Note from the National Guideline Clearinghouse: This guideline references a drug(s)/intervention(s) for which important revised regulatory and/or warning information has been released.

Note: This guideline has been updated. The National Guideline Clearinghouse (NGC) is working to update this summary. The recommendations that follow are based on the previous version of the guideline.

The levels of evidence [A-D] supporting the recommendations are defined at the end of the "Major Recommendations" field.

Aims

• If a person at risk of a myocardial infarction (MI) has an acute coronary syndrome lasting over 20 minutes, imminent MI must be suspected. Instead of chest pain, acute dyspnoea may be the primary symptom.
• An acute coronary syndrome without myocardial damage is often unstable angina, which calls for active treatment.
• The diagnosis should be made without delay since early therapy improves the prognosis decisively.
• Thrombolytic therapy is given as early as possible in all cases with a clinical picture of imminent MI and corresponding electrocardiogram (ECG) changes (See the Finnish Medical Society Duodecim guideline "Thrombolytic Therapy and Balloon Angioplasty in Acute ST Elevation Myocardial Infarction [STEMI]").
• Acute angioplasty (percutaneous transluminal coronary angioplasty [PTCA], percutaneous coronary intervention [PCI]) is an alternative or a complementary procedure to thrombolytic therapy (Grines et al., 2003; Keeley, Boura, & Grines, 2003;) [A]. Angioplasty is probably preferred, at least in ST elevation MI (Keeley, Boura, & Grines, 2003).
• If there are no contraindications, aspirin and a beta-blocker should be started for all patients and, for most patients, also an angiotensin-converting enzyme (ACE) inhibitor and a statin on the first days of treatment.
• Health care system should include a planned care pathway for coronary patients.

Diagnosis

• See Figures 1, 2, 3, and 4 in the original guideline document.
• The diagnostic criteria change in the course of treatment.
  • During first aid, pain is the primary symptom in younger patients. Presentation in the elderly is often atypical.
  • When thrombolytic therapy is considered, an ST elevation on the ECG or a recent left bundle branch block (LBBB) should be taken into account (See the Finnish Medical Society Duodecim guideline "Thrombolytic Therapy and Balloon Angioplasty in Acute ST Elevation Myocardial Infarction [STEMI]").
  • In addition to pain and ECG findings, myocardial enzyme levels are needed for definite clinical diagnosis.
• For differential diagnosis of chest pain, see the Finnish Medical Society Duodecim guideline "Differential Diagnosis of Chest Pain".
• The pain in MI lasts over 20 minutes and is localized widely in the retrosternal area, transfers to the arms, back, neck, or lower jaw.
  • The pain is squeezing and is experienced as tightness, heaviness, and pressure or pressing. Breathing or changing posture does not influence the intensity of pain. Nitroglycerin may relieve but does not remove the pain.
  • The pain is usually severe and consistent. It may be localized in the upper abdomen, in which case, if nausea and vomiting are also present, it simulates acute abdominal disease.
  • The patient is often pale, in a cold sweat, and anxious.
• MI may also present without chest pain as acute pulmonary oedema, unconsciousness, or sudden death.
• Thrombolytic therapy is indicated
  • If the pain has lasted less than 6 to 12 (24) hours and there is at least a 2-mm elevation in the ST segment in at least two chest leads, or
  • A 1-mm elevation of ST in at least two leads in the extremities, or
  • A reciprocal ST depression in V1-V4, or
  • A recent LBBB
• The contraindications for thrombolytic therapy must always be considered (See the Finnish Medical Society Duodecim guideline "Thrombolytic Therapy and Balloon Angioplasty in Acute ST Elevation Myocardial Infarction [STEMI]").
• In clinical investigation, remember that the ECG and myocardial markers change with the course of the disease: first there is an ST elevation, after that development of the Q-wave, and finally T-wave inversion. Complications must also be recognized. In a T-wave infarction (non-Q-wave infarction), no classical Q waves are present, but the diagnosis is based on an increase of myocardial enzymes, chest pain, or ST-T changes. Classical Q-wave changes, ST elevations, and T inversions may be caused by various other diseases, which should be remembered in the differential diagnosis. An old infarction, bundle branch block (BBB), and early repolarization make the diagnosis difficult, in which case the change in ECG is important and an old ECG recording valuable. When added to other criteria, "minor" signs of infarction are also important.
• The European Society of Cardiology and the American College of Cardiology have agreed on a new definition of MI ("Myocardial infarction redefined," 2000):
  • Typical increase in the concentration of serum cardiac troponins or creatine kinase isoenzyme containing muscle and brain subunits (CK-MB) associated with at least one of the following:
    • Symptoms of cardiac ischaemia
    • Recent pathological Q waves in the ECG
    • Ischaemic ST segment changes in the ECG
    • Coronary artery revascularization

