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(Circulation. 1998;98:1949-1984.)
© 1998 American Heart Association, Inc.
ACC/AHA Practice Guidelines |
Guidelines for the Management of Patients With Valvular Heart Disease
Executive SummaryA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease)
Key Words: AHA Medical/Scientific Statements • valves • regurgitation • stenosis • mitral valve
I. Introduction
This executive summary and recommendations appears in the November 3, 1998, issue of Circulation. The guidelines in their entirety, including the ACC/AHA Class I, II, and III recommendations, are published in the November 1, 1998, issue of the Journal of the American College of Cardiology. Reprints of both the full text and the executive summary and recommendations are available from both organizations.
During the past 2 decades, major advances have occurred in diagnostic techniques, the understanding of natural history, and interventional cardiological and surgical procedures for patients with valvular heart disease. The information base from which to make clinical management decisions has greatly expanded in recent years, yet in many situations, management issues remain controversial or uncertain. Unlike many other forms of cardiovascular disease, there is a scarcity of large-scale multicenter trials addressing the diagnosis and treatment of valvular disease from which to derive definitive conclusions, and the literature represents primarily the experiences reported by single institutions in relatively small numbers of patients.
The Committee on Management of Patients With Valvular Disease was given the task of reviewing and compiling this information base and making recommendations for diagnostic testing, treatment, and physical activity. These guidelines follow the format established in previous American College of Cardiology/American Heart Association (ACC/AHA) guidelines for classifying indications for diagnostic and therapeutic procedures:
Class I: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective
Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment
IIa. Weight of evidence/opinion is in favor of usefulness/efficacy
IIb. Usefulness/efficacy is less well established by evidence/opinion.
Class III: Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful and in some cases may be harmful.
This task force report overlaps with several previously published ACC/AHA guidelines for cardiac imaging and diagnostic testing, including the Guidelines for Clinical Use of Cardiac Radionuclide Imaging,1 the Guidelines for the Clinical Application of Echocardiography,2 the Guidelines for Exercise Testing,3 and the Guidelines for Coronary Angiography.4 Although these guidelines are not intended to include detailed information covered in previous guidelines on the use of imaging and diagnostic testing, a discussion of the indications for these tests in the evaluation and treatment of patients with valvular heart disease is an essential component of this summary.
The committee emphasizes the fact that many factors ultimately determine the most appropriate treatment of individual patients with valvular heart disease in individual communities. These factors include the availability of diagnostic equipment and expert diagnosticians, the expertise of interventional cardiologists and surgeons, and notably the wishes of well-informed patients. Therefore, deviation from these guidelines may be appropriate in some circumstances. These guidelines are written with the assumption that a diagnostic test can be performed and interpreted with skill levels consistent with previously reported ACC training and competency statements and ACC/AHA guidelines, that interventional cardiological and surgical procedures can be performed by highly trained practitioners within acceptable safety standards, and that the resources necessary to perform these diagnostic procedures and provide this care are readily available. This is not true in all geographic areas, which further underscores the committee's position that these recommendations are guidelines and not rigid requirements.
II. General Principles
A. Evaluation of the Patient With a Cardiac Murmur
A heart murmur may have no pathological significance or may
be an important clue to the presence of valvular, congenital,
or other structural abnormalities of the heart. Most systolic
heart murmurs do not signify cardiac disease, and many are related to
physiological increases in blood flow velocity. In
other instances, a heart murmur may be an important clue to the
diagnosis of undetected cardiac disease that may be important even when
asymptomatic or that may define the reason for cardiac
symptoms. In these situations, various noninvasive or invasive cardiac
tests may be necessary to establish a firm diagnosis and form the basis
for rational treatment of an underlying disorder. Two-dimensional (2-D)
and Doppler echocardiography is particularly
useful in this regard. Diastolic murmurs virtually always
represent pathological conditions and require further cardiac
evaluation, as do most continuous murmurs. Continuous "innocent"
murmurs include venous hums and mammary soufflés.
An important consideration in a patient with a cardiac murmur is the presence or absence of symptoms. Many asymptomatic children and young adults with grade 2/6 midsystolic murmurs and no other cardiac physical findings need no further cardiac workup after the initial history and physical examination. A particularly important group is the large number of asymptomatic elderly patients, many with systemic hypertension, who have midsystolic murmurs related to sclerotic aortic valve leaflets, flow into tortuous, noncompliant great vessels, or a combination of these. Such murmurs must be distinguished from murmurs caused by mild to severe valvular aortic stenosis (AS), which is prevalent in this age group.
Although echocardiography usually provides more specific and often quantitative information about the significance of a heart murmur and may be the only test needed, the electrocardiogram (ECG) and chest x-ray are readily available and may have already been obtained. The absence of ventricular hypertrophy, atrial abnormality, arrhythmias, conduction abnormalities, prior myocardial infarction, and evidence of active ischemia on the ECG provides useful negative information at a relatively low cost. Abnormal findings on the ECG such as ventricular hypertrophy or a prior infarction should lead to a more extensive evaluation, including 2-D and Doppler echocardiography.
Echocardiography
Echocardiography is an important noninvasive
method for assessing the significance of cardiac murmurs. 2-D
echocardiography may indicate abnormal
valvular motion and morphology but usually does not indicate
the severity of valvular stenosis or
regurgitation except in mitral stenosis (MS).
Doppler echocardiography identifies increased
velocity of flow across stenotic valves from which the severity
of stenosis may be determined. The presence of an abnormal
regurgitant jet on Doppler color flow imaging indicates
valvular regurgitation and provides
semiquantitative information about its severity.
Although 2-D echocardiography and color flow Doppler imaging can provide important information on patients with cardiac murmurs, these tests are not necessary for all patients with cardiac murmurs and usually add little but expense in the evaluation of asymptomatic patients with short grade 1 to 2 midsystolic murmurs and otherwise normal physical findings. Alternatively, if the diagnosis is still questionable after transthoracic echocardiography, transesophageal echocardiography or cardiac catheterization may be appropriate. Many recent studies indicate that Doppler ultrasound devices are very sensitive and may detect valvular regurgitation through the tricuspid and pulmonic valves in a large percentage of healthy subjects and through left-sided valves (particularly the mitral) in a variable but lower percentage.
General recommendations for performing 2-D and Doppler
echocardiography in asymptomatic and
symptomatic patients with heart murmurs follow. Of course,
individual exceptions to these indications may exist.
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There are very few data addressing the cost-effectiveness of various approaches to the patient undergoing medical evaluation of a cardiac murmur. Optimal auscultation by well-trained examiners who can recognize an insignificant midsystolic murmur with confidence results in less frequent use of expensive additional testing to define murmurs that do not indicate cardiac pathology.
Many murmurs in asymptomatic adults are innocent and have no functional significance. Such murmurs have the following characteristics: (1) grade 1 to 2 intensity at the left sternal border, (2) a systolic ejection pattern, (3) normal intensity and splitting of the second heart sound, (4) no other abnormal sounds or murmurs, and (5) no evidence of ventricular hypertrophy or dilatation and the absence of increased murmur intensity with the Valsalva maneuver. Such murmurs are especially common in high-output states such as pregnancy.
In the evaluation of heart murmurs, the purposes of echocardiography are to (1) define the primary lesion in terms of etiology and severity, (2) define hemodynamics, (3) define coexisting abnormalities, (4) detect secondary lesions, (5) evaluate cardiac chamber size and function, (6) establish a reference point for future comparisons, and (7) reevaluate the patient after an intervention.
B. Endocarditis and Rheumatic Fever Prophylaxis
1. Endocarditis Prophylaxis
Endocarditis is a serious illness associated with significant
mortality. Its prevention by appropriate administration of antibiotics
before procedures expected to produce bacteremia merits serious
consideration. Several issues must be considered in generating
recommendations for endocarditis prophylaxis. It has been suggested
that the risk of endocarditis in patients with preexisting cardiac
disorders be classified as relatively high risk, moderate risk, and low
or negligible risk, as determined by the cardiac disorder. Guidelines
for the prevention of endocarditis have been issued by the American
Heart Association,5 and the current committee
endorses those guidelines, with the following comments:
This committee recommends prophylaxis in hypertrophic
cardiomyopathy only when there is latent or resting
obstruction.
Patients with mitral valve prolapse (MVP) without
regurgitation require additional clinical judgment.
Indications for antibiotic prophylaxis in MVP are discussed in section
III.D. Patients who do not have mitral regurgitation (MR) but do have
echocardiographic evidence of thickening and/or
redundancy of the valve leaflets and especially men 
45 years may be
at increased risk for bacterial endocarditis.5
Additionally, approximately one third of patients with MVP without MR
at rest may have exercise-induced MR. Some patients may exhibit MR at
rest on 1 occasion and none on others. There are no data available to
address this latter issue, and at present, the decision must be
left to clinical judgment, taking into account the nature of the
invasive procedure, the previous history of endocarditis, and the
presence or absence of valve thickening and/or redundancy.
In patients with echocardiographic evidence
of physiological MR in the absence of a murmur and
with structurally normal valves, prophylaxis is not recommended. The
committee also does not recommend prophylaxis for
physiological tricuspid and pulmonary
regurgitation detected by Doppler in the absence of
a murmur, as such findings occur in a large number of normal
individuals and the risk of endocarditis is extremely low.
Recommendations regarding Doppler
echocardiography for purposes of antibiotic
prophylaxis in patients who have received anorectic drugs are given in
section III.H. of these guidelines.
Various dental and/or surgical procedures are associated with varying degrees and frequencies of bacteremia. Recommendations for endocarditis prophylaxis, as determined by the dental and/or surgical procedure, are provided in full in the AHA recommendations for prevention of bacterial endocarditis5 and the full text of these guidelines.
2. Rheumatic Fever Prophylaxis
Rheumatic fever is an important cause of valvular heart
disease worldwide. In the United States (and Western Europe), cases of
acute rheumatic fever have been uncommon since the 1970s. However,
starting in 1987, an increase in cases has been observed.
Patients who have had an episode of rheumatic fever are at high risk of developing recurrent episodes of acute rheumatic fever. Patients who develop carditis are especially prone to similar episodes with subsequent attacks. Thus, secondary prevention of subsequent rheumatic fever recurrences is of great importance. Continuous antimicrobial prophylaxis has been shown to be effective. Anyone who has had rheumatic fever with or without carditis (including MS) should have prophylaxis for recurrent rheumatic fever. Lifelong prophylaxis is recommended for patients who have had carditis and residual valve disease and are likely to come in contact with populations with a high prevalence of streptococcal infections, such as teachers and day-care workers. Guidelines for primary and secondary prevention have been published by the AHA6 and are reproduced in the full text of these guidelines.
III. Specific Valve Lesions
A. Aortic Stenosis
Grading the Degree of Stenosis
The aortic valve area must be reduced to one fourth its
normal size before significant changes in the circulation occur.
Because the normal adult valve orifice is 
3.0 to 4.0
cm2, an area 0.75 to 1.0
cm2 is usually not considered severe AS. In large
patients, a valve area of 1.0 cm2 may be severely
stenotic, whereas a valve area of 0.7 cm2
may be adequate for a smaller patient.
The committee used a variety of hemodynamic and natural
history data to grade the degree of AS as mild (area >1.5
cm2), moderate (area >1.0 to 1.5
cm2), or severe (area
1.0cm2). When stenosis is
severe and cardiac output is normal, the mean transvalvular
pressure gradient is generally >50 mm Hg. Some patients with
severe AS remain asymptomatic, whereas others with only
moderate stenosis develop symptoms. Therapeutic decisions,
particularly those related to corrective surgery, are based largely on
the presence or absence of symptoms. Thus, the absolute valve area (or
transvalvular pressure gradient) is not usually the primary
determinant of the need for aortic valve replacement (AVR).
An ejection systolic murmur may be heard in the presence of a normal valve, one that is thickened and minimally calcified, and one that is stenotic. The 3 conditions must be distinguished.
Natural History
The natural history of AS in the adult consists of a
prolonged latent period in which morbidity and mortality are very low.
The rate of progression of the stenotic lesion has been
estimated in a variety of hemodynamic studies performed
largely in patients with moderate AS. Cardiac
catheterization and Doppler
echocardiographic studies indicate that some patients
exhibit a decrease in valve area of 0.1 to 0.3
cm2 per year; the average rate of change is
0.12 cm2 per year. The systolic
pressure gradient across the valve may increase by as much as 10 to
15 mm Hg per year. However, more than half of the reported
patients showed little or no progression over a 3- to 9-year period.
Although it appears that progression of AS can be more rapid in
patients with degenerative calcific disease than in those with
congenital or rheumatic disease, it is not possible to predict the rate
of progression in an individual patient.
Eventually, symptoms of angina, syncope, or heart failure develop after a long latent period, and the outlook changes dramatically. After onset of symptoms, average survival is <2 to 3 years. Thus, the development of symptoms identifies a critical point in the natural history of AS.
Many asymptomatic patients with severe AS develop symptoms
within a few years and require surgery. The incidence of angina,
dyspnea, or syncope in asymptomatic patients with
Doppler outflow velocities 4 m/s has been reported to be as high
as 38% after 2 years and 79% after 3 years. Therefore, patients with
severe AS require careful monitoring for development of symptoms and
progressive disease.
Sudden death is known to occur in patients with severe AS but has rarely been documented to occur without prior symptoms. Recent prospective echocardiographic studies provide important data on the rarity of sudden death in asymptomatic patients. Although sudden death does occasionally occur in the absence of preceding symptoms in patients with AS, it must be an uncommon event—probably <1% per year.
Management of the Asymptomatic Patient
Patients with the physical findings of AS should undergo selected
laboratory examinations, including an ECG, a chest x-ray, and an
echocardiogram. The 2-D echocardiogram is valuable for confirming the
presence of aortic valve disease and determining left ventricular (LV)
size and function, degree of hypertrophy, and presence of
other associated valve disease. In most patients, the severity of the
stenotic lesion can be defined with Doppler
echocardiographic measurements of a mean
transvalvular pressure gradient and a derived valve area as
discussed in the ACC/AHA Guidelines for the Clinical Application of
Echocardiography.2
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In some patients, it may be necessary to proceed with cardiac catheterization and coronary angiography at the time of initial evaluation. This is appropriate, for example, if there is a discrepancy between the clinical and echocardiographic examinations or if the patient is symptomatic and AVR is planned.
Exercise testing in adults with AS has been discouraged largely because of concerns about safety. Furthermore, when used to assess the presence or absence of coronary artery disease (CAD), the test has limited diagnostic accuracy. Certainly, exercise testing should not be performed in symptomatic patients. However, in asymptomatic patients, exercise testing is safe and may provide information not uncovered during the initial clinical evaluation. Exercise testing in asymptomatic patients should be performed only under the supervision of an experienced physician, with close monitoring of blood pressure and the ECG. Such testing can identify patients who have a limited exercise capacity or even exercise-induced symptoms despite a negative medical history. An abnormal hemodynamic response (eg, hypotension) in a patient with severe AS is sufficient reason to consider AVR.
The frequency of follow-up visits to the physician depends on the severity of valvular stenosis and in part on the presence of comorbid conditions. Recognizing that an optimal schedule for repeated medical examinations has not been defined, many physicians perform an annual history and physical examination on patients with mild AS. Those with moderate and severe AS should be examined more frequently. Patients should be advised to promptly report the development of any exertional chest discomfort, dyspnea, lightheadedness, or syncope.
Echocardiographic studies can be an important part of an integrated approach to the asymptomatic patient. Current understanding of the natural history of AS and indications for surgical intervention do not support the use of annual echocardiographic studies to assess changes in valve area. However, serial echocardiograms are helpful for assessing changes in LV hypertrophy and function. Therefore, in patients with severe AS, a yearly echocardiogram may be appropriate. In patients with moderate AS, serial studies every 2 years or so are satisfactory, and in patients with mild AS, serial studies can be performed every 5 years. Echocardiography should be performed more frequently if there is a change in clinical findings.
Recommendations for activity are based on the clinical examination, with special emphasis on the hemodynamic severity of the stenotic lesion. Recommendations regarding participation in competitive athletics have been published by the Task Force on Acquired Valvular Heart Disease of the 26th Bethesda Conference.7 Patients with severe AS should be advised to limit activity to relatively low levels.
Indications for Cardiac Catheterization
In patients with AS, the indications for cardiac
catheterization and angiography are to assess the
coronary circulation and confirm or clarify the clinical
diagnosis. In preparation for AVR, coronary angiography is
indicated in patients suspected of having CAD, as discussed in section
VIII. If the clinical and echocardiographic data are
typical of severe isolated AS, coronary angiography may be all
that is needed before AVR. Complete left- and right-heart
catheterization may be necessary to assess the
hemodynamic severity of AS if there is a discrepancy
between clinical and echocardiographic data or evidence
of associated valvular or congenital disease or
pulmonary hypertension.
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The pressure gradient across a stenotic valve is related to the valve orifice area and transvalvular flow. Thus, in the presence of depressed cardiac output, relatively low pressure gradients are frequently obtained in patients with severe AS. On the other hand, during exercise or other high-flow states, systolic gradients can be measured in minimally stenotic valves. For these reasons, complete assessment of AS requires (1) measurement of transvalvular flow, (2) determination of the transvalvular pressure gradient, and (3) calculation of the effective valve area. Careful attention to detail with accurate measurements of pressure and flow is important, especially in patients with low cardiac output or a low transvalvular pressure gradient.
Patients with severe AS and low cardiac output often present with only modest transvalvular pressure gradients (ie, <30 mm Hg). Such patients can be difficult to distinguish from those with low cardiac output and only mild to moderate AS. In both situations, the low-flow state and low pressure gradient contribute to a calculated effective valve area that can meet criteria for severe AS. The standard valve area formula is less accurate and is known to underestimate the valve area in low-flow states; under such conditions, it should be interpreted with caution. Although valve resistance is less sensitive to flow than valve area, resistance calculations have not been proved to be substantially better than valve area calculations.
In patients with low gradient stenosis and what appears to be moderate to severe AS, it may be useful to determine the transvalvular pressure gradient and calculate valve area and resistance during a baseline state and again during exercise or pharmacological (ie, dobutamine infusion) stress. Patients who do not have true, anatomically severe stenosis exhibit an increase in the valve area during an increase in cardiac output. In patients with severe AS, these changes may result in a calculated valve area that is higher than the baseline calculation but that remains in the severe range, whereas in patients without severe AS, the calculated valve area will fall outside the severe range with administration of dobutamine and indicate that severe AS is not present.
Indications for Aortic Valve Replacement
In the vast majority of adults, AVR is the only effective
treatment for severe AS. However, younger patients may be candidates
for valvotomy (see section VI.A.).
1. Symptomatic Patients.
Patients with angina, dyspnea, or syncope exhibit
symptomatic improvement and an increase in survival after
AVR. Outcome is similar in patients with normal LV function and those
with moderate depression of contractile function. The depressed
ejection fraction in many patients in this latter group is caused by
excessive afterload (afterload mismatch), and LV function improves
after AVR in such patients. If LV dysfunction is not caused by
afterload mismatch, then improvement in LV function and resolution of
symptoms may not be complete after valve replacement. Survival is still
improved in this setting with the possible exception of patients with
severe LV dysfunction caused by CAD. Therefore, in the absence of
serious comorbid conditions, AVR is indicated in virtually all
symptomatic patients with severe AS. However, patients with
severe LV dysfunction, particularly those with so-called low gradient
AS, represent a difficult management decision (see above). AVR
should not be performed in such patients when they do not have
anatomically severe stenosis. In patients with severe AS, even
those with a low transvalvular pressure gradient, AVR results
in hemodynamic improvement and better functional
status.
