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Aldosterone blockade in heart failure.

Allan D Struthers
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Abstract

Aldosterone plays a key role in the pathophysiology of heart failure. Angiotensin converting enzyme inhibitors and angiotensin II receptor blockers may not suppress aldosterone production in the long term. This allows aldosterone to exert its effects on myocardial fibrosis and cardiac remodelling, endothelial function, electrolytes and baroreceptor response. The Randomized Aldactone Evaluation Study (RALES) tested spironolactone against placebo in patients with severe heart failure. The study found a 30% reduction in the risk of death among patients treated with spironolactone and a 31% reduction in the risk of death from cardiac causes. Patients in the spironolactone group had significantly lower risks of death from progression of heart failure and sudden cardiac death. The Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) investigated the effects of eplerenone against placebo in patients with myocardial infarction complicated by left ventricular dysfunction. Compared to placebo, the relative risk of death from any cause was 0.85 in eplerenone-treated patients, and the relative risk of death or hospitalisation for cardiovascular events was 0.87. The reduction in the risk of sudden death from cardiac causes was statistically significant. In conclusion, aldosterone blockade should form part of optimal therapy for patients with heart failure.

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Cardiac Output, LowHeartHumansMineralocorticoid Receptor AntagonistsMyocardiumRandomized Controlled Trials as TopicJournal ArticleReview

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BibTeXRIS

Allan D Struthers. 2004. Aldosterone blockade in heart failure.. https://doi.org/10.3317/jraas.2004.021

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Use of levosimendan, a new inodilator, for postoperative myocardial stunning in a premature neonate.

OBJECTIVE: To first report the successful use of the new inodilator levosimendan in a premature infant with congestive heart failure (CHF) following cardiac surgery. Although the calcium sensitizer levosimendan improves hemodynamics in adults with CHF, no data are available on the use of levosimendan in premature infants with CHF. DESIGN: Single case report. SETTING: Twenty-bed postoperative adult and pediatric cardiac intensive care unit. PATIENT: A 32 wks gestational age, 1525-g premature male twin with transposition of the great arteries. INTERVENTIONS: The patient underwent arterial switch operation. MEASUREMENTS AND MAIN RESULTS: Immediately after operation, the patient developed signs of low cardiac output syndrome. Mixed venous saturation was 56%, serum lactate increased to 14.8 mmol/L, systolic arterial pressure was 40 mm Hg, left atrial pressure was 24 mm Hg, and echocardiography showed reduced left ventricular function with a fractional shortening of 10%. There were no signs of reduced coronary perfusion. Milrinone, dobutamine, and epinephrine did not improve hemodynamics. Levosimendan was initiated at a dose of 0.05 mug.kg.min, increased to 0.1 mug.kg.min, and continuously infused for 24 hrs. Within 6 hrs after starting the levosimendan infusion, left atrial pressure decreased to 7 mm Hg and systolic arterial pressure increased to 60 mm Hg; within 24 hrs after initiation serum lactate level normalized to 1.7 mmol/L and mixed venous saturation increased to 81%. Echocardiography revealed improvement of left ventricular function with a fractional shortening of 25%. No side effects were recognized during administration of levosimendan. CONCLUSIONS: In this premature neonate with postoperative low cardiac output syndrome due to failing myocardial function, levosimendan was a potent inotropic agent.

Cardiac Output, Low↗