ECG Diagnosis

• Points for taking an ECG: acute care, emergency room, 12 hours later, on day 2, upon discharge from hospital, and thereafter as deemed necessary.
• ECG is the most important diagnostic procedure. To start with, the positions of the chest leads must be marked on the skin to allow detection of significant changes on the ECG. By monitoring the ECG, the efficacy of the treatment can be assessed. However, in the early stages there may be no changes in ECG, and the changes may be first evident after hours or even days. An ECG diagnosis is made more difficult by an old infarction, LBBB, or posterior infarction.
• In posterior wall infarction, a reciprocal ST segment depression in V1-V4 simulates ischaemia. A posterior infarction is, however, often inferoposterior and, in addition to ST segment depression, ST segment elevations are found in leads III and aVF.
• ST depression is suggestive of ischaemia and/or unstable angina pectoris. Extensive ST depressions in connection with a clinical picture of MI can indicate subendocardial damage.
• The ECG-diagnosis of myocardial infarction may be complicated by changes caused by (e.g., hypertrophic obstructive cardiomyopathy [HOCM], Wolff-Parkinson-White [WPW] syndrome, pulmonary embolism [massive], myopericarditis, hyperventilation, and tachyarrhythmias or their sequelae).

Tests Following the ECG

• Troponin is the most important new marker and is replacing creatine kinase (CK).
• CK and CK-MB or CK-MB mass
• A negative troponin T, troponin I, or CK-MB mass result 9 to 12 hours after the onset of symptoms practically rules out MI.
• Troponin T test is also valuable, if the time lapse since the beginning of the symptoms is more than 24 hours (the concentration remains elevated longer than that of CK). An elevated troponin T or troponin I concentration predicts adverse events irrespective of ECG findings (Olatidoye et al., 1998) [A].
• The tests should be performed 3 times in case of suspected infarction: on arrival of the patient and 12 and 24 hours after arrival.
• Blood haemoglobin, leucocytes, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP)
• Serum sodium and potassium, and chest x-ray if needed

Troponin-T or Troponin-I

• Principal indicators of myocardial damage, which can also be determined by means of rapid testing methods suited for primary health care. A reading device facilitates the interpretation.
• Troponin is more myocardium-specific than CK-MB and is also very sensitive.
• The concentration increases rapidly (in 4 to 6 hours) after myocardial damage, and the elevated levels persist for at least one week.
• Indications:
  • To verify or exclude MI (or myocarditis) when at least 6 hours have elapsed from the onset of pain. Unstable angina pectoris may give positive results, indicating slight myocardial damage, which means that the prognosis is serious regardless of the ECG findings and active treatment is necessary. The normal reference concentration is zero, or the method-dependent threshold is often given as <0.5 micrograms/L.
  • A negative result within 12 hours after the onset of pain excludes infarction.
  • Also used for the diagnosis of infarction when the patient's arrival for treatment is delayed, and CK has returned to normal.
  • Troponin verifies MI in cases where high CK concentration from skeletal muscle increases the CK-MB concentration over normal limits.
• Mild elevations in the concentration that exceed the threshold are often seen in cardiac surgery. Reference values that would justify the diagnosis of MI in these situations are not defined. Mild elevations may also occur when prolonged tachycardia causes a strain on the sick heart or when the right ventricle is stretched due to cardiac insufficiency or pulmonary embolism. Other, non-cardiac causes of mild increases in troponin concentrations include sepsis, liver cirrhosis, renal insufficiency, and rheumatoid arthritis.
• If the patient has an increased serum creatinine concentration, use serum CK-MB mass instead of troponin for the diagnostics of MI.