2. Asymptomatic Patients.
Management decisions in asymptomatic patients are more
controversial. The combined risk of surgery and late complications of a
prosthesis generally exceed the possibility of preventing
sudden death and prolonging survival in all asymptomatic
patients, as discussed previously. Despite these considerations, some
difference of opinion persists regarding indications for AVR in
asymptomatic patients. It is reasonable to attempt to
identify patients who may be at especially high risk of sudden death
without surgery, although data supporting this approach are limited.
Patients in this subgroup include those with an abnormal response to
exercise (eg, hypotension), LV systolic dysfunction or
marked/excessive LV hypertrophy, or evidence of severe AS.
However, it should be recognized that such "high-risk" patients are
rarely asymptomatic.
3. Patients Undergoing Coronary Artery Bypass Surgery.
Patients with severe AS, with or without symptoms, who
are undergoing coronary artery bypass surgery should undergo
AVR at the time of revascularization. Similarly,
patients with severe AS undergoing surgery on other valves (such as
mitral valve repair) or the aortic root should also undergo AVR as part
of the surgical procedure. Patients with moderate AS (for example,
gradient 30 mm Hg) may warrant AVR at the time of
coronary artery bypass surgery or surgery on the mitral valve
or aortic root. However, controversy persists regarding indications for
concomitant AVR at the time of coronary artery bypass surgery
in patients with milder forms of AS as discussed in section
VIII.D.
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Aortic Balloon Valvotomy
Percutaneous balloon aortic valvotomy has an
important role in treatment of adolescents and young adults with AS
(see section VI.A.) but a very limited role in older adults. Immediate
hemodynamic results include a moderate reduction in the
transvalvular pressure gradient, but the postvalvotomy
valve area is rarely >1.0 cm2. However, serious
complications occur with a frequency of >10%, and restenosis
and clinical deterioration occur within 6 to 12 months in most
patients. Therefore, in adults with AS, balloon valvotomy is not a
substitute for AVR.
Balloon valvotomy can play a temporary role in the management of some
symptomatic patients who are not initially candidates for
AVR. For example, patients with severe AS and refractory
pulmonary edema or cardiogenic shock may benefit from aortic
valvuloplasty as a "bridge" to surgery; an improved
hemodynamic state may reduce the risks of AVR.
Indications for palliative valvotomy in patients with serious comorbid
conditions are less well established, but most patients can expect
temporary relief of symptoms despite a very limited life expectancy.
Asymptomatic patients with severe AS who require urgent
noncardiac surgery may be candidates for valvotomy, but most such
patients can be successfully treated with more conservative
measures.
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Special Considerations in the Elderly
Because there is no effective medical therapy and balloon
valvotomy is not an acceptable alternative to surgery, AVR must be
considered in all elderly patients who have symptoms caused by AS. AVR
is technically possible at any age, but the decision to proceed with
such surgery depends on many factors, including the patient's wishes
and expectations.
In addition to the confounding effects of CAD and the potential for stroke, other considerations are specific to older patients. For example, a narrow LV outflow tract and small aortic annulus sometimes present in elderly women may require enlargement of the annulus. Heavy calcification of the valve, annulus, and aortic root may require debridement. Occasionally, a composite valve-aortic graft is needed. Excessive or inappropriate hypertrophy associated with valvular stenosis can be a marker for perioperative morbidity and mortality. Preoperative recognition of elderly patients with marked LV hypertrophy followed by appropriate perioperative management may substantially reduce this morbidity and mortality.
B. Aortic Regurgitation
1. Acute Aortic Regurgitation
In acute severe aortic regurgitation (AR), the
sudden large regurgitant volume is imposed on a left ventricle of
normal size that has not had time to accommodate to the volume
overload. LV end-diastolic and left atrial pressures may
increase rapidly and dramatically. The Frank-Starling mechanism is
used, but the inability of the ventricle to develop compensatory
chamber dilatation acutely results in a decrease in forward stroke
volume. Although tachycardia develops as a compensatory
mechanism to maintain cardiac output, this is often insufficient.
Hence, patients frequently present with pulmonary edema
and/or cardiogenic shock.
Diagnosis
Many of the characteristic physical findings of chronic AR are
modified or absent when valvular regurgitation
is acute, which may lead to underestimation of its severity.
Echocardiography is indispensable in confirming the
presence and severity of valvular
regurgitation, determining its etiology, estimating the
degree of pulmonary hypertension (if tricuspid
regurgitation [TR] is present), and determining
whether there is rapid equilibration of aortic and LV
diastolic pressure. Evidence for rapid pressure
equilibration includes short AR diastolic half-time (<300
ms), short mitral deceleration time (<150 ms), or premature closure of
the mitral valve.
Acute AR caused by aortic root dissection is a surgical emergency that requires prompt identification and management. Transesophageal echocardiography is indicated when aortic dissection is suspected. If the diagnosis remains uncertain, cardiac catheterization and aortography should be performed. Coronary angiography is an important component of the evaluation of aortic dissection and acute AR and should be performed, provided that it does not delay urgent surgery.
Treatment
Death from pulmonary edema, ventricular
arrhythmias, electromechanical dissociation, or circulatory
collapse is common in acute severe AR, even with intensive medical
management. Early surgical intervention is recommended. Nitroprusside
and possibly inotropic agents such as dopamine or
dobutamine to augment forward flow and reduce LV
end-diastolic pressure may be helpful to treat the patient
temporarily before surgery. Intra-aortic balloon counterpulsation is
contraindicated. Although ß-blockers are often used in treating
aortic dissection, they should be used cautiously, if at all, in the
setting of acute AR because they will block compensatory
tachycardia.
2. Chronic Aortic Regurgitation
Chronic AR represents a condition of combined volume
overload and pressure overload. As the disease progresses, recruitment
of preload reserve and compensatory hypertrophy permit the
ventricle to maintain normal ejection performance despite the
elevated afterload. The majority of patients remain
asymptomatic throughout this compensated phase, which may
last for decades. Vasodilator therapy has the potential to reduce the
hemodynamic burden in such patients.
For the purposes of subsequent discussion, patients with normal LV systolic function are defined as those with normal LV ejection fraction at rest. It is recognized that overall LV function is usually not "normal" in chronic severe AR and that the hemodynamic abnormalities noted above may be considerable. It is also recognized that the transition to LV systolic dysfunction represents a continuum and that no single hemodynamic measurement represents the absolute boundary between normal LV systolic function and LV systolic dysfunction.
The balance between afterload excess, preload reserve, and hypertrophy cannot be maintained indefinitely in many patients, and afterload mismatch and/or depressed contractility ultimately result in a reduction in ejection fraction, first into the low normal range and then below normal. At this point in the natural history, patients often develop dyspnea, which is related to declining systolic function or elevated filling pressures. However, this transition may be much more insidious, and it is possible for patients to remain asymptomatic until severe LV dysfunction has developed.
LV systolic dysfunction (defined as an ejection fraction below normal at rest) is initially a reversible phenomenon predominantly related to afterload excess, and full recovery of LV size and function is possible with AVR. With time, during which the ventricle develops progressive chamber enlargement and a more spherical geometry, depressed myocardial contractility predominates over excessive loading as the cause of progressive systolic dysfunction. This can progress to the extent that the full benefit of surgical correction of the regurgitant lesion in terms of recovery of LV function and improved survival can no longer be achieved.
A large number of studies have identified LV systolic function and end-systolic size as the most important determinants of survival and postoperative LV function in patients undergoing AVR for chronic AR.
Several factors are associated with worse functional and survival results after AVR for chronic AR in patients with preoperative LV systolic dysfunction. These include severity of symptoms, the severity of LV systolic dysfunction, and the duration of preoperative systolic dysfunction. Taken together, these observations support the recommendation that patients with evidence of LV systolic dysfunction, even if asymptomatic or minimally symptomatic, should undergo AVR before more severe symptoms or more severe ventricular dysfunction develop.
Natural History
1. Asymptomatic Patients With Normal Left
Ventricular Function.
The current recommendations are derived from 7 published series
involving a total of 490 patients with a mean follow-up period of 6.4
years. The rate of progression to symptoms and/or LV systolic
dysfunction averaged 4.3% per year. Sudden death occurred in 6 of the
490 patients, an average mortality rate of <0.2% per year. Six of the
7 studies reported the rate of development of
asymptomatic LV dysfunction; 36 of a total of 463 patients
developed depressed systolic function at rest without symptoms
during a mean 5.9-year follow-up period, a rate of 1.3% per year.
2. Asymptomatic Patients With Depressed
Systolic Function.
The limited data in asymptomatic patients with
depressed LV ejection fraction indicate that the majority develop
symptoms warranting surgery within 2 to 3 years. The average rate of
symptom onset in such patients is >25% per year.
3. Symptomatic Patients.
There are no recent large-scale studies of the natural history of
symptomatic patients with chronic AR, because the onset of
angina or significant dyspnea is usually an indication for valve
replacement. Data from the presurgical era indicate that
symptomatic patients have a poor outcome with medical
therapy, which is analogous to that of patients with
symptomatic AS, with mortality rates of >10% per year in
patients with angina pectoris and >20% per year in those with heart
failure.
Diagnosis and Initial Evaluation of the
Asymptomatic Patient
The diagnosis of chronic severe AR can usually be made on
the basis of physical examination. The chest x-ray and ECG are helpful
in evaluating overall heart size and rhythm, evidence of LV
hypertrophy, and evidence of conduction disorders.
Echocardiography is indicated to confirm the
diagnosis of AR if there is an equivocal diagnosis based on physical
examination; assess the cause of AR as well as valve morphology;
provide a semiquantitative estimate of severity of
regurgitation; assess LV dimension, mass, and
systolic function; and assess aortic root size. In
asymptomatic patients with preserved systolic
function, these initial measurements represent the baseline
information with which future serial measurements can be
compared.
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If the patient is asymptomatic and leads an active lifestyle and the echocardiogram is of good quality, no other testing is necessary. If the patient has severe AR and is sedentary or has equivocal symptoms, exercise testing is helpful to assess functional capacity, symptomatic responses, and hemodynamic effects of exercise. If the echocardiogram is of insufficient quality to assess LV function, radionuclide angiography should be used in asymptomatic patients to measure LV ejection fraction at rest and estimate LV volumes. When patients are symptomatic on initial evaluation, it is reasonable to proceed directly with cardiac catheterization and angiography if the echocardiogram is of insufficient quality to assess LV function or severity of AR.
The exercise ejection fraction and change in ejection fraction
from rest to exercise are often abnormal, even in
asymptomatic patients. However, these have not been proved
to have independent diagnostic or prognostic value when LV
function at rest and severity of LV volume overload by
echocardiography are already known.
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Asymptomatic patients with normal LV systolic function may participate in all forms of normal daily physical activity, including mild-intensity forms of exercise and in some cases competitive athletics. Isometric exercise should be avoided. Recommendations for participation in competitive athletics were published by the Task Force on Acquired Valvular Heart Disease of the 26th Bethesda Conference.7
Medical Therapy
Therapy with vasodilating agents is designed to improve forward
stroke volume and reduce regurgitant volume. These effects should
translate into reductions in LV end-diastolic volume, wall
stress, and afterload, resulting in preservation of LV systolic
function and reduction in LV mass. These effects have been observed in
small numbers of patients who received oral therapy with
hydralazine and nifedipine for 1 to 2 years. Less
consistent results have been reported with
angiotensin converting enzyme (ACE) inhibitors,
depending on the degree of reduction in arterial pressure
and end-diastolic volume.
Only 1 study, in which long-acting nifedipine was compared with digoxin therapy in 143 patients followed up for 6 years, has evaluated whether vasodilating therapy alters the long-term natural history of chronic asymptomatic AR in a favorable manner. Over 6 years, long-acting nifedipine reduced the need for valve replacement from 34% to 15%. Moreover, when patients who received nifedipine did undergo AVR because of symptoms or impaired systolic function, all survived surgery, and LV size and function improved considerably in all patients.
The goal of vasodilator therapy is to reduce systolic blood pressure. Drug dosage should be increased until there is a measurable decrease in systolic blood pressure or the patient develops side effects. It is rarely possible to decrease systolic blood pressure to normal because of the increased LV stroke volume, and drug dosage should not be increased excessively in an attempt to achieve this goal. Vasodilator therapy is of unknown benefit and is not indicated in patients with normal blood pressure and/or normal cavity size.
Vasodilator therapy is not recommended for
asymptomatic patients with mild AR and normal LV function
in the absence of systemic hypertension, as these patients have an
excellent outcome with no therapy. Vasodilator therapy is not an
alternative to surgery for asymptomatic or
symptomatic patients with severe AR and LV systolic
dysfunction. Whether symptomatic patients who have
preserved systolic function can be safely treated with
aggressive medical management and whether aggressive medical management
is as good or better than AVR have not been determined. It is
recommended that symptomatic patients undergo surgery
rather than long-term medical therapy.
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Serial Testing
In general, the stability and chronicity of the regurgitant lesion
and the LV response to the volume load must be established when the
patient first presents to the physician, especially if AR is
moderate to severe. If the chronic nature of the lesion is uncertain
and the patient does not present initially with 1 or more
indications for surgery, the physical examination and echocardiogram
should be repeated 2 to 3 months after the initial evaluation to ensure
that a subacute process with rapid progression is not under way.
Once the chronicity and stability of the process have been established,
the frequency of clinical reevaluation and repeat noninvasive testing
depends on severity of valvular regurgitation,
degree of LV dilatation, level of systolic function, and
whether previous serial studies have revealed progressive changes in LV
size or function. In most patients, serial testing during the long-term
follow-up period should include a detailed history, physical
examination, and echocardiography. Serial chest
x-rays and ECGs are of less value but are helpful in selected
patients.
Asymptomatic patients with mild AR, little or no LV dilatation, and normal LV systolic function can be seen on a yearly basis with instructions to alert the physician if symptoms develop in the interim. Yearly echocardiography is not necessary unless there is clinical evidence that regurgitation has worsened. Routine echocardiography can be performed every 2 to 3 years in such patients.
Asymptomatic patients with normal systolic function but severe AR and significant LV dilatation (end-diastolic dimension >60 mm) require more frequent and careful reevaluation, with a history and physical examination every 6 months and echocardiography every 6 to 12 months, depending on severity of dilatation and stability of measurements. If the patient's condition is stable, echocardiographic measurements are not required more frequently than every 12 months. It is reasonable to obtain serial echocardiograms as often as every 4 to 6 months in patients with more advanced LV dilatation (end-diastolic dimension >70 mm or end-systolic dimension >50 mm) for whom the risk of developing symptoms or LV dysfunction ranges from 10% to 20% per year. Serial chest x-rays and ECGs are of less value but are helpful in selected patients.
Chronic AR may develop from disease processes involving the proximal ascending aorta. In patients with aortic root dilatation, serial echocardiograms are indicated to evaluate aortic root size as well as LV size and function.
Repeat echocardiograms are also recommended when the patient has onset of symptoms, there is an equivocal history of changing symptoms or exercise tolerance, or there are clinical findings suggesting worsening regurgitation or progressive LV dilatation. Patients with echocardiographic evidence of progressive ventricular dilatation or declining systolic function have a greater likelihood of developing symptoms or LV dysfunction and should have more frequent follow-up examinations (every 6 months) than those with stable LV function.
In some centers with expertise in nuclear cardiology, serial radionuclide ventriculography to assess LV volume and function at rest may be an accurate and cost-effective alternative to serial echocardiography. However, there is no justification for routine serial testing with both echocardiography and radionuclide ventriculography. Serial radionuclide ventriculograms are also recommended in patients with suboptimal echocardiograms and when there is a discrepancy between clinical assessment and echocardiographic data. In centers with specific expertise in cardiac MRI, serial MRI may be performed in place of radionuclide angiography for the indications listed above.
Indications for Cardiac Catheterization
Cardiac catheterization is not required in
patients with chronic AR unless there are questions about the severity
of AR, hemodynamic abnormalities, or LV
systolic dysfunction despite physical examination and
noninvasive testing or unless AVR is contemplated and there is a need
to assess coronary anatomy (see section VIII).
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Hemodynamic and angiographic assessment of severity of AR and LV function may be necessary in some patients being considered for surgery when there are conflicting data between clinical assessment and noninvasive tests. Hemodynamic measurements during exercise are occasionally helpful in determining the effect of AR on LV function or in making decisions about medical or surgical therapy. In selected patients with severe AR, borderline or normal LV systolic function, and LV chamber enlargement that is approaching the threshold for operation (defined below), measurement of cardiac output and LV filling pressures at rest and during exercise with a right-heart catheter may be valuable for identifying patients with severe hemodynamic abnormalities in whom surgery is warranted.
Indications for Aortic Valve Replacement
In patients with pure chronic AR, AVR should be considered only if
AR is severe. Patients with only mild AR are not candidates for valve
replacement, and if they have symptoms or LV dysfunction, other causes
should be considered, such as CAD, hypertension, or
cardiomyopathic processes. The following discussion
applies only to those patients with pure severe AR.
1. Symptomatic Patients With Normal Left
Ventricular Systolic Function.
AVR is indicated in patients with normal systolic function
(defined as ejection fraction 0.50 at rest) who have New York Heart
Association (NYHA) functional Class III or IV symptoms or Canadian
Heart Association functional Class II to IV angina pectoris. In many
patients with NYHA functional Class II dyspnea, the cause of symptoms
is often unclear, and it may be difficult to differentiate the effects
of deconditioning or aging from true cardiac symptoms. In such
patients, exercise testing may be valuable. If the cause of these mild
symptoms is uncertain and if they are not severe enough to interfere
with the patient's lifestyle, a period of observation may be
reasonable. However, new onset of mild dyspnea has different
implications in severe AR, especially in patients with increasing LV
chamber size or evidence of declining LV systolic function into
the low normal range. Mild symptoms are an indication for AVR in such
patients.
2. Symptomatic Patients With Left
Ventricular Dysfunction.
Patients with NYHA functional Class II, III, or IV symptoms and
mild to moderate LV systolic dysfunction (ejection fraction
0.25 to 0.49) should undergo AVR. Patients with functional Class IV
symptoms have worse postoperative survival rates and lower likelihood
of recovery of systolic function than patients with less severe
symptoms, but AVR will improve ventricular loading
conditions and expedite subsequent management of LV dysfunction.
Symptomatic patients with advanced LV dysfunction (ejection fraction <0.25 and/or end-systolic dimension >60 mm) present difficult management issues, as many have developed irreversible myocardial changes. AVR should be more strongly considered in patients with NYHA functional Class II and III symptoms, especially if (1) symptoms and evidence of LV dysfunction are of recent onset and (2) intensive short-term therapy with vasodilators, diuretics, and/or intravenous positive inotropic agents results in substantial improvement in hemodynamics or systolic function. However, even in patients with NYHA functional Class IV symptoms and ejection fraction <0.25, the high risks associated with AVR and subsequent medical management of LV dysfunction are usually a better alternative than the higher risks of long-term medical management alone.
3. Asymptomatic Patients.
AVR in asymptomatic patients remains a controversial
topic, but it is generally agreed that valve replacement is indicated
in patients with LV systolic dysfunction. As noted previously,
for the purposes of these guidelines, LV systolic dysfunction
is defined as an ejection fraction below normal at rest, ie, 0.50. It
is recognized that this lower limit is technique dependent and may vary
among institutions.
