Comparison of the effects of dobutamine and nesiritide (B-type natriuretic peptide) on ventricular ectopy in acutely decompensated ischemic versus nonischemic cardiomyopathy

Abstract

Congestive heart failure (CHF) involves many complex autonomic and neurohormonal responses (such as activation of the renin-angiotensin-aldosterone and sympathetic systems) that can exert deleterious effects on the heart, leading to further cardiac decompensation. Inotropic therapy with dobutamine can improve cardiac hemodynamics, but also may cause arrhythmogenesis.1,2 Nesiritide (B-type natriuretic peptide, an endogenous cardiac hormone) is a systemic arterial and venous vasodilator,3–5 and has been shown to significantly reduce symptoms and improve hemodynamics in hospitalized patients with acute decompensated CHF without increasing heart rate. Nesiritide also suppresses norepinephrine, endothelin-1, and the renin-angiotensin-aldosterone system while promoting natriuresis.6–8 In the Prospective Randomized Evaluation of Cardiac Ectopy with Dobutamine or Nesiritide Therapy (PRECEDENT) trial, dobutamine was associated with significant increases in ventricular tachycardia (VT) and heart rate, especially in patients without a history of VT, suggesting that proarrythmic effects may be due to sympathetic activation of a dormant substrate.9 In contrast, nesiritide was associated with an actual reduction in VT without an increase in heart rate. The objective of this study was to determine the differential effects of dobutamine and nesiritide on ventricular arrhythmias and on heart rate in patients with ischemic and nonischemic cardiomyopathy.