Serum CK-MB Mass

• More specific and sensitive than CK-MB
• Abnormal within 6 to 8 hours from the beginning of the pain, and remains abnormal for 1 to 2 days.
• Slightly positive values may indicate mild myocardial damage that requires active treatment. Unlike with troponin, the normal concentration of CK-MB is not zero. There is an uncertain borderline area of 5 to 10 micrograms/L between the positive and negative result.

Differential Diagnosis of Chest Pain

• The most important differential diagnoses include
  • Myopericarditis (See the Finnish Medical Society Duodecim guideline "Myocarditis")
  • Aortic dissection (See the Finnish Medical Society Duodecim guideline "Aortic Aneurysm and Dissection").
  • Pulmonary embolism (See the Finnish Medical Society Duodecim guideline "Pulmonary embolism [PE]")
  • Unstable angina pectoris (See the Finnish Medical Society Duodecim guideline "Unstable Angina Pectoris").
  • Oesophageal pain (See the Finnish Medical Society Duodecim guideline "Heartburn; Reflux Oesophagitis")
• See the Finnish Medical Society Duodecim guideline "Differential Diagnosis of Chest Pain."

Treatment

• Oxygen, if there are problems in oxygenation (pulmonary oedema)
• For treating pain
  • Glyceryl nitrate: mouth spray or sublingual tablet
  • Morphine 4 to 6 mg intravenously (i.v.), additionally 4 mg 1 to 3 times at 5-minute intervals, if necessary. Oxycodone 3 to 5 mg i.v. is an alternative.
  • A beta-blocker (metoprolol, atenolol, practolol) 2 to 5 mg i.v. may sometimes ease the pain.
• Aspirin 250 mg, chewable tablet or dissolved in water, unless there are contraindications (active ulcer, hypersensitivity to aspirin, anticoagulation) (Antithrombotic Trialists' Collaboration, 2002) [A].
• A beta-blocker (Danchin, De Benedetti, & Urban, 2002) [A] is always instituted, unless there are contraindications (asthma, hypotension, heart insufficiency, conduction disturbance, bradycardia). The first dose can be given intravenously (Chen et al., 2005) [A] if the patient is in pain, or orally if the patient is pain-free and time has passed since the infarction. Beta-blockers are useful especially in patients who are tachycardic and hypertensive but do not have heart failure.
  • i.v. dose: metoprolol or atenolol 5 mg
  • Orally: metoprolol or atenolol 25 to 50 mg x 2
• Thrombolytic therapy, unless there are contraindications (See the Finnish Medical Society Duodecim guideline "Thrombolytic Therapy and Balloon Angioplasty in Acute ST Elevation Myocardial Infarction ( STEMI)." ("Indications for fibrinolytic therapy," 1994) [A].
• Immediate PTCA (Grines et al., 2003; Keeley, Boura, & Grines, 2003) [A] if available. May be performed when thrombolytic therapy is contraindicated. The effect is better than that of thrombolysis in the acute phase and also in long-term follow-up. Stenting probably improves the outcome (Meads, et al, 2000) [A] (Grines et al., 1999). Further treatment is aspirin combined with clopidogrel for 3 to 6 months to prevent thrombosis and restenosis. Endothelialization of drug-eluting stents is slow, and therefore an uninterrupted antithrombotic medication is especially important during the first months. (Iakovou et al., 2005)
• An ACE inhibitor to all patients with signs or symptoms of heart failure or ejection fraction (EF) <40, anterior wall infarction, or reinfarction (Domanski et al., 1999; Danchin, De Benedetti, & Urban, 2002) [A]. Therapy is not usually started on the first day.
  • For example: captopril. Start with 6.25 mg and increase the dose rapidly.
• Continuous nitrate therapy (Mehta & Yusuf, 2000) [A]
  • Administered as an infusion, if the patient has ischaemic pain and pain medication has no effect. Nitrate infusion (see the Finnish Medical Society Duodecim guideline "Nitrate Infusion in Angina Pectoris and Myocardial Infarction").
  • Orally (e.g., isosorbide dinitrate 10 to 20 mg x 2 to 3)
• Heparinization (with low molecular weight [LMW] or unfractionated heparin) is often indicated
  • Treatment dose is used, if the patient has a thromboembolic complication or the condition remains otherwise unstable.
    • If the unstable situation is prolonged, it is advisable to continue with heparin up to one month.
  • Prophylactic dose is given if the bed rest is prolonged and the patient is significantly overweight.
  • If the patient has ventricular aneurysm or atrial fibrillation, anticoagulation therapy is gradually switched over to warfarin (possibly permanent), when the haemostatic situation is stabilized.
• Anticoagulation with warfarin is often started in massive anterior infarction and when transient ischemic attack (TIA) or stroke (mural thrombosis) occurs with MI.