Valve replacement is also recommended in patients with severe LV dilatation (end-diastolic dimension >75 mm or end-systolic dimension >55 mm), even if ejection fraction is normal. Such patients appear to represent a high-risk group with an increased incidence of sudden death, and thus far the results of valve replacement have been excellent. In contrast, postoperative mortality is considerable once patients with severe LV dilatation develop symptoms and/or LV systolic dysfunction.
Women tend to develop symptoms and/or LV dysfunction with less LV
dilatation than men; this appears to be related to body size, as these
differences are not apparent when LV dimensions are corrected for body
surface area. Hence, LV dimensions alone may be misleading in small
patients of either gender, and the threshold values of
end-diastolic and end-systolic dimension
recommended for AVR in asymptomatic patients (75 mm
and 55 mm, respectively) may need to be reduced for such patients.
There are no data from which to derive guidelines for LV dimensions
corrected for body size, and clinical judgment is required.
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Concomitant Aortic Root Disease
In addition to causing acute AR, diseases of the proximal aorta
may also contribute to chronic AR. If AR is mild and/or the left
ventricle is only mildly dilated, management should focus on treating
the underlying aortic root disease, which is beyond the scope of these
guidelines. However, in many patients, AR may be severe, in which case
decisions about medical therapy and timing of surgery must take into
account both conditions. In general, AVR and aortic root reconstruction
are indicated in patients with disease of the proximal aorta and AR of
any severity when the degree of aortic root dilatation is 50 mm
by echocardiography.
Evaluation of Patients After Aortic Valve Replacement
After AVR, careful follow-up is necessary during the early and
long-term postoperative course to evaluate prosthetic valve
function and assess LV function, as discussed in detail in section
VII.C. An echocardiogram should be performed soon after surgery to
assess the results of surgery on LV size and function and to serve as a
baseline for comparison of subsequent echocardiograms. In the first few
weeks after surgery, there is little change in LV systolic
function, and ejection fraction may deteriorate, compared with
preoperative values, because of the reduced preload. A better predictor
of subsequent LV systolic function is the reduction in LV
end-diastolic dimension, which declines significantly
within the first week or two of operation. This is an excellent marker
of the functional success of AVR, as the magnitude of early reduction
in end-diastolic dimension after operation correlates with
the magnitude of late increase in ejection fraction.
Patients with persistent LV dilatation on the initial postoperative echocardiogram should receive the same treatment, including ACE inhibitors, as any other patient with symptomatic or asymptomatic LV dysfunction.
C. Mitral Stenosis
The normal mitral valve area is 4.0 to 5.0 cm2. Narrowing of the valve area to <2.5 cm2 must occur before development of symptoms.
A mitral valve area >1.5 cm2 usually does not produce symptoms at rest. However, if there is an increase in transmitral flow or a decrease in the diastolic filling period, there will be a rise in left atrial pressure and development of symptoms. Thus, the first symptoms of dyspnea in patients with mild MS are usually precipitated by exercise, emotional stress, infection, pregnancy, or atrial fibrillation with a rapid ventricular response.
Natural History
MS is a continuous, progressive, lifelong disease, usually
consisting of a slow, stable course in the early years and progressive
acceleration later in life. In developed countries, there is a long
latent period of 20 to 40 years from the occurrence of rheumatic fever
to onset of symptoms. Once symptoms develop, there is another period of
almost a decade before symptoms become disabling. Overall, the 10-year
survival of untreated patients with MS is 50% to 60%, depending on
symptoms at presentation. In the asymptomatic
or minimally symptomatic patient, survival is >80% at 10
years, with 60% of patients having no progression of symptoms.
However, once significant limiting symptoms occur, there is a dismal
10-year survival rate of 0% to 15%, and when there is severe
pulmonary hypertension, mean survival drops to <3 years.
Mortality of untreated patients with MS is caused by progressive heart
failure in 60% to 70%, systemic embolism in 20% to 30%,
pulmonary embolism in 10%, and infection in 1% to 5%.
Evaluation and Management of the Asymptomatic Patient
The diagnosis of MS should be based on the history, physical
examination, chest x-ray, and ECG. The diagnostic tool of
choice in the evaluation of a patient with MS is 2-D and Doppler
echocardiography. The morphological appearance of
the mitral valve apparatus should be assessed by 2-D
echocardiography, including leaflet mobility,
leaflet thickness, leaflet calcification, subvalvular fusion,
and appearance of the commissures. These features may be important when
considering the timing and type of intervention to be performed.
Chamber size and function as well as other structural valvular,
myocardial, or pericardial abnormalities should also be assessed.
The hemodynamic severity of the obstruction
should be assessed with Doppler
echocardiography. The mean transmitral gradient can
be accurately and reproducibly measured from the continuous wave
Doppler signal across the mitral valve with the modified Bernoulli
equation, and the mitral valve area can be noninvasively measured by
either the diastolic half-time method or the continuity
equation. The half-time method may be inaccurate in patients with
abnormalities of left atrial or LV compliance, those with associated
AR, and those with previous mitral valvotomy. Doppler
echocardiography should also be used when possible
to estimate pulmonary artery systolic pressure from the
TR velocity signal and assess severity of concomitant MR or AR. Formal
hemodynamic exercise testing can be done noninvasively
by either a supine bicycle or upright treadmill with Doppler
recordings of transmitral and tricuspid velocities. This allows
measurement of both the transmitral gradient and pulmonary
artery systolic pressure at rest and with exercise.
Dobutamine stress testing with Doppler
recordings may also be performed.
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In the asymptomatic patient who has documented mild MS (valve area >1.5 cm2 and mean gradient <5 mm Hg), no further evaluation is needed on the initial workup. These patients usually remain stable for many years. If MS is more significant, further evaluation should be considered if the mitral valve morphology appears to be suitable for mitral valvotomy with pliable, noncalcified valves with little or no subvalvular fusion and no calcification in the commissures. Patients with moderate pulmonary hypertension at rest (pulmonary artery systolic pressure >50 mm Hg) and pliable mitral valve leaflets may be considered for percutaneous mitral valvotomy even if they deny symptoms. In patients who lead a sedentary lifestyle, a hemodynamic exercise test with Doppler echocardiography is useful. Objective limitation of exercise tolerance with a rise in transmitral gradient >15 mm Hg and pulmonary artery systolic pressure >60 mm Hg may be an indication to consider percutaneous valvotomy if mitral valve morphology is suitable.
All patients should be informed that any change in symptoms warrants reevaluation. In the asymptomatic patient, yearly reevaluation is recommended; at this time, a history, physical examination, chest x-ray, and ECG should be obtained. A yearly echocardiogram is not recommended unless there is a change in clinical status. Ambulatory ECG monitoring to detect paroxysmal atrial fibrillation is indicated in patients with palpitations.
Medical Therapy
1. General Principles.
Because MS is primarily caused by rheumatic fever, prophylaxis against
rheumatic fever is recommended. Appropriate endocarditis prophylaxis is
also recommended. Patients who have more than a mild degree of MS
should be counseled to avoid unusual physical stresses. Agents with
negative chronotropic properties, such as ß-blockers or calcium
channel blockers, may be of benefit in patients with sinus rhythm who
have exertional symptoms if the symptoms occur with high heart rates.
Salt restriction and intermittent administration of a diuretic
are useful if there is evidence of pulmonary vascular
congestion. Digitalis does not benefit patients with MS in sinus rhythm
unless there is left and/or right ventricular
dysfunction.
2. Atrial Fibrillation.
Atrial fibrillation develops in 30% to 40% of patients with
symptomatic MS. Significant hemodynamic
consequences may result from acute development of atrial fibrillation,
with loss of atrial contribution to LV filling, and from the rapid
ventricular rate. Atrial fibrillation occurs more commonly
in older patients and is associated with a poorer prognosis, with a
10-year survival rate of 25% compared with 46% in patients who remain
in sinus rhythm. The risk of arterial embolization,
especially stroke, is significantly increased in patients with atrial
fibrillation. Treatment of an acute episode of rapid atrial
fibrillation consists of anticoagulation with heparin and control of
the heart rate response. Intravenous digoxin, calcium
channel blockers, or ß-blockers should be used to control
ventricular response. If there is
hemodynamic instability, electrical cardioversion
should be undertaken urgently, with intravenous heparin
before, during, and after the procedure. Patients who have been in
atrial fibrillation >24 to 48 hours without anticoagulation are
at an increased risk for embolic events after cardioversion, but
patients may also have an embolic event with <24 hours of atrial
fibrillation. The decision to proceed with elective cardioversion
depends on multiple factors, including duration of atrial fibrillation,
hemodynamic response to onset of atrial fibrillation,
documented history of prior episodes of atrial fibrillation, and
history of prior embolic events. If the decision has been made to
proceed with elective cardioversion in a patient who has had documented
atrial fibrillation for >24 to 48 hours and who has not been on
long-term anticoagulation, 1 of 2 approaches is recommended, based on
data from patients with nonrheumatic atrial fibrillation. The first is
anticoagulation with warfarin for 3 weeks, followed by elective
cardioversion. The second is anticoagulation with heparin and
transesophageal echocardiography to
look for left atrial thrombus. In the absence of left atrial thrombus,
cardioversion is performed with intravenous heparin before,
during, and after the procedure. It is important to continue
anticoagulation after cardioversion to prevent thrombus formation
caused by atrial mechanical inactivity and to then maintain the patient
on long-term warfarin unless there is a strong contraindication to
anticoagulation. Controversy surrounds whether
percutaneous mitral valvotomy should be performed in
patients with new-onset atrial fibrillation and moderate to severe MS
who are otherwise asymptomatic.
3. Prevention of Systemic Embolization.
Systemic embolization may occur in 10% to 20% of patients with MS.
The risk of embolization is related to age, the presence of atrial
fibrillation, and history of previous embolic events. One third of
embolic events occur 1 month after onset of atrial fibrillation, and
two thirds occur within 1 year. The frequency of embolic events does
not seem to be related to severity of MS, cardiac output, size of left
atrium, or presence of symptoms. An embolic event may thus be the
initial manifestation of MS. In patients who have experienced an
embolic event, the frequency of recurrence is as high as 15 to
40 events per 100 patient months. There are no data to support the
concept that oral anticoagulation is beneficial in patients with MS who
have not had atrial fibrillation or an embolic event. It is
controversial whether patients who have not had atrial fibrillation or
an embolic event and who might be at higher risk for future embolic
events (ie, severe stenosis or enlarged left atrium) should be
considered for long-term warfarin therapy.
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Physical Activity and Exercise
The 26th Bethesda Conference on Recommendations for Determining Eligibility for Competition in Athletes With Cardiovascular Abnormalities has published guidelines for patients with MS who wish to engage in competitive athletics.7
Evaluation of the Symptomatic Patient
Patients who develop symptoms should undergo evaluation with a
history, physical examination, ECG, chest x-ray, and
echocardiography to evaluate mitral valve
morphology, mitral valve hemodynamics, and
pulmonary artery pressure. Patients with NYHA functional Class
II symptoms and moderate or severe stenosis (mitral valve area
1.5 cm2 or mean gradient 5 mm Hg) may
be considered for mitral balloon valvotomy if they have suitable mitral
valve morphology. Patients with NYHA functional Class III or IV
symptoms and evidence of severe MS have a poor prognosis if left
untreated, and intervention with either balloon valvotomy or surgery
should be considered.
A subset of patients have significant limiting symptoms yet resting
hemodynamics that do not indicate moderate to severe
MS. If there is a discrepancy between symptoms and
hemodynamic data, formal exercise testing or
dobutamine stress testing may be useful to differentiate
symptoms caused by MS from other causes. Exercise tolerance, heart rate
and blood pressure response, transmitral gradient, and
pulmonary artery pressure can be obtained at rest and during
exercise. This can usually be accomplished by either supine bicycle or
upright exercise with Doppler recording of TR and
transmitral velocities. Right- and left-heart
catheterization with exercise may also be helpful.
Patients who are symptomatic with a significant elevation
of pulmonary artery pressure (>60 mm Hg), mean
transmitral gradient (>15 mm Hg), or pulmonary artery
wedge pressure (25 mm Hg) on exertion have
hemodynamically significant MS and should be considered
for further intervention. Alternatively, patients who do not manifest
elevation in pulmonary artery, pulmonary artery wedge,
or transmitral pressures coincident with development of exertional
symptoms most likely would not benefit from intervention on the mitral
valve.
Indications for Cardiac Catheterization
In most instances, Doppler measurements of transmitral
gradient, valve area, and pulmonary pressure correlate well
with each other. Catheterization is indicated to assess
hemodynamics when there is a discrepancy between
Doppler-derived hemodynamics and the clinical
status of a symptomatic patient. Absolute left- and
right-sided pressure measurements should be obtained by
catheterization when there is elevation of
pulmonary artery pressure out of proportion to mean gradient
and valve area. Catheterization including left
ventriculography (to evaluate severity of MR) is indicated when there
is a discrepancy between Doppler-derived mean gradient and valve
area. Coronary angiography may be required in selected patients
who may need to undergo intervention (see section VIII).
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Indications for Surgical or Percutaneous Valvotomy
With the development of cardiopulmonary bypass in the 1960s, open mitral commissurotomy and replacement of the mitral valve became the surgical procedures of choice for treatment of MS. Percutaneous mitral balloon valvotomy emerged in the mid 1980s. This procedure has become an accepted alternative to surgical approaches in selected patients. The procedure itself is technically challenging and involves a steep learning curve. There is a higher success rate and lower complication rate in experienced high-volume centers. Thus, results of the procedure are highly dependent on the experience of the operators, which must be taken into consideration when making recommendations for proceeding with this technique.
The immediate results of percutaneous mitral
valvotomy are similar to those of mitral commissurotomy. The mean valve
area usually doubles (from 1.0 cm2 to 2.0
cm2), with a 50% to 60% reduction in
transmitral gradient. Overall, 80% to 95% of patients may have a
successful procedure, which is defined as a mitral valve area >1.5
cm2 and a decrease in left atrial pressure to
18 mm Hg in the absence of complications. The most common acute
complications reported in large series include severe MR, which occurs
in 2% to 10%, and a residual atrial septal defect. A large atrial
septal defect (>1.5:1 left-to-right shunt) occurs in up to 12% of
patients with the double balloon technique and in <5% with the Inoue
balloon technique. Smaller atrial septal defects may be detected by
transesophageal echocardiography in
larger numbers of patients. Less frequent complications include
perforation of the left ventricle (0.5% to 4.0%), embolic events
(0.5% to 3%), and myocardial infarction (0.3% to 0.5%). The
mortality for patients who undergo balloon valvotomy in larger series
has ranged from 1% to 2%; however, with increasing experience in the
procedure, percutaneous mitral valvotomy can be done in
selected patients with a mortality of <1%.
Follow-up information after percutaneous balloon valvotomy is limited. Event-free survival (freedom from death, repeat valvotomy, or mitral valve replacement) overall is 50% to 65% over 3 to 7 years, with an event-free survival of 80% to 90% in patients with favorable mitral valve morphology. More than 90% of patients free of events remain in NYHA functional Class I or II after percutaneous mitral valvotomy. Randomized trials have compared percutaneous balloon valvotomy with both closed and open surgical commissurotomy. There was no significant difference in acute hemodynamic results or complication rate between percutaneous mitral valvotomy and surgery, and early follow-up data indicate no difference in hemodynamics, clinical improvement, or exercise time. However, longer-term follow-up studies at 3 to 7 years indicate more favorable hemodynamic and symptomatic results with percutaneous balloon valvotomy than with closed commissurotomy and results equivalent to those of open commissurotomy.
The immediate results, acute complications, and follow-up results of percutaneous balloon valvotomy depend on multiple factors. It is of utmost importance that this procedure be performed in centers with skilled, experienced operators. Other factors include age, NYHA functional class, severity of stenosis, LV end-diastolic pressure, cardiac output, and pulmonary artery wedge pressure. The underlying mitral valve morphology is the most important factor in determining outcome, and patients with valvular calcification, thickened fibrotic leaflets with decreased mobility, and subvalvular fusion have a higher incidence of acute complications and a higher rate of recurrent stenosis on follow-up. In patients with noncalcified pliable valves and no calcium in the commissures, the procedure can be performed with a high success rate (>90%), low complication rate (<2% to 3%), and sustained improvement in 80% to 90% over a 3- to 7-year follow-up period.
Relative contraindications to percutaneous balloon valvotomy include the presence of a left atrial thrombus and significant (3+ to 4+) MR. Transesophageal echocardiography is frequently performed before the procedure to determine the presence of left atrial thrombus, specifically examining the left atrial appendage. If a thrombus is found, 3 months of anticoagulation with warfarin may result in resolution of the thrombus.
In centers with skilled, experienced operators,
percutaneous balloon valvotomy should be considered the
initial procedure of choice for symptomatic patients with
moderate to severe MS who have a favorable valve morphology in the
absence of significant MR or a left atrial thrombus. In
asymptomatic patients with a favorable valve morphology,
percutaneous mitral valvotomy may be considered if
there is evidence of a hemodynamic effect on left
atrial pressure (new-onset atrial fibrillation) or pulmonary
circulation (pulmonary artery pressure >50 mm Hg at rest
or >60 mm Hg with exercise). The strength of evidence for this
recommendation is low because there are no data comparing the results
of percutaneous balloon valvotomy and medical therapy
in such patients. It is controversial whether severely
symptomatic patients with less favorable valve morphology
should undergo this catheter-based procedure. Although there is a
higher acute complication rate and lower event-free survival
(approximately 50% at 5 years in these patients, compared with 80% to
90% in patients with favorable valve morphology), this must be weighed
against the risks and potential complications of surgical mitral valve
replacement.
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Indications for Mitral Valve Replacement
Mitral valve replacement (MVR) is an accepted surgical procedure for patients with severe MS who are not candidates for surgical commissurotomy or percutaneous mitral valvotomy. The risk of MVR is dependent on multiple factors, including functional status, age, LV function, cardiac output, concomitant medical problems, and concomitant CAD. In the young, healthy person, MVR can be performed with a risk of <5%. However, in the older patient with concomitant medical problems or pulmonary hypertension at systemic levels, the risk of MVR may be 10% to 20%.
If there is significant calcification, fibrosis, and
subvalvular fusion of the mitral valve apparatus,
commissurotomy or percutaneous balloon valvotomy is
less likely to be successful, and MVR will be necessary. Given the risk
of MVR and the potential long-term complications of a
prosthetic valve, there are stricter indications for mitral
valve operation in these patients with calcified fibrotic valves. For
the patient with NYHA functional Class III symptoms due to severe MS or
combined MS/MR, MVR results in excellent symptomatic
improvement. Postponement of surgery until the patient reaches the
functional Class IV symptomatic state should be avoided
because operative mortality is high and long-term outcome suboptimal.
However, if the patient presents in NYHA functional Class IV heart
failure, surgery should not be denied because the outlook without
surgical intervention is grave. It is controversial whether
asymptomatic or mildly symptomatic patients
with severe MS (valve area <1 cm2) and severe
pulmonary hypertension (pulmonary artery
systolic pressure >60 to 80 mm Hg) should undergo MVR to
prevent right ventricular failure, but surgery is generally
recommended in such patients. It is recognized that patients with such
severe pulmonary hypertension are rarely
asymptomatic.
