Renal Effects of Levosimendan in Patients Admitted With Acute Decompensated Heart Failure - Full Text View

Sponsored by:	University of Roma La Sapienza
Information provided by:	University of Roma La Sapienza
ClinicalTrials.gov Identifier:	NCT00527059

Purpose

The purpose of this study is to evaluate the effect of levosimendan infusion, in addition to standard therapy,on renal function in patients with Acute Heart Failure,compared with standard therapy alone.

Condition	Intervention	Phase
Heart Failure Renal Insufficiency	Drug: Levosimendan in addition to standard therapy Drug: spironolactone, beta-blockers,ecc	Phase IV

MedlinePlus related topics: Heart Failure

Drug Information available for: Levosimendan Simendan Spironolactone

U.S. FDA Resources

Study Type:	Interventional
Study Design:	Treatment, Randomized, Open Label, Active Control, Parallel Assignment, Efficacy Study
Official Title:	Renal Effects of Levosimendan in Patients Admitted With Acute Decompensated Heart Failure

Further study details as provided by University of Roma La Sapienza:

Primary Outcome Measures:

Primary endpoint: GFR measured by inulin Clearance. [ Time Frame: 0, 24. 48 and 72 hours after Levosimendan infusion starting ]

Secondary Outcome Measures:

Secondary endpoints: •Other renal function measures: BUN, albumin, urine volume, sodium excretion and plasma sodium, and cystatin. •Hemodynamic parameters: PCWP, PAP, cardiac output, HR, BP, renal blood flow. [ Time Frame: 0,1,24,48 and 72 hours after Levosimendan infusion started ]

Estimated Enrollment:	21
Study Start Date:	October 2007
Estimated Study Completion Date:	March 2008

Arms	Assigned Interventions
1: Experimental patients with acute heart failure	Drug: Levosimendan in addition to standard therapy intravenous infusion of levosimendan (10 minutes bolus with 6 mcg/Kg according to physician judgement, followed by 0.1 mcg/Kg/min for 24 hours) in addition to standard therapy
2: Active Comparator standard therapy for heart failure	Drug: spironolactone, beta-blockers,ecc

Detailed Description:

The term "cardiorenal syndrome" has been applied to the presence or development of a renal dysfunction in HF patients and may be the major precipitant of decompensation and cause for admission in these patients. The renal hypoperfusion that occurs with cardiac injury can lead to sodium and water retention and activation of the renin-angiotensin-aldosterone system and neurohormonal pathways with resultant deleterious effects on the myocardium. A vicious cycle may then ensue and be associated with increased cardiovascular complications. In this regard, renal dysfunction is of a functional nature and thus means to intervene with this vicious cycle need to be sought.

Several studies already demonstrated the deleterious effects of renal dysfunction on prognosis in patients with HF due to chronic left ventricular dysfunction.

Levosimendan increases myocardial contractility without significant changes in the intracellular calcium ion and cyclic adenosine monophosphate concentrations and does not enhance myocardial oxygen demand. By its action on the potassium channels this drug also dilates the coronary and peripheral arteries and exerts an anti-ischemic,anti-stunning effect. To date, the effects of levosimendan on renal function in patients with worsening chronic HF, remain unknown.

Eligibility

Genders Eligible for Study:	Both
Accepts Healthy Volunteers:	No

Criteria

Inclusion Criteria:

an ejection fraction (EF) 40% by transthoracic echocardiogram,
a baseline pulmonary capillary wedge pressure (PCWP) 20 mm Hg
a MDRD (Modification of Diet Renal Disease) score > 30 and < 60
and a standard therapy for HF that should include angiotensin converting enzyme inhibitors, angiotensin receptor blockers, aldosterone blocking agents (spironolactone) and beta-blockers, unless contraindicated

Exclusion Criteria:

patients receiving other oral or i.v. inotropes,
oral or i.v. diuretics
or receiving nitroglycerine or nitroprusside,
patients with systolic blood pressure <110 mmHg,
mechanical ventilation,
anticipated survival <30 days,
absence of thoracic windows for echocardiography,
acute coronary syndromes,
sustained ventricular tachycardia or ventricular fibrillation,
documented renal artery stenosis, requiring dialysis,
requiring admission primarily for concurrent morbidity,
severe aortic or mitral regurgitation,
left ventricular failure primarily from uncorrected obstructive valvular disease, hypertrophic obstructive cardiomyopathy, restrictive/obstructive cardiomyopathy,
uncorrected thyroid disease,
known amyloid cardiomyopathy
or known malfunctioning artificial heart valve.

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT00527059

Contacts

Contact: Francesco Fedele, professor

0039-0649979020

francesco.fedele@uniroma1.it

Locations

Italy
Department of Cardiovascular, Respiratory and Morphological Sciences, University of Rome La Sapienza
Rome, viale del Policlinico 155, Italy, 00161

Sponsors and Collaborators

University of Roma La Sapienza

Investigators

Principal Investigator:

Francesco Fedele, professor

Department of Cardiovascular, Respiratory and Morphological Sciences, University of Rome La Sapienza

More Information

Study ID Numbers:	LEV1068
Study First Received:	September 7, 2007
Last Updated:	September 7, 2007
ClinicalTrials.gov Identifier:	NCT00527059
Health Authority:	Italy: Ethics Committee

Keywords provided by University of Roma La Sapienza:

Cardiorenal syndrome

Study placed in the following topic categories:

Heart Failure
Renal Insufficiency
Heart Diseases
Urologic Diseases

Kidney Diseases
Spironolactone
Simendan

Additional relevant MeSH terms:

Vasodilator Agents
Molecular Mechanisms of Pharmacological Action
Cardiotonic Agents
Hormone Antagonists
Diuretics
Physiological Effects of Drugs
Hormones, Hormone Substitutes, and Hormone Antagonists
Enzyme Inhibitors
Cardiovascular Agents

Protective Agents
Pharmacologic Actions
Phosphodiesterase Inhibitors
Aldosterone Antagonists
Natriuretic Agents
Therapeutic Uses
Cardiovascular Diseases
Anti-Arrhythmia Agents

ClinicalTrials.gov processed this record on January 14, 2009