Arrhythmias in Myocardial Infarction

Objectives

• To prevent sudden death and treat severe arrhythmias immediately
• To prevent arrhythmias by treating the underlying conditions

Causes of Arrhythmias

• Myocardial damage, ischaemia, and sympathetic stimulation are associated with ventricular arrhythmias.
• Ejection failure causes supraventricular tachyarrhythmias and atrial fibrillation.
• Vagal stimulation causes bradyarrhythmias and atrioventricular (AV) conduction disturbances, especially in cases of inferior-posterior wall infarction.
• Reperfusion often causes benign ventricular rhythm; however, it also causes severe ventricular arrhythmias.

Ventricular Fibrillation

• Often occurs within 2 to 4 hours of infarction. After 12 hours, a primary ventricular fibrillation is rare. Ventricular fibrillation that is rapidly treated in the initial phase does not necessarily worsen the prognosis.
• An early ectopic beat may initiate ventricular fibrillation in an ischaemic myocardium. Ectopic beats are not treated if cardiac monitoring is effective.
• Treatment
  • Acute ventricular fibrillation is treated by immediate defibrillation starting with 200 joules. Prolonged ventricular fibrillation frequently calls for cardiopulmonary resuscitation (CPR).
  • To prevent recurrence of fibrillation, lidocaine was formerly often used (initially as a bolus of 100 mg, repeated if necessary, and continued as an infusion of 1 to 3 mg/minutes). Lidocaine has currently been replaced by amiodarone: 5 mg/kg/30 min intravenously, thereafter infusion at 900 to 1200 mg/24 hours.
  • A beta-blocker is usually added to the therapy.

Ventricular Tachycardia

• More than three ectopic beats and a heart rate over 120 beats per minute (bpm).
• Brief, spontaneously ending bursts are seen in over 50% of patients with infarction during the first two days. They occur mainly 8 to 14 hours after, not immediately after the infarction, as does ventricular fibrillation.
• Ventricular tachycardia (VT) leads to haemodynamic collapse or ventricular fibrillation. The severity depends on the duration, variability, frequency, and timing of tachycardia.
• Ventricular tachycardia may be monomorphic or polymorphic.
• Treatment
  • Beta-blocker: metoprolol 5 mg i.v., repeatedly if necessary
  • Lidocaine boluses and infusion as in ventricular fibrillation, if haemodynamics compromise. Amiodarone may be a better alternative.
  • If necessary, synchronized cardioversion shock with 50 joules is performed.
  • Late in infarction, ventricular tachycardia is, like ventricular fibrillation, a serious problem considering the prognosis and requires further specialist examinations and treatment.