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Management of Patients After Valvotomy or Commissurotomy
Recurrent symptoms after successful surgical commissurotomy have been reported to occur in as many as 60% of patients after 9 years, but recurrent stenosis accounts for symptoms in <20%. In patients with adequate initial results, progressive MR and development of other valvular or coronary problems are more frequently responsible for recurrent symptoms. Thus, in patients presenting with symptoms late after commissurotomy, a comprehensive evaluation is required to look for other causes of the symptoms. Patients undergoing percutaneous mitral valvotomy have a higher incidence of recurrent symptoms at 1- to 2-year follow-up if there was an unfavorable mitral valve morphology due to either an initial inadequate result or restenosis.
The management of patients after successful
percutaneous balloon valvotomy or surgical
commissurotomy is similar to that of the asymptomatic
patient with MS. A baseline echocardiogram should be performed after
the procedure to assess hemodynamics as well as to
exclude significant complications such as MR, LV dysfunction, or atrial
septal defect (in the case of percutaneous valvotomy).
The echocardiogram should be performed 72 hours after the
procedure because acute changes in atrial and ventricular
compliance immediately after the procedure affect the reliability of
the half-time method in calculating valve area. Patients with severe MR
or a large atrial septal defect should be considered for early
operation. However, the majority of small left-to-right shunts at the
atrial level will close spontaneously over the course of 6 months. In
patients with a history of atrial fibrillation, warfarin should be
restarted 1 to 2 days after the procedure.
Repeat percutaneous balloon valvotomy can be performed in the patient who has restenosis after either a prior surgical commissurotomy or balloon valvotomy. The results of these procedures are less satisfactory than the overall results of initial valvotomy because there is usually more valve deformity, calcification, and fibrosis than with the initial procedure. MVR should be considered in those patients with recurrent severe symptoms and severe deformity of the mitral apparatus.
D. Mitral Valve Prolapse
MVP is the most common form of valvular heart disease and occurs in 2% to 6% of the population. MVP often occurs as a clinical entity with little or no MR but is also the most common cause of significant MR in the United States.
Primary and secondary MVP must be distinguished from normal variants by cardiac auscultation and/or echocardiography; these variations can result in an incorrect diagnosis of MVP, particularly in patients with hyperkinetic hearts or dehydration. Other auscultatory findings may be misinterpreted as midsystolic clicks or late systolic murmurs. Patients with mild to moderate billowing of 1 or more nonthickened leaflets toward the left atrium with the leaflet coaptation point on the LV side of the mitral annulus and minimal or no MR by Doppler echocardiography are probably normal. Unfortunately, many such patients are overdiagnosed as having the MVP syndrome.
Natural History
In most patient studies, the MVP syndrome is associated with a
benign prognosis. The age-adjusted survival rate of both men and women
with MVP is similar to that of individuals without this common clinical
entity. The gradual progression of MR in patients with MVP may result
in progressive dilatation of the left atrium and ventricle. Left atrial
dilatation may result in atrial fibrillation, and moderate to severe MR
may eventually result in LV dysfunction and development of congestive
heart failure. Pulmonary hypertension may occur with associated
right ventricular dysfunction. In some patients, after an
initially prolonged asymptomatic interval, the entire
process may enter an accelerated phase as a result of left atrial and
LV dysfunction, atrial fibrillation, and in certain instances, ruptured
mitral valve chordae.
Several long-term prognostic studies suggest that complications occur most commonly in patients with a mitral systolic murmur, thickened redundant mitral valve leaflets, and increased LV or left atrial size, especially in men >45 years of age. Sudden death is a rare complication of MVP, occurring in <2% of known cases during long-term follow-up, with annual mortality rates <1% per year.
Infective endocarditis is a serious complication of MVP, which is the leading predisposing cardiovascular diagnosis in most series of patients reported with endocarditis. Because the absolute incidence of endocarditis is extremely low for the entire MVP population, there has been much controversy about the risk of endocarditis in MVP.
Evaluation and Management of the Asymptomatic Patient
The primary diagnostic evaluation of the patient with
MVP is a careful physical examination. The principal cardiac
auscultatory feature of this syndrome is the midsystolic click,
which may vary considerably in intensity and timing according to LV
loading conditions and contractility. Clicks result
from sudden tensing of the mitral valve apparatus as the
leaflets prolapse into the left atrium during systole. The
midsystolic click(s) is frequently followed by a late
systolic murmur, usually medium- to high-pitched and loudest at
the cardiac apex. Dynamic auscultation is often useful for establishing
the clinical diagnosis of the MVP syndrome. Changes in LV
end-diastolic volume result in changes in the timing of the
midsystolic click(s) and murmur. When end-diastolic
volume is decreased (as with standing), the critical volume is achieved
earlier in systole, and the click-murmur complex occurs shortly after
the first heart sound. By contrast, any maneuver that augments the
volume of blood in the ventricle (eg, squatting), reduces myocardial
contractility, or increases LV afterload, lengthens the
time from onset of systole to initiation of MVP, and the
systolic click and/or murmur move toward the second heart
sound.
2-D and Doppler
echocardiography is the most useful
noninvasive test for defining MVP. The M-mode
echocardiographic definition of MVP includes 2-mm
posterior displacement of 1 or both leaflets or holosystolic
posterior "hammocking" >3 mm. On 2-D
echocardiography, systolic displacement of
1 or both mitral leaflets in the parasternal long-axis view,
particularly when they coapt on the atrial side of the annular plane,
indicates a high likelihood of MVP. There is disagreement about the
reliability of echocardiographic diagnosis of MVP when
observed in only the apical 4-chamber view. The diagnosis of MVP is
even more certain when leaflet thickness is >5 mm. Leaflet
redundancy is often associated with an enlarged mitral annulus and
elongated chordae tendineae. On Doppler
echocardiography, the presence or absence of MR is
an important consideration, and MVP is more likely when MR is detected
as a high-velocity eccentric jet in late systole.
At present, there is no consensus on the 2-D echocardiographic criteria for MVP. Because echocardiography is a tomographic cross-sectional technique, no single view should be considered diagnostic. The parasternal long-axis view permits visualization of the medial aspect of the anterior mitral leaflet and middle scallop of the posterior leaflet. If the findings of prolapse are localized to the lateral scallop in the posterior leaflet, they would be best visualized by the apical 4-chamber view. All available echocardiographic views should be used, with the provision that billowing of the anterior leaflet alone in the 4-chamber apical view is not evidence of prolapse; however, displacement of the posterior leaflet or coaptation point in any view, including the apical view, suggests the diagnosis of prolapse. The echocardiographic criteria for MVP should include structural changes, such as leaflet thickening, redundancy, annular dilatation, and chordal elongation.
Patients with echocardiographic evidence for MVP but no
evidence of thickened/redundant leaflets or definite MR are more
difficult to classify. If such patients have clinical auscultatory
findings of MVP, the echocardiogram usually confirms the diagnosis.
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Although there is controversy concerning the need for
echocardiography in patients with classic
auscultatory findings of MVP, the usefulness of
echocardiography for risk stratification in
patients with MVP has been demonstrated in 6 published studies. All
patients with MVP should have an initial echocardiogram. Serial
echocardiograms are not usually necessary in the
asymptomatic patient with MVP unless there are clinical
indications of severe or worsening MR.
Reassurance is a major part of the management of patients with MVP, most of whom are asymptomatic or have no cardiac symptoms and lack a high-risk profile. These patients with mild or no symptoms and findings of milder forms of prolapse should be reassured of the benign prognosis. A normal lifestyle and regular exercise are encouraged.
Antibiotic prophylaxis for prevention of infective endocarditis
during procedures associated with bacteremia is recommended for most
patients with a definite diagnosis of MVP, as indicated in section
II.B. There has been some disagreement about whether patients with an
isolated systolic click and no systolic murmur should
undergo endocarditis prophylaxis. Patients with only a systolic
click who have echocardiographic evidence of a
higher-risk profile for endocarditis, such as leaflet thickening,
elongated chordae, left atrial enlargement, or LV dilatation, should
receive endocarditis prophylaxis.
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Evaluation and Management of the Symptomatic Patient
Patients with MVP and palpitations associated with mild
tachyarrhythmias or increased adrenergic symptoms and
those with chest pain, anxiety, or fatigue often respond to therapy
with ß-blockers. However, in many cases, the cessation of stimulants
such as caffeine, alcohol, and cigarettes may be sufficient to control
symptoms. In patients with recurrent palpitations, continuous or
event-activated ambulatory ECG recordings may reveal
whether arrhythmias are the cause of symptoms and indicate
appropriate treatment of existing arrhythmias. The indications
for electrophysiological testing are
similar to those in the general population (eg, aborted sudden death,
recurrent syncope of unknown cause, and symptomatic or
sustained ventricular tachycardia).
Cardiac catheterization is not required for the diagnosis of MVP. It is helpful in evaluating associated conditions (eg, CAD and atrial septal defect) and may be needed to assess the hemodynamic effects of severe MR (as well as coronary artery anatomy) before consideration for valve repair or replacement.
Daily aspirin therapy (80 to 325 mg/d) is recommended for patients with
MVP and documented focal neurological events who are in sinus rhythm
with no atrial thrombi. Such patients should also avoid smoking
cigarettes and using oral contraceptives. Long-term anticoagulation
therapy with warfarin is recommended for poststroke patients with MVP
and patients with MVP and recurrent transient ischemic attacks
while receiving aspirin therapy (INR 2 to 3). Warfarin therapy is
indicated in patients >65 years with MVP and atrial fibrillation and
those with MR, hypertension, or a history of heart failure (INR 2 to
3). Aspirin therapy is satisfactory in patients with atrial
fibrillation who are <65, have no MR, and have no history of
hypertension or heart failure. Daily aspirin therapy is also often
recommended for patients with high-risk
echocardiographic characteristics.
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Asymptomatic patients with MVP and no significant MR can be clinically evaluated every 3 to 5 years. Serial echocardiography is not necessary in most of these patients and is performed only if there is development of symptoms consistent with cardiovascular disease and a change in physical findings suggesting development of significant MR, and in patients with high-risk characteristics observed on the initial echocardiogram. Patients with high-risk characteristics, including those with moderate to severe MR, should receive a follow-up once a year.
Patients with severe MR with symptoms and/or impaired LV systolic function require cardiac catheterization and evaluation for mitral valve surgery. The thickened, redundant mitral valve can often be repaired rather than replaced with lower operative mortality and excellent short- and long-term results, as discussed in section III.E.
Surgical Considerations
Management of MVP may require valve surgery, particularly for
those who develop a flail mitral leaflet as a result of rupture of
chordae tendineae or their marked elongation. Most such valves can be
successfully repaired by surgeons experienced in mitral valve repair,
especially when the posterior leaflet of the mitral valve is
predominantly affected. Symptoms of heart failure, severity of MR, the
presence or absence of atrial fibrillation, LV systolic
function, LV end-diastolic and end-systolic
volumes, and pulmonary artery pressure (at rest and during
exercise) all influence the decision to recommend mitral valve surgery.
Recommendations for surgery in patients with MVP and MR are the same as
those with other forms of nonischemic severe MR, as indicated
in section III.E.4.
E. Mitral Regurgitation
1. Acute Severe Mitral Regurgitation
In acute severe MR, acute volume overload increases LV preload,
allowing for a modest increase in total LV stroke volume. However,
forward stroke volume and cardiac output are reduced, and the
regurgitant volume results in pulmonary congestion. In acute
severe MR, the hemodynamic overload often cannot be
tolerated, and mitral valve repair or replacement must often be
performed urgently.
Diagnosis
The patient with acute severe MR is almost always
symptomatic. Physical examination of the precordium may
be misleading because a normal-sized left ventricle does not produce a
hyperdynamic apical impulse. The systolic murmur of MR, which
may or may not be holosystolic, and a third heart sound may be
the only abnormal physical findings present. A fourth heart sound
is common. Transthoracic
echocardiography may demonstrate the disruption of
the mitral valve and help provide semiquantitative information about
lesion severity. However, transthoracic
echocardiography may underestimate lesion severity
by inadequate imaging of the color flow jet. Because
transesophageal echocardiography
can more accurately assess the color flow jet,
transesophageal imaging should be performed if mitral
valve morphology and regurgitant severity are still in question after
transthoracic echocardiography.
Transesophageal echocardiography is
also helpful in demonstrating the anatomic cause of MR and directing
successful surgical repair.
If ischemia is not the cause of MR and there is no reason to suspect CAD, mitral valve repair can usually be performed without cardiac catheterization. However, if CAD is suspected or there are risk factors for CAD, coronary arteriography is necessary before surgery.
Medical Therapy
In acute severe MR, the goal of nonsurgical therapy is to diminish
the amount of MR, in turn increasing forward output and reducing
pulmonary congestion. In the normotensive patient,
administration of nitroprusside may effectively accomplish all 3 goals.
Nitroprusside alone should not be administered to patients with
hypotension, but combination therapy with an inotropic agent (such as
dobutamine) and nitroprusside is of benefit in some
patients. In such patients, aortic balloon counterpulsation increases
forward output and mean arterial pressure while diminishing
regurgitant volume and LV filling pressure and can be used to stabilize
hemodynamics while preparing for surgery. If infective
endocarditis is the cause of acute MR, identification and treatment of
the infectious organism are essential.
2. Chronic Mitral Regurgitation
In chronic severe MR, the increase in LV end-diastolic
volume permits an increase in total stroke volume, allowing for
restoration of forward cardiac output. Augmented preload and reduced or
normal afterload (provided by unloading of the left ventricle into the
left atrium) facilitate LV ejection. At the same time, the increase in
LV and left atrial size allows accommodation of the regurgitant volume
at a lower filling pressure. In this phase of compensated MR, the
patient may be entirely asymptomatic, even during vigorous
exercise.
The duration of the compensated phase of MR varies but may last for many years. However, the prolonged burden of volume overload may eventually result in LV dysfunction. In this phase, contractile dysfunction impairs ejection, and end-systolic volume increases. There may be further LV dilatation and increased LV filling pressure. These hemodynamic events result in reduced forward output and pulmonary congestion. However, the still favorable loading conditions often maintain ejection fraction in the low normal range (0.50 to 0.60) despite the presence of significant muscle dysfunction. Correction of MR should occur before advanced LV decompensation.
Diagnosis
In evaluating the patient with chronic MR, a careful history is
invaluable. A well-established estimation of baseline exercise
tolerance is important in gauging the subtle onset of symptoms at
subsequent evaluations. Physical examination should demonstrate
displacement of the LV apical impulse, which indicates that MR is
severe and chronic, producing cardiac enlargement. A third heart sound
is usually present and does not necessarily indicate heart failure.
An ECG and a chest x-ray are useful in establishing rhythm and heart
size, respectively. An initial echocardiogram, including Doppler
interrogation of the mitral valve, is indispensable in the management
of MR. The echocardiogram provides a baseline estimation of LV and left
atrial volume, an estimation of LV ejection fraction, and approximation
of the severity of regurgitation. Changes from these
baseline values are subsequently used to guide the timing of mitral
valve surgery. In addition, the echocardiogram can often disclose the
anatomic cause of the patient's condition. In the presence of even
mild TR, interrogation of the tricuspid valve yields an estimate of
pulmonary artery pressure.
In some patients, Doppler studies show that MR worsens with exercise, possibly reconciling exercise-induced symptoms with resting echocardiograms that show only mild or moderate regurgitation.
Serial Testing
Asymptomatic patients with mild MR and no evidence of
LV enlargement or dysfunction or pulmonary hypertension can be
followed up on a yearly basis with instructions to alert the physician
if symptoms develop in the interim. Yearly
echocardiography is not necessary unless there is
clinical evidence that regurgitation has worsened. In
patients with moderate MR, clinical evaluations should be performed
annually, and echocardiography is not necessary
more than once a year.
Asymptomatic patients with severe MR should be followed up with a history, physical examination, and echocardiography every 6 to 12 months to assess symptoms or transition to asymptomatic LV dysfunction. Serial chest x-rays and ECGs are of less value but are helpful in selected patients. Most patients develop symptoms before developing LV dysfunction. Exercise stress testing may be used to add objective evidence of symptoms and changes in exercise tolerance. Exercise testing is especially important if a good history of the patient's exercise capacity cannot be obtained.
Several studies have indicated that preoperative ejection fraction is
an important predictor of postoperative survival in patients with
chronic MR. The loading conditions of MR facilitate ejection and
increase ejection fraction, and the ejection fraction in a patient with
MR with normal LV function is usually 0.60. Consistent with
this concept, postoperative survival is reduced in patients with a
preoperative ejection fraction <0.60 compared with patients with
higher ejection fractions.
Alternatively or in concert, echocardiographic LV
end-systolic dimension (or volume) can be used in the timing of
mitral valve surgery. End-systolic dimension, which may be less
load dependent than ejection fraction, should be <45 mm before
surgery to ensure normal postoperative LV function. If patients become
symptomatic, they should undergo mitral valve surgery even
if LV function is normal.
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Medical Therapy
For the asymptomatic patient with chronic MR, there is
no generally accepted medical therapy. Although intuitively the use of
vasodilators may appear to be logical for the same reasons that they
are effective in acute MR and chronic AR, there are no large long-term
studies to indicate that they are beneficial. Furthermore, because MR
with normal ejection fraction is a disease in which afterload is not
increased, drugs that reduce afterload might produce a
physiological state of chronic low afterload for
which there is very little experience. Thus, in the absence of systemic
hypertension, there is no known indication for the use of vasodilating
drugs in asymptomatic patients with preserved LV
function.
In patients with MR who develop symptoms but have preserved LV function, surgery is the most appropriate therapy. If atrial fibrillation develops, heart rate should be controlled with digitalis, rate-lowering calcium channel blockers, ß-blockers, or, rarely, amiodarone. Although the risk of embolism with the combination of MR and atrial fibrillation may be less than that of MS and atrial fibrillation, INR should be maintained between 2 and 3 in patients with MR who develop atrial fibrillation.
Indications for Cardiac Catheterization
Cardiac catheterization, with or without
exercise, is necessary when there is a discrepancy between clinical and
noninvasive findings. Catheterization is also performed
when surgery is contemplated and there is uncertainty about the
severity of MR after noninvasive testing or when there is a need to
assess extent and severity of CAD before surgery. In patients with MR
who have risk factors for CAD (advanced age,
hypercholesterolemia, hypertension, etc) or
when there is suspicion that MR is ischemic in etiology (either
because of known myocardial infarction or suspected ischemia),
coronary angiography should be performed before surgery. For
cases in which no reasonable suspicion of CAD exists, coronary
angiography can be avoided.
Obviously, patients should not undergo valve surgery unless the
valve lesion is severe. In cases of chronic MR, noninvasive imaging
should demonstrate anatomic disruption of the valve or its
apparatus, and color flow Doppler should indicate
severe MR. Although the standard semiquantitative approach to
determining severity of MR from ventriculography has its own
limitations, ventriculography does provide an additional method to
assess LV dilatation and function and to gauge severity of MR. Exercise
hemodynamics and quantitative angiography may provide
additional information that is helpful for decision making.
During the catheterization procedure, a
right-heart catheterization should be performed if
severity of MR is uncertain.