Ventricular Ectopic Beats

• Occur in nearly all patients with painful MI
• May cause complications if they are frequent (more than 5/min), are variable, or occur concomitantly with an early T wave
• Treatment is usually not necessary if cardiac monitoring is effective. A beta-blocker may be indicated. Potassium level should be kept above 4.0.

Idioventricular Rhythm

• Idioventricular rhythm is an arrhythmia often associated with MI. In the reperfusion phase, it may even indicate that thrombolysis has been successful. The frequency is often 70 to 80 bpm but may be as high as 120 bpm; drug therapy is not necessary.

Atrial Fibrillation

• Atrial fibrillation (AF) in a patient with infarction is often associated with cardiac insufficiency and it worsens the prognosis. Atrial fibrillation increases the risk of stroke, which is why low molecular weight (LMW) heparin and warfarin therapy are indicated if AF is prolonged.
• AF is common in the acute phase of myocardial infarction (15 to 20%), is often self-terminated, and does not always require treatment.
• In cardiac insufficiency, rapid atrial fibrillation requires active direct current (DC) cardioversion. Often, the achieved sinus rhythm does not remain. In such a case, haemodynamics must be stabilised (oxygenation, treatment of pulmonary oedema, controlling of ventricular response with a beta-blocker and digitalis) after which spontaneous reversal of the rhythm is waited for. The effect of the beta-blocker is seen rapidly but that of digitalis not before several hours. Rapid ventricular response may be controlled even if cardiac insufficiency is present: the benefit often outweighs the disadvantage.
• Selective beta-blockers are best suited for maintaining the achieved sinus rhythm.
• Intravenous amiodarone will not reduce the contraction of the myocardium. It is effective in prophylaxis of AF (together with a beta-blocker) and it may be used in cardioversion of AF and/or slowing down the ventricular response.
• Ibutilide is a new class III drug with a single indication: treatment of AF and flutter. There are limited data on its use in patients with infarction.
• Note: A broad QRS complex tachycardia in a patient with infarction must always be treated as a ventricular tachycardia.

Bradyarrhythmias

• A strong vagal reaction in the early stages of infarction may lead to a circulatory collapse.
• Postero-inferior wall infarction is often associated with a functional atrioventricular (AV) block. The QRS complex is narrow and the heart rhythm is 50 to 60 even in cases of a total block. A pacemaker is rarely needed.
• In anterior wall infarction, the proximal conduction system may be blocked: the QRS complex is wide, the substituting rhythm is slow (30 to 40), the patient is in a poor condition, and pacing is necessary. Prognosis is poor even with pacing.
• Drug treatment
  • Atropine 0.5 mg i.v., repeated as necessary, for treatment of functional sinus bradycardia if the heart rate is less than 40 bpm.

Pacemaker

• In anterior wall infarction, pacing is indicated if there is a 2nd or 3rd degree block. Pacing should be anticipated in case of a trifascicular block, alternating right and left bundle branch block, or if an extensive infarction is associated with left anterior fascicular block (LAFB) or left posterior fascicular block (LPFB).
• Postero-inferior wall infarction associated with a 3rd degree AV block requires pacing if bradycardia is detrimental to haemodynamics and not responsive to treatment with atropine.
• If temporary pacing is not possible, isoprenaline may be cautiously administered.

Right Ventricle Infarction

• The clinical picture and treatment principles of right ventricle infarction differ from pure left ventricle infarction.
• The clinical picture is dominated by hypotonia without pulmonary oedema or without severe dysfunction of the left ventricle. Simulates pulmonary embolism.
• Verified in lead V4R on the ECG.
• Treated with hydration, even if venous pressure is high.
• Occurs in connection with extensive inferoposterior infarction (occlusion of the stem of the right coronary artery).