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Indications for Surgery
Three different mitral valve operations are used to correct
MR: mitral valve repair, MVR with preservation of part or all of the
mitral apparatus, and MVR with removal of the mitral
apparatus. In most cases, mitral valve repair is the
operation of choice when the valve is suitable for repair and
appropriate surgical skill and expertise are available. This procedure
preserves the patient's native valve without a prosthesis,
avoiding the risk of long-term anticoagulation (except in patients in
atrial fibrillation) or prosthetic valve failure late after
surgery. In addition, preservation of the mitral apparatus
leads to better postoperative LV function and survival than in cases
when the apparatus is removed. However, mitral valve repair
is technically more demanding than MVR, may require longer
extracorporeal circulation time, and may occasionally fail.
The advantage of MVR with preservation of the chordal apparatus is that this operation ensures postoperative mitral valve competence, preserves LV function, and enhances postoperative survival compared with MVR, in which the apparatus is disrupted. Its disadvantage is the use of a prosthetic valve, with the risks of deterioration in biological valves or the need for anticoagulation in mechanical valves.
MVR in which the mitral valve apparatus is destroyed should almost never be performed. It should be reserved for those circumstances in which the native valve and apparatus are so distorted by the preoperative pathology (eg, rheumatic disease) that the mitral apparatus cannot be saved.
Many factors are useful in the preoperative prediction of success of mitral valve repair. This prediction is based on the surgeon's skill and experience in performing repair and on the location and type of mitral valve disease that caused MR. Nonrheumatic posterior leaflet prolapse due to degenerative mitral valve disease or a ruptured chorda tendineae can usually be repaired. Involvement of the anterior leaflet diminishes the likelihood of repair, and consequently the skill and experience of the surgeon are probably the most important determinants of whether the operation is eventually performed. In general, rheumatic and ischemic involvement of the mitral valve and calcification of the mitral valve leaflets or annulus diminish the likelihood of repair even in experienced hands.
1. Symptomatic Patients With Normal Left
Ventricular Function.
Patients with severe MR and symptoms of congestive heart failure
despite normal LV function on echocardiography
(ejection fraction >0.60 and end-systolic dimension <45
mm) require surgery. The feasibility of mitral valve repair is
dependent on several factors, including valve anatomy and
surgical expertise. Successful surgical repair improves symptoms,
preserves LV function, and avoids problems associated with
prosthetic valves. When repair is not feasible, MVR with
chordal preservation should relieve symptoms and maintain LV
function.
2. Asymptomatic or Symptomatic Patients
With Left Ventricular Dysfunction.
The timing of surgery for asymptomatic patients was once
controversial, but most now agree that mitral valve surgery is
appropriate once the echocardiographic indicators of LV
dysfunction have appeared. These include LV ejection fraction 0.60
and/or LV end-systolic dimension 45 mm. Although some
would recommend a slightly lower threshold ejection fraction (0.55), it
must be emphasized that, unlike timing of AVR for AR, LV ejection
fraction should not be allowed to fall into the low normal range in
patients with chronic MR. The data regarding postoperative survival are
much stronger with LV ejection fraction than end-systolic
dimension, whereas both ejection fraction and end-systolic
dimension strongly influence postoperative LV function and heart
failure.
Mitral valve surgery should also be recommended for
symptomatic patients with evidence of LV systolic
dysfunction (ejection fraction 0.60, end-systolic dimension
45 mm).
Determining the surgical candidacy of the symptomatic
patient with MR and far-advanced LV dysfunction is a common clinical
dilemma. If mitral valve repair appears likely, surgery should still be
contemplated, provided ejection fraction is 0.30. Even though such a
patient is likely to have persistent LV dysfunction, surgery is likely
to improve symptoms and prevent further deterioration of LV
function.
3. Asymptomatic Patients With Normal Left
Ventricular Function.
Repair of a severely regurgitant valve may be contemplated in an
asymptomatic patient with normal LV function to preserve LV
size and function and prevent the sequelae of chronic MR. Although
there are no data with which to recommend this approach to all
patients, the committee recognizes that some experienced centers are
moving in this direction when there is a high likelihood of successful
repair. This approach is often recommended in
hemodynamically stable patients with newly acquired
severe MR, as might occur with ruptured chordae. Surgery is also
recommended in asymptomatic patients with chronic MR with
recent onset of episodic or chronic atrial fibrillation in whom there
is a high likelihood of successful valve repair (see below).
4. Atrial Fibrillation.
Atrial fibrillation is a common, potentially morbid arrhythmia
associated with MR. Preoperative atrial fibrillation is an independent
predictor of reduced long-term survival after mitral valve surgery for
chronic MR. The persistence of atrial fibrillation after mitral valve
surgery partially nullifies an advantage of mitral repair by requiring
anticoagulation. Predictors of persistent atrial fibrillation after
successful valve surgery are the presence of atrial fibrillation
for >1 year and left atrial size >50 mm. In 1 study, an
even shorter duration of preoperative atrial fibrillation (3 months)
was a predictor of persistent atrial fibrillation after mitral valve
repair. Although patients who develop atrial fibrillation usually
manifest other symptomatic or functional changes that would
warrant mitral valve repair or replacement, many clinicians consider
the onset of episodic or chronic atrial fibrillation to be an
indication in and of itself for surgery.
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3. Ischemic Mitral Regurgitation
The outlook for the patient with ischemic MR is
substantially worse than that for regurgitation from
other causes, as ischemic MR is usually caused by LV
dysfunction and/or papillary muscle dysfunction. On the other hand,
coronary artery bypass graft surgery may improve LV function
and reduce ischemic MR, and in many patients with transient
severe MR due to ischemia, myocardial
revascularization can eliminate episodes of severe
MR.
Hypotension and pulmonary edema often occur in severe MR secondary to acute myocardial infarction. Treatment is aimed at hemodynamic stabilization, usually with insertion of an intra-aortic balloon pump. Occasionally, revascularization of the coronary artery supplying an ischemic papillary muscle can lead to improvement in mitral valve competence. However, such improvement is rare, and correction of acute severe ischemic MR usually requires valve surgery. Unlike nonischemic MR, in which mitral repair is clearly the operation of choice, the best operation for ischemic MR is controversial.
F. Multiple Valve Disease
Remarkably few data exist to objectively guide management of mixed valve disease. Each case must be considered individually and management based on understanding the potential derangements in hemodynamics and LV function and the probable benefit of medical versus surgical therapy. The committee has developed no specific recommendations for treatment of multiple valve disease. Specific valve lesions are discussed in the full text of these guidelines.
G. Tricuspid Valve Disease
Tricuspid valve dysfunction can occur with normal or abnormal valves. Normal tricuspid valves develop regurgitation with elevation of right ventricular systolic and/or diastolic pressure, right ventricular cavity enlargement, and tricuspid annular dilatation. Right ventricular systolic hypertension occurs in MS, pulmonic valve stenosis, and the various causes of pulmonary hypertension. Right ventricular diastolic hypertension occurs in dilated cardiomyopathy and right ventricular failure of any cause.
Diagnosis
The physical examination is the initial key to diagnosis of
tricuspid valve disease. Echocardiography is
valuable in assessing valve structure and motion, measuring annular
size, and identifying other cardiac abnormalities that might influence
tricuspid valve function. Doppler
echocardiography estimates severity of TR, right
ventricular systolic pressure, and the tricuspid
valve diastolic gradient. It should be pointed out that
clinically insignificant TR is detected by color Doppler imaging in
many normal persons. This is not an indication for either routine
follow-up or prophylaxis against bacterial endocarditis. Thus, clinical
correlation and judgment must accompany the
echocardiographic results. Systolic
pulmonary artery pressure estimation combined with information
about annular circumference will further improve the accuracy of
clinical assessment.
Management
In patients with severe MS and pulmonary hypertension with
resulting right ventricular dilatation and TR, relief of MS
and the resulting decrease in pulmonary artery pressure may
result in substantial diminution of the degree of TR. Although the
timing of surgery for TR remains controversial, as do the surgical
techniques, this controversy has diminished since the advent of 2-D and
Doppler echocardiography for preoperative
assessment. Intraoperative transesophageal Doppler
echocardiography allows refinement of annuloplasty
techniques to optimize outcome.
Patients with severe TR of any cause have a poor long-term outcome because of right ventricular dysfunction and/or systemic venous congestion. Tricuspid valve and chordal reconstruction can be attempted in some cases of TR that are the result of endocarditis and trauma. In recent years, annuloplasty has become an established surgical approach to significant TR.
When the valve leaflets themselves are diseased, abnormal, or
destroyed, valve replacement with a low-profile mechanical valve or
bioprosthesis is often necessary. A biological
prosthesis is preferred because of the high rate of
thromboembolic complications with mechanical prostheses in the
tricuspid position.
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H. Valvular Heart Disease Associated With Anorectic Drugs
In the summer of 1997, the association between anorexigens and valvular heart disease was reported in 24 patients receiving the drug combination of fenfluramine and phentermine; unusual valve morphology and associated regurgitation were identified in both left- and right-sided heart valves. The echocardiographic and histopathologic findings were similar to those described in patients with carcinoid or ergotamine-induced valvular heart disease. All 24 patients were symptomatic and had heart murmurs; thus, the frequency of valvular pathology in asymptomatic patients receiving the combination of fenfluramine-phentermine could not be determined. The FDA has reported 5 echocardiographic prevalence surveys in which 86 of 271 patients (32%) who received a combination of fenfluramine and phentermine for 6 to 24 months had evidence of significant AR and/or MR, as did 6 of 20 patients (30%) who received dexfenfluramine with or without phentermine.
In light of this information, fenfluramine and dexfenfluramine have been withdrawn from the market. The risk of valvular heart disease associated with exposure to fenfluramine or dexfenfluramine, alone or in combination with phentermine, has been addressed in recent peer-reviewed studies in which the prevalence of AR and/or MR in patients exposed to these drugs varied widely. It does appear that the prevalence of significant valvular regurgitation may be related to the duration of exposure to the anorectic agents and that patients exposed for only brief periods of time have less risk of developing valvular regurgitation.
In addition to the uncertainties regarding the prevalence of valvular disease in patients receiving combination or single-drug therapy, the natural history of the valve disease during anorectic drug treatment and after drug withdrawal is unknown and awaits further clinical investigation. Thus, the risk of valvular heart disease relative to the benefit of weight reduction in patients with morbid obesity is unknown.
Considering these unknown variables, it is not possible to derive definitive diagnostic and treatment guidelines for patients who have received these anorectic drugs. Hence, clinical judgment is important. The US Department of Health and Human Services (DHHS), through the Centers for Disease Control and Prevention and the National Institutes of Health, has published interim recommendations.8
The Committee on Management of Patients With Valvular Heart Disease recommends that all patients with a history of use of fenfluramine or dexfenfluramine undergo a careful history and thorough cardiovascular physical examination. Physical examination should include auscultation with the patient in the upright position at end expiration to detect AR and in the left lateral decubitus position to detect MR. 2-D and Doppler echocardiography should be performed in those patients with symptoms, cardiac murmurs, or other signs of cardiac involvement (eg, widened pulse pressure or regurgitant c or v waves in the jugular venous pulse). Patients whose body habitus prevents adequate cardiac auscultation should also undergo 2-D and Doppler echocardiography. For example, mild AR may be difficult to detect on auscultation in an obese patient. Patients with clinical and echocardiographic evidence of valvular heart disease should then undergo treatment and/or further testing according to the recommendations developed for the specific valve lesions addressed earlier in these guidelines. Modification of these recommendations may be necessary as more information on the natural history of these specific valve lesions becomes available.
In light of the current evidence, echocardiographic
screening of all patients with a history of fenfluramine or
dexfenfluramine use, especially asymptomatic patients
without murmurs or associated findings, is not recommended. However,
because of possible progression of subclinical valvular
disease, asymptomatic patients without murmurs should
undergo repeat physical examinations in 6 to 8 months.
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IV. Evaluation and Management of Infective Endocarditis
A. Antimicrobial Therapy
Antimicrobial therapy in endocarditis is guided by identification
of the causative organism. Eighty percent of endocarditis cases are due
to streptococci and staphylococci. The majority of native valve
endocarditis is caused by Streptococcus viridans (50%) and
Staphylococcus aureus (20%). With prosthetic valve
endocarditis, a wide spectrum of organisms can be responsible within
the first year of operation. However, in "early" prosthetic
valve endocarditis, usually defined as endocarditis during the first 2
months after surgery, Staphylococcus epidermidis is the
frequent offending organism. Late-onset prosthetic valve
endocarditis follows the profile of native valve endocarditis.
Enterococcus faecalis and Enterococcus faecium
account for 90% of enterococcal endocarditis, usually associated with
malignancy or manipulation of the genitourinary or gastrointestinal
tract. Gram-positive and gram-negative bacilli are relatively uncommon
causes of endocarditis. In recent years, the HACEK group of organisms
(Haemophilus, Actinobacillus, Cardiobacterium, Eikenella,
and Kingella species) have become important causes of
endocarditis. Fungi, especially Candida, are important
causes of endocarditis in patients with prosthetic valves,
compromised immune systems, and intravenous drug abuse.
Recommended antimicrobial regimens for treatment of bacterial
endocarditis have been published by the AHA9 and
are reproduced in the full-text version of these guidelines.
B. Culture-Negative Endocarditis
Culture-negative endocarditis most frequently (62%) results
from prior antibiotic treatment before blood cultures were drawn. The
other reasons for negative blood cultures are infections caused by
Candida; Aspergillus; or fastidious, slow-growing
organisms and noninfective endocarditis, such as Libman-Sacks
endocarditis in patients with systemic lupus
erythematosus. The recommended regimen for
culture-negative presumed bacterial endocarditis is a 6-week course of
intravenous vancomycin (15 mg/kg every 12 hours) plus
intravenous or intramuscular gentamycin (1 mg/kg every
8 hours).
C. Endocarditis in HIV Seropositive Patients
Endocarditis in patients who are HIV seropositive usually occurs
as a complication of drug injections or long-term indwelling central
catheters. S aureus is the most frequent pathogen.
Endocarditis-related mortality in patients with AIDS exceeds that of
HIV-positive patients without AIDS. Thus, it is recommended that
endocarditis in patients with AIDS be treated with maximum-duration
antibiotic regimens.
D. Indications for Echocardiography in
Endocarditis
Echocardiography is useful for detection and
characterization of the hemodynamic and pathological
consequences of infection. These consequences include valvular
vegetations; valvular regurgitation;
ventricular dysfunction; and associated lesions such as
abscesses, shunts, and ruptured chordae. The indications for
transthoracic and transesophageal
echocardiography are discussed in the ACC/AHA
Guidelines for the Clinical Application of
Echocardiography.2
Transesophageal imaging is more sensitive for detecting
vegetations than transthoracic imaging.
Echocardiography may be useful in the case of
culture-negative endocarditis or the diagnosis of a persistent
bacteremia whose source remains unidentified after appropriate
evaluation.
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E. Indications for Surgery in Patients With Active
Infective Endocarditis
Surgery is indicated in patients with life-threatening congestive
heart failure or cardiogenic shock due to surgically treatable
valvular heart disease with or without established infective
endocarditis if the patient's prospects for recovery are reasonable,
with satisfactory quality of life after the operation. Surgery should
not be delayed in the setting of acute infective endocarditis when
congestive heart failure intervenes. Surgery is not indicated if
complications (severe embolic cerebral damage) or comorbid conditions
make the prospect of recovery remote.
The indications for surgery for infective endocarditis in patients with stable hemodynamics are less clear. Early consultation with a cardiovascular surgeon is recommended as soon as the diagnosis of aortic or mitral valve endocarditis is made so that the surgical team is aware of the patient who may suddenly need surgery. Surgery is recommended for patients with annular or aortic abscesses, infections resistant to antibiotic therapy, and fungal endocarditis.
When endocarditis develops in patients with prosthetic
valves who are receiving warfarin anticoagulation, warfarin should be
discontinued and replaced with heparin. This recommendation is less
related to the possibility of hemorrhagic complications of endocarditis
than the possibility of urgent surgery. If surgery is required, the
effects of warfarin will have dissipated, and heparin can easily be
reversed. Likewise, aspirin, if part of the medical regimen, should
also be discontinued. If neurological symptoms develop, anticoagulation
should be discontinued until an intracranial hemorrhagic event is
excluded by MRI or computed tomographic scanning.
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V. Management of Valvular Disease in Pregnancy
A. Physiological Changes of Pregnancy
The evaluation and management of valvular heart disease in
the pregnant patient requires an understanding of the normal
physiological changes associated with gestation,
labor, delivery, and the early postpartum period. On average, there is
a 50% increase in circulating blood volume during pregnancy, which is
accompanied by a commensurate increase in cardiac output that usually
peaks between the midportion of the second and third trimesters. The
augmented cardiac output is caused by an increase in stroke volume,
although there is also a smaller increase in heart rate, averaging 10
to 20 bpm. Because of the effects of uterine circulation and
endogenous hormones, systemic vascular resistance falls
with a disproportionately greater lowering of diastolic
blood pressure and a wide pulse pressure. Inferior vena
caval obstruction from a gravid uterus in the supine position can
result in an abrupt decrease in cardiac preload, leading to hypotension
with weakness and lightheadedness. These symptoms resolve quickly with
a change in position.
There is a further abrupt increase in cardiac output during labor and delivery related in part to the associated anxiety and pain. Uterine contractions can lead to marked increases in both systolic and diastolic blood pressure. After delivery, there is an initial surge in preload related to the autotransfusion of uterine blood into the systemic circulation and to caval decompression.
Pregnancy is also associated with a hypercoagulable state, owing to relative decreases in protein S activity, stasis, and venous hypertension. Estrogens may interfere with collagen deposition within the media of the medium- and large-sized muscular arteries. Circulating elastase can break up the elastic lamellae and weaken the aortic media during pregnancy. Weakening of the vascular wall may in turn predispose to dissection with or without an underlying connective tissue disorder.
The increased blood volume and enhanced cardiac output associated with normal pregnancy can accentuate the murmurs associated with stenotic heart valve lesions (eg, MS, AS). On the other hand, murmurs of AR or MR may actually attenuate in the face of lowered systemic vascular resistance.
B. Echocardiography
Normal pregnancy is accompanied by
echocardiographic evidence of mild
ventricular chamber enlargement. Pulmonic and tricuspid
valvular regurgitation, as assessed by
Doppler interrogation, is the rule rather than the exception. A
large minority of women will demonstrate Doppler evidence of
"physiological" MR in the absence of structural
valve disease. Atrioventricular valve incompetence may
be derived from the annular dilatation that accompanies
ventricular enlargement. Appreciation of these
echocardiographic and Doppler findings in normal
individuals is an important foundation for noninvasive evaluation of
subjects with suspected valvular disease. The use of ultrasound
during pregnancy poses no risk to the mother or fetus.
C. General Management Guidelines
Clinical experience has shown several cardiac conditions in which
the physiological changes of pregnancy are poorly
tolerated. Most experts would agree that pregnancy should be
discouraged for some conditions, such as cyanotic heart disease,
Eisenmenger syndrome, or severe pulmonary hypertension.
Valvular heart lesions associated with increased maternal and
fetal risk during pregnancy include severe AS with or without symptoms,
MR or AR with NYHA functional Class III to IV symptoms, MS with NYHA
functional Class II to IV symptoms, valve disease resulting in severe
pulmonary hypertension (pulmonary pressure >75% of
systemic pressures), valve disease with severe LV dysfunction (EF
<0.40), mechanical prosthetic valves requiring
anticoagulation, and AR in Marfan syndrome.
Individual counseling usually requires a multidisciplinary approach and should include information about contraception, maternal and fetal risks of pregnancy, and expected long-term outcomes. However, many patients with valvular heart disease can be successfully managed throughout pregnancy and during labor and delivery with conservative medical measures designed to optimize intravascular volume and systemic loading conditions.
Simple interventions such as bed rest and avoidance of the supine position should not be overlooked. Whenever possible, symptomatic or severe valvular lesions should be addressed and resolved before conception and pregnancy. Contemporaneous management with a dedicated obstetrical team accustomed to working with high-risk patients is encouraged.
D. Specific Lesions
1. Mitral Stenosis
Young pregnant women with a previous history of acute rheumatic
fever and carditis should continue to receive penicillin prophylaxis as
indicated in the nonpregnant state. Patients with mild to moderate MS
can almost always be managed with judicious use of diuretics
and ß-blockade. Care must be taken to avoid vigorous volume depletion
to protect against uretero-placental hypoperfusion. ß-Blockers are
chiefly indicated to treat or prevent tachycardia to
optimize diastolic filling.
Patients with severe MS who are symptomatic before conception will not predictably tolerate the hemodynamic burden of pregnancy and should be considered for percutaneous balloon mitral valvotomy before conception, provided the valve is anatomically suitable. Patients with severe MS who develop NYHA functional Class III-IV symptoms during pregnancy should undergo percutaneous balloon valvotomy.
Rarely, medical management of patients with MS does not prevent repetitive or persistent heart failure during pregnancy. However, there is now a near 10-year experience with balloon mitral valvotomy, with either very limited fluoroscopy (<1 to 2 minutes' exposure with both pelvic and abdominal shielding) or echocardiographic guidance. The reported results with mitral balloon valvotomy have been excellent, with few maternal and/or fetal complications. Percutaneous mitral balloon valvotomy should be performed only in experienced centers and only after aggressive medical measures have been exhausted. In developing countries, there is a long history of successful surgical closed commissurotomy for the pregnant woman.
2. Mitral Regurgitation
MVP is the most common cause of MR in pregnant women. The
physical findings pertinent to MVP may be obscured or varied by the
physiological changes of pregnancy, especially
increased blood volume and reduced systemic vascular resistance. The
associated MR can usually be managed medically, although on rare
occasions, mitral valve surgery is required because of ruptured chordae
and acute, severe worsening of the regurgitant lesion. When mitral
valve surgery is required, repair is always preferred, as would be the
case for any young patient, but especially in relation to the
desirability of avoiding the potential need for anticoagulation.
3. Aortic Stenosis
The most common cause of AS in pregnant women is congenital
bicuspid disease. Patients with mild to moderate obstruction and normal
LV systolic function can usually be managed conservatively
through the entire pregnancy. Patients with more severe obstruction
(pressure gradient >50 mm Hg) or symptoms should be advised to
delay conception until relief of AS is obtained. There is an
association between the presence of a bicuspid aortic valve and cystic
medial necrosis, which may predispose to spontaneous aortic dissection,
usually in the third trimester.
4. Aortic Regurgitation
Isolated AR, like MR, can usually be managed medically with a
combination of diuretics and if necessary vasodilator therapy.
Women with symptoms and/or signs of LV failure should be carefully
monitored throughout labor and delivery with strict attention to volume
status and blood pressure. As with MR, surgery during pregnancy should
be contemplated only for the control of refractory Class III or IV
symptoms. Consideration of LV size or systolic function in less
symptomatic patients should not apply.
5. Pulmonary Valve Stenosis
Isolated pulmonic stenosis is rarely a significant
impediment to a successful pregnancy. This lesion can be approached
with percutaneous valvotomy under
echocardiographic guidance when necessary.
6. Marfan Syndrome
Spontaneous aortic dissection and/or rupture are the most
feared cardiovascular complications of Marfan syndrome
associated with pregnancy. Dissection can occur at any point along the
aorta but most commonly originates in the ascending portion.
Enlargement of the aortic root >4.0 cm identifies a particularly
high-risk group, although a normal dimension is by no means a guarantee
against this catastrophic complication.
Any woman with Marfan syndrome who is contemplating pregnancy should
have a screening transthoracic echocardiogram with careful
assessment of aortic root dimensions. Enlargement 5.0 cm is
considered an indication for elective repair before conception, usually
with a composite valve-graft conduit and reimplantation of the
coronary arteries. If aortic root enlargement (>4.0 cm) is
first detected during pregnancy, some authorities recommend termination
with prompt aortic repair, especially if serial
echocardiographic studies demonstrate progressive
dilatation over time. Dissection and rupture are most likely to occur
during the third trimester or near the time of delivery. Special care
must be taken to provide adequate analgesia to prevent wide surges in
blood pressure during labor and delivery. Obstetrical techniques to
shorten the second stage of labor are appropriate. General
anesthesia and cesarean section may allow more optimal
hemodynamic control. The use of
prophylactic ß-blockade throughout pregnancy is strongly
recommended. Finally, it should be pointed out that patients with
Marfan syndrome and no identifiable cardiovascular
abnormalities on examination or echocardiographic study
can be safely shepherded through pregnancy and a normal vaginal
delivery.
E. Endocarditis Prophylaxis
The Committee on Rheumatic Fever, Endocarditis, and Kawasaki
Disease of the American Heart Association does not recommend routine
antibiotic prophylaxis in patients with valvular heart disease
undergoing uncomplicated vaginal delivery or cesarean section unless
infection is suspected. Antibiotics are optional for high-risk patients
with prosthetic heart valves, a previous history of
endocarditis, complex congenital heart disease, or a surgically
constructed systemic-pulmonary conduit. Many
practitioners routinely provide antibiotics.
F. Cardiac Valve Surgery
Cardiac valve surgery is a difficult and complex undertaking in
the pregnant patient. Even under ideal conditions, including the use of
cardiopulmonary bypass techniques that promote high flow rates
and warm perfusion temperatures, there is a high incidence of fetal
distress, growth retardation, or wastage. If possible, it is always
preferable to delay surgery until the fetus is viable and a cesarean
section can be performed as part of a concomitant procedure. Surgery
should be pursued only in the setting of medically refractory symptoms
(pulmonary congestion), especially if a low output syndrome
intervenes.
G. Anticoagulation
Pregnant patients with mechanical valve prostheses have an
obligate need for anticoagulation. Unfortunately, significant problems
remain, along with an impressive risk to both mother and fetus of
either hemorrhage or thrombosis with the use of either warfarin
or heparin.
1. Warfarin
Warfarin crosses the placenta and has been associated with
an increased incidence of spontaneous abortion, fetal deformity,
prematurity, and stillbirth. The true incidence of warfarin embryopathy
has been difficult to ascertain from the reported case series and has
ranged from <5% to 67%; an estimate of 4% to 10% seems reasonable,
based on recent reports. The risk may be dose related and appears to be
highest if exposure occurs during the 6th to 12th week of gestation.
Fetal cerebral hemorrhage can complicate labor and delivery,
especially if forceps evacuation is necessary.
2. Heparin
Heparin does not cross the placenta and is generally
considered safer. However, its longer-term use is complicated by
sterile abscesses, osteoporosis (albeit with a small risk of fracture),
thrombocytopenia, and bleeding. Numerous reports attest to an
unacceptable incidence of thromboembolic complications, including fatal
valve thrombosis, in high-risk pregnant women managed with subcutaneous
heparin (12% to 24%). These studies have several limitations, such as
inclusion of a predominant population of women with older-generation
and more thrombogenic prostheses, inadequate heparin dosing, and/or
lack of meticulous monitoring strategies. Unfortunately, the efficacy
of adjusted-dose subcutaneous heparin has not been definitively
established.
The choice of anticoagulant must be carefully considered and should
consider the mother's preferences regarding the competing risks to her
and the fetus. For many women, a 4% to 10% risk of warfarin
embryopathy is unacceptable. These women may be unwilling to take
warfarin at any time during the first trimester or throughout the
entire pregnancy. However, implicit in their choice of heparin is
the acceptance of increased risk of maternal hemorrhage
or prosthetic valve thrombosis. Certainly, a full discussion of
these issues is indicated before conception.
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Low-molecular-weight heparins offer several potential advantages over unfractionated heparin, including greater bioavailability, ease of administration, lack of need for laboratory monitoring, and a lower incidence of thrombocytopenia and osteoporosis. Low-molecular-weight heparins do not cross the placenta. Although they have been used to treat deep venous thrombosis in pregnant patients, there are no data to guide their use in the management of patients with mechanical heart valves. Dipyridamole is not an acceptable alternative to aspirin because of its harmful effects on the fetus. Neither warfarin nor heparin is contraindicated in postpartum mothers who breast-feed.
VI. Management of Valvular Heart Disease in Adolescents and Young Adults
Many patients with congenital heart disease have some valvular involvement. Frequently, it is part of a more complex congenital cardiac anomaly. The management of these complex diseases with multiple valve involvement is beyond the scope of these guidelines. Rather, this section concerns isolated valve involvement in which it is the primary anatomic abnormality in adolescents and young adults.
A. Aortic Stenosis
Adolescents and young adults with isolated aortic valve
stenosis almost always have congenital fusion of one or more
commissures, resulting in a bicuspid or unicuspid valve. Although the
prevalence of bicuspid and unicuspid valves may be as high as 2%, only
1 of 50 children born with these abnormalities will actually have
significant obstruction or regurgitation by
adolescence.
The rate of progression of AS during childhood and adolescence differs from that in the adult with acquired AS. One third of children manifest an increase in the transaortic gradient over a 4- to 8-year period. However, patients >12 years of age show very small increases. Those with higher initial gradients have a greater likelihood of progression.
Over the course of 20 years, only 20% of those with initial peak LV to
peak aortic pressure gradients <25 mm Hg require any
intervention. However, in those with an initial peak gradient >50
mm Hg, arrhythmias, sudden death, and other morbid events
(including endocarditis, congestive heart failure, syncope, angina,
myocardial infarction, stroke, and pacemaker insertion) occur at a rate
of 1.2% per year. Based on the experience of 370 patients followed
up for 8000 patient-years, the incidence of sudden death is 0.3%
per year. The severity of obstruction in those who died cannot be
determined, and a higher-risk subgroup cannot be
excluded.
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Balloon valvotomy is an efficacious treatment option for children and adolescents with AS caused by fusion of commissures. Although balloon dilation has become standard in children and adolescents with AS, it is rarely recommended in older adults because even short-term palliation is uncommon. There are insufficient published data to establish an age cutoff. Until more information becomes available, recommendations for balloon valvotomy should be limited to adolescents and young adults in their early 20s, although some older young adults without heavily calcified valves may also benefit.
Because balloon valvotomy has resulted in good long-term palliation with little morbidity and little or no short- or intermediate-term mortality in children, adolescents, and young adults in their early 20s, the indications for intervention are considerably more liberal than those in older adults, for whom intervention usually involves valve replacement.
Children and young adults with Doppler gradients 70 to
80 mm Hg (peak velocity >4.2 m/s), those who develop LV
repolarization or ischemic changes on the ECG (T-wave inversion
or ST depression) at rest or with exercise, and those with symptoms may
be considered for cardiac catheterization and possible
balloon dilation. The gradient should be confirmed
hemodynamically before proceeding with dilation, and it
is reasonable to perform valvotomy in patients with
catheterization gradients >60 mm Hg. Patients
with less severe gradients (50 to 70 mm Hg by Doppler
echocardiography) who are interested in
participating in vigorous athletics or those contemplating pregnancy
are also commonly referred for balloon dilation. In most centers,
balloon valvotomy has replaced surgical valvotomy, but the latter
remains a reasonable alternative if skilled interventional
cardiologists are not available.
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When balloon aortic valvotomy is ineffective or significant AR is
present, valve replacement may be necessary. Replacement of the
aortic valve with a pulmonary autograft, in which a
pulmonary or aortic homograft replaces the native
pulmonary valve, as first performed by Ross, has recently
gained acceptance at some centers. Preliminary results indicate
low surgical risk, with the majority of autograft valves performing
well for 1 decade. This approach has the advantage of not requiring
anticoagulation, an important issue for active adolescents and younger
adults, including women contemplating pregnancy.
B. Aortic Regurgitation
The indications for surgery in adolescents and young adults with a
bicuspid aortic valve with isolated AR or mixed aortic valve disease
are at present similar to adults; ie, symptoms, LV dysfunction
(ejection fraction <0.50), or greatly increased LV
end-diastolic or end-systolic diameter, taking into
account variations in body size. If the durability of pulmonary
autograft and homograft valves in the right ventricular
outflow tract is substantiated in long-term studies, the indications
for autograft valve replacement are likely to become more
liberal.
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C. Mitral Regurgitation
Isolated congenital MR is an extremely uncommon cardiac
condition. The most common cause of MR in children is
atrioventricular septal defects. MR can be associated
with MVP in adolescents or young adults. The pathophysiology,
diagnosis, and medical therapy of MR in adolescents is similar to that
discussed for the adult (see section III.E.). When symptoms or
deteriorating LV systolic function develop, surgery should be
performed. Under most circumstances, it is possible to decrease
regurgitation with a mitral annuloplasty. Occasionally,
MVR with a mechanical or biological valve is necessary. When valve
repair rather than MVR is likely, surgery for severe MR may be
contemplated in the absence of heart failure or LV
dysfunction.
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D. Mitral Stenosis
In developed countries, virtually all MS in adolescents and young
adults is congenital in origin. In the developing areas of the world,
MS is more likely to result from rheumatic fever. Congenital MS may be
associated with a wide variety of other congenital cardiac
malformations of the left side of the heart, including coarctation of
the aorta.
The clinical, ECG, and radiological features of congenital MS are
similar to those of acquired MS in adults. The echocardiogram is
beneficial for evaluating the mitral valve apparatus and
papillary muscles and may provide considerable insight into the
feasibility of successful valve repair. The information obtained from
transthoracic imaging is usually sufficient, but in older
children, adolescents, and young adults, a
transesophageal echocardiogram is sometimes
necessary.
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The surgical management of congenital MS has improved considerably with the improved appreciation of the mechanism of mitral valve function and ability to visualize the valve afforded by transesophageal echocardiography. In those with a parachute mitral valve, creation of fenestrations among the fused chordae may increase effective orifice area and improve symptoms dramatically. MVR may occasionally be necessary but is especially problematic in those with a hypoplastic mitral annulus, who may require an annulus-enlarging operation. Balloon dilation of congenital MS was recently attempted, but its usefulness is unproved. This is one of the most difficult and dangerous therapeutic catheterization procedures and should be undertaken only in centers with operators who have established experience and skill in this interventional technique.
E. Tricuspid Valve Disease
Acquired disease of the tricuspid valve is very uncommon in
adolescents and young adults and is usually the result of trauma,
bacterial endocarditis in intravenous drug abusers, and
small ventricular septal defects. Most cases of tricuspid
valve disease are congenital, with Ebstein's anomaly of the tricuspid
valve being the most common.
There is variation in the severity of the valve leaflet abnormalities
and TR. An interatrial communication, usually in the form of a patent
foramen ovale, is present in most patients. If TR elevates right
atrial pressure above left atrial pressure, right-to-left shunting can
occur with resulting hypoxemia. One or more accessory conduction
pathways are quite common, with a risk of paroxysmal atrial
tachycardia of 25%.
Patients with Ebstein's anomaly may be asymptomatic
with no cyanosis and no atrial arrhythmias. More commonly, they
are cyanotic because of right-to-left shunting, which is associated
with exercise intolerance. Right ventricular dysfunction
may eventually lead to right-sided congestive heart failure frequently
exacerbated by an atrial arrhythmia such as atrial
tachycardia, atrial flutter, or atrial
fibrillation.
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The natural history of Ebstein's anomaly varies. In patients who present in the perinatal period, the 10-year actuarial survival is 61%. In a study that included more children who presented after the perinatal period, the probability of survival was 50% at 47 years of age. Predictors of poor outcome were NYHA functional Class III or IV symptoms, a cardiothoracic ratio >65%, or atrial fibrillation. However, patients with Ebstein's anomaly who reach late adolescence and adulthood often have an excellent outcome.
The surgical management of Ebstein's anomaly remains challenging. For older children, adolescents, and young adults, tricuspid valve repair may be performed. Reconstruction of the valve is possible occasionally, especially when there is a mobile anterior leaflet not tethered to the ventricular septum.
Occasionally, the tricuspid valve is not reparable, and
replacement with a bioprosthesis or a mechanical valve may be
necessary. When present, atrial communications should be closed. If
an accessory pathway is present, it should be mapped and
obliterated either preoperatively in the electrophysiology
laboratory or at the time of surgery.
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F. Pulmonic Stenosis
Because the pulmonary valve is the least likely valve to
be affected by acquired heart disease, virtually all cases of
pulmonary valve stenosis or
regurgitation are congenital in origin. Most patients
with stenosis have a conical or dome-shaped pulmonary
valve formed by fusion of the valve leaflets, which project
superiorly into the main pulmonary artery. Occasionally, the
valve may be thickened and dysplastic, with stenosis caused by
the inability of the valve leaflets to move sufficiently during
ventricular systole.
Symptoms are unusual in children or adolescents with pulmonary valve stenosis, even when severe. Adults with long-standing severe obstruction may have dyspnea and fatigue secondary to an inability to increase cardiac output adequately with exercise. Exertional syncope or light-headedness may occur, but sudden death is very unusual. Eventually, TR and right ventricular failure may occur.
At any age, if the foramen ovale is patent, right
ventricular compliance may be reduced sufficiently to
elevate right atrial pressure, allowing right-to-left shunting and
cyanosis. This increases the risk of paradoxical emboli.
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Clinical Course
The clinical course of children and young adults with
pulmonary valve stenosis has been well described. The
second Natural History Study of Congenital Heart Defects, reported in
1993, found that the probability of 25-year survival was 96%. Less
than 20% of patients initially managed medically subsequently required
a valvotomy, and only 4% of operated patients required a second
operation. For patients with an initial transpulmonary gradient
<25 mm Hg, 96% did not require surgery over a 25-year
period.
Infective endocarditis is very uncommon, occurring with an incidence of 0.94 per 10 000 patient years.
Surgical relief of severe obstruction by valvotomy with a
transventricular or transpulmonary artery approach
predates the introduction of cardiopulmonary bypass. Balloon
valvotomy has now become the procedure of choice for the typically
domed, thickened valve in both children and adults virtually everywhere
in the United States. Surgery is still required for the dysplastic
valve often seen in Noonan syndrome. Although long-term follow-up of
pulmonary balloon valvotomy is not yet available, early and
midterm results (up to 10 years) suggest that the results will be
similar to surgical valvotomy, ie, little or no recurrence over
a 22- to 30-year period.
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In those with severe or long-standing
valvular obstruction, infundibular hypertrophy may
cause secondary obstruction when the pulmonary valve is
successfully dilated. This frequently regresses over time without
treatment. Some have advocated transient pharmacological ß-blockade,
but there is insufficient information to determine whether this is
effective or necessary.
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G. Pulmonary Regurgitation
Pulmonary valve regurgitation is an
uncommon congenital lesion occasionally seen with what has been
described as idiopathic dilation of the pulmonary artery. Mild
pulmonary regurgitation may be a normal finding
on Doppler echocardiography.