Symptoms and Signs

• Hypotension, bradycardia, and high venous pressure without pulmonary oedema and cold limbs are characteristic symptoms.
• The lead V4R on the ECG gives a conclusive diagnosis: a 1-mm elevation is sensitive (70%) and specific (nearly 100%) (see Figure 5 in the original guideline document). ECG usually shows a concomitant left ventricular inferoposterior wall infarction.
• The tricuspidal valve is insufficient, but regurgitation is usually not audible (detected on echocardiography).
• As the right coronary artery usually (90%) supplies blood to the AV node, a partial or complete AV block is often present.

Differential Diagnosis

• All diseases that cause hypotension, pulmonary embolism being the most important.

Treatment

• Thrombolytic therapy with tissue plasminogen activator (TPA), which does not cause hypotension. See the Finnish Medical Society Duodecim guideline "Thrombolytic Therapy and Balloon Angioplasty in Acute ST Elevation Myocardial Infarction (STEMI)."
• Rapid correction of the hypotension by hydration is essential.
• Hypotensive drugs (nitrates) must be avoided.
• Atropine for bradycardia
• If pacing is required, a sequential pacemaker is preferable

Treatment in Hospital

Follow-up and Treatment

• Pain: morphine, nitro, beta-blocker
• Blood pressure
• Skin, peripheral circulation
• Increased respiratory rate suggests cardiac insufficiency.
• Monitoring of arrhythmias
• ST segment changes
• Oxygen saturation; oxygen or continuous positive airway pressure (CPAP)
• A comfortable posture
• Informing and reassuring the patient
• Nicotine replacement therapy is started already in the hospital. Nicotine addiction may be evaluated by using the Fagerstrom test, and the planning of further treatment may be based on it.
• In an uncomplicated infarction, patients are allowed to sit as soon as they want, they can eat unassisted, and they can be helped to a portable toilet at the bedside. Intensive monitoring is usually needed for 1 to 2 days.
• The infarction is complicated and treatment lasts longer if the patient has had
  • Shock
  • Hypotension
  • Obvious cardiac insufficiency (usually requires thrombosis prophylaxis or anticoagulation, especially if in connection with atrial fibrillation)
  • Prolonged chest pain
  • Serious ventricular arrhythmias
  • Thromboembolic complications
  • Anatomical complications (papillary muscle dysfunction or rupture)
  • Pericarditis on days 2 to 4
• Treatment of the patient in primary health care (in a primary health care hospital) is justifiable if the patient's prognosis is otherwise poor: those who are permanent inpatients or otherwise severely disabled and for whom invasive treatment has not been planned.

Assessment of Risk Factors in a Patient with Myocardial Infarction

• The most important causes of mortality are
  • Reinfarction
  • Cardiac insufficiency
  • Arrhythmias: especially late phase ventricular tachycardia
• During hospitalization, a poor prognosis is indicated by
  • Cardiac insufficiency and extensive infarction (EF < 25%)
  • Chest pain and ischaemic ST changes (send to angiography)
  • In connection with non-Q-wave infarction, risk factors for CHD and especially diabetes mellitus
• Evaluation of ischaemia and need for active treatment
  • Risk is highest during the first few weeks and months after infarction. Therefore, at the end of the hospital treatment, an early symptom-limited exercise test is performed on many patients to estimate the need for angioplasty and coronary surgery in particular (see Table below).
• For indications of coronary angiography, see the Finnish Medical Society Duodecim guideline "Diagnostic Coronary Angiography."

Table: Assessment of Risk of Reinfarction and Patient's Prognosis

*Mean workload of last 4 minutes

Care After Myocardial Infarction

Drug Treatment

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