Pulmonary regurgitation is an almost unavoidable result of either surgical or balloon valvuloplasty of valvular pulmonic stenosis or surgical repair of tetralogy of Fallot. Among patients who undergo surgical valvotomy, 87% have pulmonary regurgitation by Doppler echocardiography, although it is audible in only 58%. Pulmonary regurgitation after successful repair of tetralogy of Fallot usually has no long-term clinical consequence. However, a small group with long-standing pulmonary regurgitation has developed right ventricular dilatation and systolic dysfunction, which can lead to inability to augment cardiac output with exercise and in some cases congestive heart failure. This group has also had a significant incidence of ventricular arrhythmias associated with late sudden death. Pulmonary valve replacement, usually with a homograft, has been performed, but follow-up data are too preliminary to develop recommendations at this time.
VII. Management of Patients With Prosthetic Heart Valves
A. Antibiotic Prophylaxis
1. Infective Endocarditis
All patients with prosthetic valves need appropriate
antibiotics for prophylaxis against infective endocarditis (section
II.B.).
2. Recurrence of Rheumatic Carditis
Patients with rheumatic heart disease continue to need antibiotics
for prophylaxis against recurrence of rheumatic carditis
(section II.B.).
B. Antithrombotic Therapy
All patients with mechanical valves require warfarin therapy. The
risk of embolism is greater with a valve in the mitral position
(mechanical or biological) compared with a valve in the aortic
position. With either type of prosthesis or valve location, the
risk of emboli is probably higher in the first few days and months
after valve insertion, before the valve is fully
endothelialized.
1. Mechanical Valves
For mechanical prostheses in the aortic position, INR should be
maintained between 2.0 and 3.0 for bileaflet valves and Medtronic Hall
valves and between 2.5 and 3.5 for other disk valves and Starr-Edwards
valves; for prostheses in the mitral position, INR should be maintained
between 2.5 and 3.5 for all mechanical valves. There was a difference
of opinion regarding the Starr-Edwards valve in the aortic position,
with a minority opinion recommending maintaining INR between 2.0 and
3.0. The recommendation for higher INR values in the mitral position is
based on the greater risk of thromboembolic complications with
mechanical valves in the mitral position and the greater risk of
bleeding at higher INRs. In patients with aortic mechanical prostheses
who are at higher risk of thromboembolic complications (see below), INR
should be maintained at 2.5 to 3.5 and the addition of aspirin
considered. Some valves are thought to be more thrombogenic than others
(particularly the tilting disk valves), and a case could be made for
increasing INR to between 3 and 4.5; however, this is associated with a
considerably increased risk of bleeding.
The addition of low-dose aspirin (80 to 100 mg/d) to warfarin therapy (INR 2.0 to 3.5) further decreases the risk of thromboembolism and decreases mortality due to other cardiovascular diseases. A slight increase in risk of bleeding with this combination should be kept in mind. The risk of gastrointestinal irritation and hemorrhage with aspirin is dose dependent over the range of 100 to 1000 mg/d, and the antiplatelet effects are independent of dose over this range. There are no data in patients with prosthetic heart valves who are taking warfarin and aspirin in doses of 100 to 325 mg/d. Doses of 500 to 1000 mg/d clearly increase risk of bleeding. The addition of aspirin (80 to 100 mg/d) to warfarin should be strongly considered unless there is a contraindication to the use of aspirin (ie, bleeding or aspirin intolerance). This combination is particularly appropriate for patients who have had an embolus while on warfarin therapy, those with known vascular disease, and/or those known to be particularly susceptible to hypercoagulability.
It is important to note that thromboembolic risk is increased early after insertion of the prosthetic valve. The use of heparin early after prosthetic valve replacement and before warfarin achieves therapeutic levels is controversial. In some patients, achievement of therapeutic INR can be delayed several days postoperatively because of mitigating complications.
2. Biological Valves
Because of an increased risk of thromboemboli in the first 3
months after implantation of a biological prosthetic valve,
anticoagulation with warfarin is usually recommended, although in
several centers, only aspirin is used for biological valves in the
aortic position. Risk is particularly high in the first few days after
surgery, and heparin should be started as soon as the risk of increased
surgical bleeding is reduced. After 3 months, the biological valve can
be treated like native valve disease, and warfarin can be discontinued
in over two thirds of patients with biological valves. In the remaining
patients with associated risk factors for thromboembolism, such as
atrial fibrillation, previous thromboembolism, or a hypercoagulable
condition, lifelong warfarin therapy is indicated to achieve an INR of
2.0 to 3.0. Many would also recommend continuing anticoagulation in
patients with severe LV dysfunction (ejection fraction <0.30).
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3. Embolic Events During Adequate Antithrombotic Therapy
In the patient who has a definite embolic episode(s) while
receiving adequate antithrombotic therapy, antithrombotic therapy
should be increased as follows:
- Warfarin, INR 2 to 3: warfarin dose increased to achieve INR of 2.5 to 3.5
- Warfarin, INR 2.5 to 3.5: warfarin dose may need to be increased to achieve INR of 3.5 to 4.5
- Not on aspirin: aspirin 80 to 100 mg/d should be initiated
- Warfarin plus aspirin 80 to 100 mg/d dose may also need to be increased to 325 mg/d if the higher dose of warfarin is not achieving the desired clinical result
- Aspirin alone: aspirin dose may need to be increased to 325 mg/d and/or warfarin added to achieve an INR of 2 to 3
4. Excessive Anticoagulation
In most patients with INR above the therapeutic range, excessive
anticoagulation can be managed by withholding warfarin and following
the level of anticoagulation with serial INR determinations. Excessive
anticoagulation (INR >5) greatly increases the risk of
hemorrhage. However, rapid decreases in INR that lead to INR
falling below the therapeutic level increase the risk of
thromboembolism. Patients with prosthetic heart valves with INR
in the range of 5 to 10 who are not bleeding can be managed by
withholding warfarin and administering 2.5 mg of vitamin
K1 orally. INR should be determined after 24
hours and subsequently as needed. Warfarin therapy is restarted and
dose appropriately adjusted to ensure that INR is in the therapeutic
range. In emergency situations, the use of fresh frozen plasma is
preferable to high-dose vitamin K1, especially if
given parenterally.
5. Antithrombotic Therapy in Patients Requiring Noncardiac
Surgery/Dental Care
The risk of increased bleeding during a procedure performed on a
patient receiving antithrombotic therapy has to be weighed against the
increased risk of thromboembolism caused by stopping the therapy. The
risk of stopping warfarin can be estimated and is relatively slight if
the drug is withheld for only a few days. When warfarin therapy is
reinstituted, there are theoretic concerns about a hypercoagulable
state caused by suppression of protein C and protein S before the drug
affects the thrombotic factors. Although these risks are only
hypothetical, individuals at very high risk should be treated with
heparin therapy until INR returns to the desired range.
Admission to the hospital or a delay in discharge to give heparin is
usually unnecessary. Determining which patients are at very high risk
of thrombosis and require heparin until warfarin can be reinstated may
be difficult, and clinical judgment is required. Heparin can usually be
reserved for those who have had a recent thrombosis or embolus
(arbitrarily within 1 year), those with demonstrated thrombotic
problems when previously off therapy, those with the Björk-Shiley
valve, and those with 3 "risk factors." Risk factors are atrial
fibrillation, previous thromboembolism, a hypercoagulable condition,
and mechanical prosthesis; many would also include LV
dysfunction (ejection fraction <0.30) as a risk factor. A lower
threshold for recommending heparin should be considered in patients
with mechanical valves in the mitral position, in whom a single risk
factor would be sufficient evidence of high risk. Low-molecular-weight
heparin is attractive as it is even more easily used outside the
hospital; however, there are no data on patients with
prosthetic heart valves, and low-molecular-weight heparins
cannot be recommended at this time.
6. Antithrombotic Therapy in Patients Needing Cardiac
Catheterization/Angiography
In an emergent or semiemergent situation, cardiac
catheterization can be performed with a patient taking
warfarin but preferably the drug should be stopped 72 hours before
the procedure so that INR is 1.5 (see above). The drug should be
restarted as soon as the procedure is completed. If a patient has 1 or
more risk factors that predispose to thromboembolism, heparin should be
started when INR falls below 2.0 and continued when warfarin is
restarted. After an overlap of 3 to 5 days, heparin may be discontinued
when the desired INR is achieved.
7. Thrombosis of Prosthetic Heart Valves
Prosthetic valve obstruction may be caused by thrombus
formation, pannus ingrowth, or a combination of these. If the
prosthesis is obstructed by pannus,
thrombolytic therapy will be ineffective, and the valve
needs to be replaced. Thrombolytic therapy for a
prosthetic valve obstructed by thrombus is associated with
significant risks and is often ineffective. Thrombolytic
therapy is ineffective in 16% to 18% of patients, and the rate of
acute mortality is 6%. Risk of thromboembolism is 12%; stroke, 3% to
10%; major bleeding episodes, 5%; nondisabling bleeding, 14%; and
recurrent thrombosis, 11%. Patients who have a large clot or evidence
of valve obstruction and who are in NYHA functional Classes
III or IV because of prosthetic thrombosis should undergo
early/immediate reoperation. Thrombolytic therapy in such
patients is reserved for those for whom surgical intervention carries
high risk and those with contraindications to surgery. Streptokinase
and urokinase are the most frequently used thrombolytic
agents. The duration of thrombolytic therapy depends on
resolution of pressure gradients and valve areas to near normal by
Doppler echocardiography.
Thrombolytic therapy should be stopped at 24 hours if there
is no hemodynamic improvement or after 72 hours, even
if hemodynamic recovery is incomplete. If
thrombolytic therapy is successful, it should be
followed with intravenous heparin until warfarin achieves
an INR of 3 to 4 for aortic prosthetic valves and 3.5 to 4.5
for mitral prosthetic valves. If partially successful,
thrombolytic therapy may be followed by a combination
of subcutaneous heparin twice daily (to achieve aPTT of 55 to 80
seconds) plus warfarin (INR 2.5 to 3.5) for a 3-month period.
Patients with a "small clot" who are in NYHA functional Class I or II and those with LV dysfunction should have in-hospital, short-term intravenous heparin therapy. If this is unsuccessful, they may receive a trial of continuous infusion thrombolytic therapy over several days. If this is unsuccessful or there is an increased risk associated with thrombolytic therapy, they may need reoperation. An alternative to thrombolytic therapy in patients who remain hemodynamically stable is to convert intravenous heparin to combined therapy with subcutaneous heparin (twice daily to an aPTT of 55 to 80 seconds) and warfarin (INR 2.5 to 3.5) for 1 to 3 months on an outpatient basis to allow endogenous thrombolysis. If intravenous heparin, heparin/thrombolytic therapy, or heparin/warfarin is successful, warfarin doses should be increased so that INR is between 3.0 and 4.0 (around 3.5) for prosthetic aortic valves and 3.5 and 4.5 (around 4.0) for prosthetic mitral valves. These patients should also receive low-dose aspirin.
C. Follow-up Visits
1. First Outpatient Postoperative Visit
The workup on this visit should include an interval or complete
history and physical examination, ECG, chest x-ray, 2-D and Doppler
echocardiography, complete blood count,
BUN/creatinine, electrolytes, lactase
dehydroxygenase (LDH), and INR, if indicated.
Echocardiography is the most useful noninvasive
test. It provides information about prosthesis
stenosis/regurgitation, valve area, assessment
of other valve disease(s), pulmonary hypertension, atrial size,
left and right ventricular hypertrophy, left
and right ventricular size and function, and pericardial
effusion/thickening. Echocardiography is an
essential component of the first postoperative visit because it
assesses the effects and results of surgery and serves as a baseline
for comparison should complications and/or deterioration occur
later.
2. Follow-up Visits in Patients Without Complications
Patients who have undergone valve replacement are not cured but
still have serious heart disease. They have exchanged native valve
disease for prosthetic valve disease and must be followed with
the same care as patients with native valvular disease.
The asymptomatic patient without complications needs to be
seen only at 1-year intervals. The frequency with which 2-D and
Doppler echocardiography should be performed
routinely in patients without complications is uncertain, and there are
no data on which to base this decision. The committee did not reach
consensus on this issue. The majority recommended no further
echocardiographic testing after the initial
postoperative evaluation in patients with mechanical valves whose
condition is stable and who have no symptoms or clinical evidence of LV
dysfunction, prosthetic valve dysfunction, or dysfunction of
other heart valves in keeping with the ACC/AHA Guidelines for the
Clinical Application of
Echocardiography.2 The
committee also failed to reach consensus about serial
echocardiography in patients with
bioprosthetic valves, who have an increasing risk of structural
deterioration of the valve after 5 years in the mitral position and 8
years in the aortic position. A minority opinion recommended annual
echocardiography, whereas the majority recommended
detailed histories and cardiac physical examinations with
echocardiography when dictated by clinical
circumstances, such as a regurgitant murmur or a change in symptoms.
Once regurgitation is detected, close follow-up with
2-D and Doppler echocardiography every 3 to 6
months is indicated. The committee agreed that
echocardiography is indicated for any patient with
a prosthetic heart valve whenever there is evidence of a new
murmur, there are questions of prosthetic valve integrity and
function, or there are concerns about ventricular
function.
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3. Follow-up Visits in Patients With Complications
LV dysfunction and clinical heart failure after valve replacement
may be the result of (1) preoperative LV dysfunction that persists or
improves only partially; (2) perioperative myocardial
damage; (3) other valve disease that has progressed; (4) complications
of prosthetic heart valves; and (5) associated heart disease,
such as CAD and systemic hypertension.
Any patient with a prosthetic heart valve who does not improve after surgery or who later shows deterioration of functional capacity should undergo appropriate testing, including 2-D and Doppler echocardiography and, if necessary, transesophageal echocardiography and cardiac catheterization with angiography to determine the cause.
D. Major Criteria for Valve Selection
In general, mitral valve repair is preferable to
replacement, provided that it is feasible and the appropriate skill and
experience are available to perform the procedure successfully.
The major advantages of a mechanical valve are an extremely low rate of
structural deterioration and a better survival rate in patients <65
years old after AVR and for MVR in patients 50 years old after MVR.
The major disadvantages are increased incidence of bleeding due to the
need for antithrombotic therapy and cost and disadvantages of
antithrombotic therapy.
The major advantage of a bioprosthesis (whether porcine or
pericardial) is lack of need for antithrombotic therapy. In addition,
the rate of structural valve deterioration in the aortic position in
patients 65 years is lower than in patients <65, especially in the
aortic position. In patients 65 years undergoing AVR with a porcine
bioprosthesis, the rate of structural deterioration is <10%
at 10 years. The major disadvantage is the increased rate of structural
valve deterioration and hence the need for reoperation in patients <65
years, particularly in those 50 years. Pericardial bioprostheses may
have a lower rate of structural valve deterioration than porcine
bioprostheses in patients 65 years.
Pregnancy after valve replacement poses a difficult problem. The disadvantages of a mechanical valve are that the patient is at risk for complications of warfarin therapy that may affect the patient and/or fetus and complications of heparin therapy (see section V.G.). The disadvantage of a bioprosthesis is the relatively higher rate of early structural valve deterioration. The Ross procedure (pulmonary autograft) or an aortic valve homograft is associated with a lower rate of such complications in young women and does not require anticoagulation. These procedures are strongly recommended for women who wish to become pregnant, provided that the necessary surgical skill and experience in performing these procedures are available.
If the patient needs antithrombotic therapy for any reason, for example, atrial fibrillation or presence of a mechanical valve in another position, the major advantage of a biological valve is reduced substantially.
Biological valves have a much higher rate of structural deterioration
when implanted in patients with renal failure, those on hemodialysis,
and those with hypercalcemia. Adolescent patients who are still growing
have a high risk for accelerated biological valve calcification.
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VIII. Evaluation and Treatment of Coronary Artery Disease in Patients With Valvular Heart Disease
Many patients with valvular heart disease have concomitant CAD, but the data are limited regarding optimal strategies for diagnosis and treatment of CAD in such patients. Thus, management decisions are usually developed by blending information from the randomized studies of treatment of CAD and smaller published series of patients undergoing surgical treatment of valvular heart disease.
A. Probability of Coronary Artery Disease in Patients With
Valvular Heart Disease
Ischemic symptoms in patients with valvular heart
disease may have multiple causes, such as LV chamber enlargement,
increased wall stress or wall thickening with subendocardial
ischemia, and right ventricular
hypertrophy. In general, because angina is a poor marker of
CAD in patients with AS, coronary arteriography is recommended
in symptomatic patients before AVR, especially in men >35
years of age, premenopausal women >35 years of age with
coronary risk factors, and postmenopausal women.
CAD is less prevalent in patients with AR and those with MS than in those with AS. Nonetheless, in symptomatic patients and/or those with LV dysfunction, preoperative coronary angiography is recommended in men >35 years old, premenopausal women >35 years old with coronary risk factors, and postmenopausal women.
The relation between MR and CAD is unique in that CAD is frequently the cause of this valve lesion. The management of these patients is discussed in section III.E.
B. Diagnosis of Coronary Artery Disease
The resting ECG in patients with valvular heart disease
frequently shows ST-segment changes due to LV hypertrophy,
LV dilatation, or bundle branch block, which reduce the accuracy of the
ECG at rest and during exercise for the diagnosis of concomitant
CAD.
Similarly, resting or exercise-induced regional wall motion
abnormalities are nonspecific markers for CAD in patients with
underlying valvular heart disease who have LV
hypertrophy and/or chamber dilatation, as are myocardial
perfusion abnormalities induced by exercise or pharmacological stress.
Thus, there are few indications for myocardial perfusion imaging with
thallium 201 or technetium 99m perfusion agents in patients
with severe valvular disease, and coronary
arteriography remains the most appropriate method for definitive
diagnosis of CAD. Noninvasive imaging is useful when CAD is suspected
in patients with mild valve stenosis or
regurgitation and normal LV cavity size and wall
thickness.
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C. Treatment of Coronary Artery Disease at the
Time of Aortic Valve Replacement
As noted previously, 33% of patients with AS undergoing AVR
have concomitant CAD. More than 50% of patients >70 years old have
CAD. Combined coronary artery bypass surgery has had little or
no adverse effect on operative mortality. Moreover, combined
coronary bypass grafting and AVR reduces the rates of
perioperative myocardial infarction, operative
mortality, and late mortality and morbidity, compared with
patients with significant CAD who do not undergo
revascularization at the time of AVR.
Incomplete revascularization is associated with
greater postoperative systolic dysfunction and reduced survival
rates after surgery compared with patients who receive complete
revascularization. For 1 decade, improved
myocardial preservation techniques have been associated with reduced
overall operative mortality, and it has become standard practice
to bypass all significant coronary artery stenoses when
possible in patients undergoing AVR. The committee recommends
this approach.
D. Aortic Valve Replacement in Patients Undergoing
Coronary Artery Bypass Surgery
Patients undergoing coronary artery bypass surgery
who have severe AS should undergo AVR at the time of
revascularization. Decision making is less clear in
patients with mild to moderate AS and CAD requiring coronary
bypass surgery. Controversy persists regarding the indications for
"prophylactic" AVR at the time of coronary
bypass surgery in such patients. This decision should be made only
after the severity of AS is carefully determined by Doppler
echocardiography and cardiac
catheterization.
It is difficult to predict whether a given patient with CAD and
mild AS is likely to develop significant AS after
revascularization. As noted previously (section
III.A.), the natural history of mild AS is variable, with some
patients manifesting a relatively rapid progression of AS, with a
decrease in valve area of up to 0.3 cm2 per year
and an increase in pressure gradient of 15 to 19 mm Hg per year;
however, the majority may show little or no change. The average rate of
reduction in valve area is 0.12 cm2 per year,
but the rate of change in an individual patient is difficult to
predict.
Although definitive data are not yet available, patients with
intermediate aortic valve gradients (30 to 50 mm Hg mean gradient
at catheterization or 3 to 4 m/s transvalvular
velocity by Doppler echocardiography) who are
undergoing coronary artery bypass surgery may warrant AVR at
the time of revascularization, but this is
controversial because there are limited data to indicate the wisdom of
this general policy.
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Footnotes
When citing this document, the American College of Cardiology and the American Heart Association recommend that the following format be used: Bonow RO, Carabello B, de Leon AC Jr, Edmunds LH Jr, Fedderly BJ, Freed MD, Gaasch WH, McKay CR, Nishimura RA, O'Gara PT, O'Rourke RA, Rahimtoola SH. ACC/AHA guidelines for the management of patients with valvular heart disease: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease). Circulation. 1998;98:1949-1984.
"Guidelines for the Management of Patients With Valvular Heart Disease: Executive Summary" was approved by the American College of Cardiology in August 1998 and the American Heart Association Science Advisory and Coordinating Committee in July 1998.
A single reprint of this document (Executive Summary) is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Avenue, Dallas, TX 75231-4596. Ask for reprint No. 71-0154. To obtain a reprint of the full text of the Guidelines published in the November 1998 issue of the Journal of the American College of Cardiology, ask for reprint No. 71-0153. To purchase additional reprints, specify version and reprint number: up to 999 copies, call 800-611-6083 (US only) or fax 413-665-2671; 1000 or more copies, call 214-706-1466, fax 214-691-6342, or . To make photocopies for personal or educational use, call the Copyright Clearance Center, 978-750-8400.
Circulation. 1998;98:1949-1984.
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W.R. E. Jamieson, S. D. Moffatt-Bruce, P. Skarsgard, M. A. Hadi, J. Ye, G. J. Fradet, J. G. Abel, M. T. Janusz, A. Cheung, and E. Germann Early Antithrombotic Therapy for Aortic Valve Bioprostheses: Is There an Indication for Routine Use? Ann. Thorac. Surg., February 1, 2007; 83(2): 549 - 557. [Abstract] [Full Text] [PDF]
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K. Kuwaki, N. Kawaharada, K. Morishita, T. Koyanagi, H. Osawa, T. Maeda, and T. Higami Mitral Valve Repair Versus Replacement in Simultaneous Mitral and Aortic Valve Surgery for Rheumatic Disease Ann. Thorac. Surg., February 1, 2007; 83(2): 558 - 563. [Abstract] [Full Text] [PDF]
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P. Varadarajan, N. Kapoor, R. C. Bansal, and R. G. Pai Clinical Profile and Natural History of 453 Nonsurgically Managed Patients With Severe Aortic Stenosis Ann. Thorac. Surg., December 1, 2006; 82(6): 2111 - 2115. [Abstract] [Full Text] [PDF]
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R. G. Pai, N. Kapoor, R. C. Bansal, and P. Varadarajan Malignant Natural History of Asymptomatic Severe Aortic Stenosis: Benefit of Aortic Valve Replacement Ann. Thorac. Surg., December 1, 2006; 82(6): 2116 - 2122. [Abstract] [Full Text] [PDF]
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J. Aboulhosn and J. S. Child Left Ventricular Outflow Obstruction: Subaortic Stenosis, Bicuspid Aortic Valve, Supravalvar Aortic Stenosis, and Coarctation of the Aorta Circulation, November 28, 2006; 114(22): 2412 - 2422. [Full Text] [PDF]
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R. M. Weiss, M. Ohashi, J. D. Miller, S. G. Young, and D. D. Heistad Calcific Aortic Valve Stenosis in Old Hypercholesterolemic Mice Circulation, November 7, 2006; 114(19): 2065 - 2069. [Abstract] [Full Text] [PDF]
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M Weber, M Hausen, R Arnold, H Nef, H Moellman, A Berkowitsch, A Elsaesser, R Brandt, V Mitrovic, and C Hamm Prognostic value of N-terminal pro-B-type natriuretic peptide for conservatively and surgically treated patients with aortic valve stenosis Heart, November 1, 2006; 92(11): 1639 - 1644. [Abstract] [Full Text] [PDF]
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W. B. Meijboom, N. R. Mollet, C. A.G. Van Mieghem, J. Kluin, A. C. Weustink, F. Pugliese, E. Vourvouri, F. Cademartiri, A. J.J.C. Bogers, G. P. Krestin, et al. Pre-Operative Computed Tomography Coronary Angiography to Detect Significant Coronary Artery Disease in Patients Referred for Cardiac Valve Surgery J. Am. Coll. Cardiol., October 17, 2006; 48(8): 1658 - 1665. [Abstract] [Full Text] [PDF]
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M. Toyama, A. Usui, T. Abe, H. Oshima, T. Akita, and Y. Ueda Mitral Valve Surgery for Dilated Cardiomyopathy with Mitral Regurgitation Asian Cardiovasc Thorac Ann, October 1, 2006; 14(5): 371 - 376. [Abstract] [Full Text] [PDF]
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M. El-Husseiny, K. Salhiyyah, S. G. Raja, and J. Dunning Should warfarin be routinely prescribed for the first three months after a bioprosthetic valve replacement? Interactive CardioVascular and Thoracic Surgery, October 1, 2006; 5(5): 616 - 623. [Abstract] [Full Text] [PDF]
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J. O. Bohm, C. A. Botha, A. Horke, W. Hemmer, D. Roser, G. Blumenstock, F. Uhlemann, and J.-G. Rein Is the Ross operation still an acceptable option in children and adolescents? Ann. Thorac. Surg., September 1, 2006; 82(3): 940 - 947. [Abstract] [Full Text] [PDF]
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V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society J. Am. Coll. Cardiol., August 15, 2006; 48(4): e149 - e246. [Full Text] [PDF]
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V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society Circulation, August 15, 2006; 114(7): e257 - e354. [Full Text] [PDF]
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D. S. Jassal, T. G. Neilan, A. D. Pradhan, K. E. Lynch, G. Vlahakes, A. K. Agnihotri, and M. H. Picard Surgical Management of Infective Endocarditis: Early Predictors of Short-Term Morbidity and Mortality Ann. Thorac. Surg., August 1, 2006; 82(2): 524 - 529. [Abstract] [Full Text] [PDF]
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W. Flameng, B. Meuris, P. Herijgers, and M.-C. Herregods Prosthesis-Patient Mismatch is Not Clinically Relevant in Aortic Valve Replacement Using the Carpentier-Edwards Perimount Valve Ann. Thorac. Surg., August 1, 2006; 82(2): 530 - 536. [Abstract] [Full Text] [PDF]
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M. G. St. John Sutton and R. C. Gorman Surgery for Asymptomatic Severe Mitral Regurgitation in the Elderly: Early Surgery or Wait and Watch? Circulation, July 25, 2006; 114(4): 258 - 260. [Full Text] [PDF]
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D. Detaint, T. M. Sundt, V. T. Nkomo, C. G. Scott, A. J. Tajik, H. V. Schaff, and M. Enriquez-Sarano Surgical Correction of Mitral Regurgitation in the Elderly: Outcomes and Recent Improvements Circulation, July 25, 2006; 114(4): 265 - 272. [Abstract] [Full Text] [PDF]
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A. Kulik, I. G. Burwash, V. Kapila, T. G. Mesana, and M. Ruel Long-Term Outcomes After Valve Replacement for Low-Gradient Aortic Stenosis: Impact of Prosthesis-Patient Mismatch Circulation, July 4, 2006; 114(1_suppl): I-553 - I-558. [Abstract] [Full Text] [PDF]
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S. Fukuda, A. M. Gillinov, P. M. McCarthy, W. J. Stewart, J.-M. Song, T. Kihara, M. Daimon, M.-S. Shin, J. D. Thomas, and T. Shiota Determinants of Recurrent or Residual Functional Tricuspid Regurgitation After Tricuspid Annuloplasty Circulation, July 4, 2006; 114(1_suppl): I-582 - I-587. [Abstract] [Full Text] [PDF]
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T. Walther, A. Rastan, V. Falk, S. Lehmann, J. Garbade, A. K. Funkat, F. W. Mohr, and J. F. Gummert Patient prosthesis mismatch affects short- and long-term outcomes after aortic valve replacement. Eur. J. Cardiothorac. Surg., July 1, 2006; 30(1): 15 - 19. [Abstract] [Full Text] [PDF]
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T. W. Waterbolk, E. S. Hoendermis, I. J. den Hamer, and T. Ebels Pulmonary valve replacement with a mechanical prosthesis. Promising results of 28 procedures in patients with congenital heart disease. Eur. J. Cardiothorac. Surg., July 1, 2006; 30(1): 28 - 32. [Abstract] [Full Text] [PDF]
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G. Maurer Aortic regurgitation. Heart, July 1, 2006; 92(7): 994 - 1000. [Full Text] [PDF]
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D. Messika-Zeitoun, B. D. Johnson, V. Nkomo, J.-F. Avierinos, T. G. Allison, C. Scott, A. J. Tajik, and M. Enriquez-Sarano Cardiopulmonary Exercise Testing Determination of Functional Capacity in Mitral Regurgitation: Physiologic and Outcome Implications J. Am. Coll. Cardiol., June 20, 2006; 47(12): 2521 - 2527. [Abstract] [Full Text] [PDF]
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L. A. Cuniberti, P. G. Stutzbach, E. Guevara, G. G. Yannarelli, R. P. Laguens, and R. R. Favaloro Development of Mild Aortic Valve Stenosis in a Rabbit Model of Hypertension J. Am. Coll. Cardiol., June 6, 2006; 47(11): 2303 - 2309. [Abstract] [Full Text] [PDF]
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P. Vaughan and P. D. Waterworth Anticoagulation after bioprosthetic aortic valve replacement J. Thorac. Cardiovasc. Surg., June 1, 2006; 131(6): 1425 - 1425. [Full Text] [PDF]
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G. M. Feuchtner, W. Dichtl, T. Schachner, S. Muller, A. Mallouhi, G. J. Friedrich, and D. z. Nedden Diagnostic performance of MDCT for detecting aortic valve regurgitation. Am. J. Roentgenol., June 1, 2006; 186(6): 1676 - 1681. [Abstract] [Full Text] [PDF]
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A. Vincentelli, B. Jude, and S. Belisle Antithrombotic therapy in cardiac surgery: [Traitement antithrombotique en chirurgie cardiaque]. Can J Anesth, June 1, 2006; 53(6_suppl): S89 - S102. [Abstract] [Full Text] [PDF]
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B. E. Ickx and A. Steib Perioperative management of patients receiving vitamin K antagonists: [Prise en charge perioperatoire des patients traites aux antagonistes de la vitamine K] Can J Anesth, June 1, 2006; 53(6_suppl): S113 - S122. [Abstract] [Full Text] [PDF]
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B. P. Griffin Timing of Surgical Intervention in Chronic Mitral Regurgitation: Is Vigilance Enough? Circulation, May 9, 2006; 113(18): 2169 - 2172. [Full Text] [PDF]
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R. Rosenhek, F. Rader, U. Klaar, H. Gabriel, M. Krejc, D. Kalbeck, M. Schemper, G. Maurer, and H. Baumgartner Outcome of Watchful Waiting in Asymptomatic Severe Mitral Regurgitation Circulation, May 9, 2006; 113(18): 2238 - 2244. [Abstract] [Full Text] [PDF]
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T. Walther, T. Dewey, G. Wimmer-Greinecker, M. Doss, R. Hambrecht, G. Schuler, F. W. Mohr, and M. Mack Transapical approach for sutureless stent-fixed aortic valve implantation: experimental results. Eur. J. Cardiothorac. Surg., May 1, 2006; 29(5): 703 - 708. [Abstract] [Full Text] [PDF]
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G. M. Feuchtner, W. Dichtl, G. J. Friedrich, M. Frick, H. Alber, T. Schachner, J. Bonatti, A. Mallouhi, T. Frede, O. Pachinger, et al. Multislice Computed Tomography for Detection of Patients With Aortic Valve Stenosis and Quantification of Severity J. Am. Coll. Cardiol., April 4, 2006; 47(7): 1410 - 1417. [Abstract] [Full Text] [PDF]
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C. Marquie, G. De Geeter, D. Klug, C. Kouakam, F. Brigadeau, O. Jabourek, N. Trillot, D. Lacroix, and S. Kacet Post-operative use of heparin increases morbidity of pacemaker implantation. Europace, April 1, 2006; 8(4): 283 - 287. [Abstract] [Full Text] [PDF]
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R. L. Sacco, R. Adams, G. Albers, M. J. Alberts, O. Benavente, K. Furie, L. B. Goldstein, P. Gorelick, J. Halperin, R. Harbaugh, et al. Guidelines for Prevention of Stroke in Patients With Ischemic Stroke or Transient Ischemic Attack: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association Council on Stroke: Co-Sponsored by the Council on Cardiovascular Radiology and Intervention: The American Academy of Neurology affirms the value of this guideline. Circulation, March 14, 2006; 113(10): e409 - e449. [Abstract] [Full Text] [PDF]
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P. Engelfriet, J. Tijssen, H. Kaemmerer, M. A. Gatzoulis, E. Boersma, E. Oechslin, E. Thaulow, J. Popelova, P. Moons, F. Meijboom, et al. Adherence to guidelines in the clinical care for adults with congenital heart disease: The Euro Heart Survey on Adult Congenital Heart Disease Eur. Heart J., March 2, 2006; 27(6): 737 - 745. [Abstract] [Full Text] [PDF]
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V. Chan, W.R. E. Jamieson, A. G. Fleisher, D. Denmark, F. Chan, and E. Germann Valve Replacement Surgery in End-Stage Renal Failure: Mechanical Prostheses Versus Bioprostheses. Ann. Thorac. Surg., March 1, 2006; 81(3): 857 - 862. [Abstract] [Full Text] [PDF]
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J. G. Webb, M. Chandavimol, C. R. Thompson, D. R. Ricci, R. G. Carere, B. I. Munt, C. E. Buller, S. Pasupati, and S. Lichtenstein Percutaneous Aortic Valve Implantation Retrograde From the Femoral Artery Circulation, February 14, 2006; 113(6): 842 - 850. [Abstract] [Full Text] [PDF]
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A. Kulik, F. D. Rubens, P. S. Wells, C. Kearon, T. G. Mesana, J. van Berkom, and B.-K. Lam Early Postoperative Anticoagulation After Mechanical Valve Replacement: A Systematic Review Ann. Thorac. Surg., February 1, 2006; 81(2): 770 - 781. [Abstract] [Full Text] [PDF]
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R. L. Sacco, R. Adams, G. Albers, M. J. Alberts, O. Benavente, K. Furie, L. B. Goldstein, P. Gorelick, J. Halperin, R. Harbaugh, et al. Guidelines for Prevention of Stroke in Patients With Ischemic Stroke or Transient Ischemic Attack: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association Council on Stroke: Co-Sponsored by the Council on Cardiovascular Radiology and Intervention: The American Academy of Neurology affirms the value of this guideline. Stroke, February 1, 2006; 37(2): 577 - 617. [Abstract] [Full Text] [PDF]
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W. M. Popescu Ghost-Boostering Phantom Gradients Anesth. Analg., February 1, 2006; 102(2): 654 - 654. [Full Text] [PDF]
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P. Meurin, J. Y. Tabet, H. Weber, N. Renaud, and A. B. Driss Low-Molecular-Weight Heparin as a Bridging Anticoagulant Early After Mechanical Heart Valve Replacement Circulation, January 31, 2006; 113(4): 564 - 569. [Abstract] [Full Text] [PDF]
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F. di Marco, G. Meneghetti, and G. Gerosa Early anticoagulation after aortic valve replacement with bioprostheses: Time to abandon it? J. Thorac. Cardiovasc. Surg., November 1, 2005; 130(5): 1482 - 1483. [Full Text] [PDF]
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E. B. Schelbert, G. E. Rosenthal, K. F. Welke, and M. S. Vaughan-Sarrazin Treatment Variation in Older Black and White Patients Undergoing Aortic Valve Replacement Circulation, October 11, 2005; 112(15): 2347 - 2353. [Abstract] [Full Text] [PDF]
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B. Mahesh, G. Angelini, M. Caputo, X. Y. Jin, and A. Bryan Prosthetic Valve Endocarditis Ann. Thorac. Surg., September 1, 2005; 80(3): 1151 - 1158. [Abstract] [Full Text] [PDF]
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M. Kupari, H. Turto, and J. Lommi Left ventricular hypertrophy in aortic valve stenosis: preventive or promotive of systolic dysfunction and heart failure? Eur. Heart J., September 1, 2005; 26(17): 1790 - 1796. [Abstract] [Full Text] [PDF]
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E. R. Nowicki What is the Future of Mortality Prediction Models in Heart Valve Surgery? Ann. Thorac. Surg., August 1, 2005; 80(2): 396 - 398. [Full Text] [PDF]
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T R D Shaw, D B Northridge, and N Sutaria Mitral balloon valvotomy and left atrial thrombus Heart, August 1, 2005; 91(8): 1088 - 1089. [Full Text] [PDF]
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M. Briand, J. G. Dumesnil, L. Kadem, A. G. Tongue, R. Rieu, D. Garcia, and P. Pibarot Reduced Systemic Arterial Compliance Impacts Significantly on Left Ventricular Afterload and Function in Aortic Stenosis: Implications for Diagnosis and Treatment J. Am. Coll. Cardiol., July 19, 2005; 46(2): 291 - 298. [Abstract] [Full Text] [PDF]
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F. Thuny, G. Disalvo, O. Belliard, J.-F. Avierinos, V. Pergola, V. Rosenberg, J.-P. Casalta, J. Gouvernet, G. Derumeaux, D. Iarussi, et al. Risk of Embolism and Death in Infective Endocarditis: Prognostic Value of Echocardiography: A Prospective Multicenter Study Circulation, July 5, 2005; 112(1): 69 - 75. [Abstract] [Full Text] [PDF]
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A. Pelliccia, R. Fagard, H. H. Bjornstad, A. Anastassakis, E. Arbustini, D. Assanelli, A. Biffi, M. Borjesson, F. Carre, D. Corrado, et al. Recommendations for competitive sports participation in athletes with cardiovascular disease: A consensus document from the Study Group of Sports Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology Eur. Heart J., July 2, 2005; 26(14): 1422 - 1445. [Full Text] [PDF]
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P. Das, H. Rimington, and J. Chambers Exercise testing to stratify risk in aortic stenosis Eur. Heart J., July 1, 2005; 26(13): 1309 - 1313. [Abstract] [Full Text] [PDF]
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R. Zegdi, M. Debieche, C. Latremouille, D. Lebied, C. Chardigny, J.-M. Grinda, S. Chauvaud, A. Deloche, A. Carpentier, and J.-N. Fabiani Long-Term Results of Mitral Valve Repair in Active Endocarditis Circulation, May 17, 2005; 111(19): 2532 - 2536. [Abstract] [Full Text] [PDF]
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D. Detaint, D. Messika-Zeitoun, J.-F. Avierinos, C. Scott, H. Chen, J. C. Burnett Jr, and M. Enriquez-Sarano B-Type Natriuretic Peptide in Organic Mitral Regurgitation: Determinants and Impact on Outcome Circulation, May 10, 2005; 111(18): 2391 - 2397. [Abstract] [Full Text] [PDF]
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