Sanjiv J Shah1, Andrew D Michaels. 1. Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Abstract
BACKGROUND: Although nesiritide is a potent vasodilator, studies using myocytes and isolated muscle strips have shown that recombinant B-type natriuretic peptide (BNP; nesiritide) decreases contractility. We sought to determine whether nesiritide decreases contractility in heart failure patients. METHODS AND RESULTS: Twenty-five heart failure patients underwent left heart catheterization (using a pressure-volume conductance catheter) and echocardiography at baseline and after a 2 mcg/kg bolus and 30-minute nesiritide infusion (0.01 mcg.kg.min). From invasive and noninvasive measurements, left ventricular (LV) systolic function indices were calculated, including ejection fraction, end-systolic elastance (E(es); single-beat invasive and noninvasive methods) and preload-recruitable stroke work (PRSW; noninvasive, single-beat method). The mean age was 60 +/- 11 years, 48% were male, 56% had coronary disease, and 64% had hypertension. Although nesiritide did not change LV ejection fraction, it did decrease contractility on pressure-volume analysis. Noninvasive E(es) decreased from 2.6 +/- 1.6 to 2.0 +/- 1.4 mm Hg/mL (P = .02). For those with reduced ejection fraction, E(es) decreased by invasive (P = .006) and noninvasive (P = .02) methods. PRSW decreased from 76 +/- 37 to 62 +/- 28 g/cm(2) (P = .003). On tissue Doppler imaging, nesiritide reduced the systolic annular tissue velocity of the mitral annulus from 8.0 +/- 1.9 to 6.9 +/- 1.3 cm/s (P = .04). CONCLUSIONS: Nesiritide infusion acutely decreases derived measures of contractility and systolic function in patients with chronic heart failure.
BACKGROUND: Although nesiritide is a potent vasodilator, studies using myocytes and isolated muscle strips have shown that recombinant B-type natriuretic peptide (BNP; nesiritide) decreases contractility. We sought to determine whether nesiritide decreases contractility in heart failurepatients. METHODS AND RESULTS: Twenty-five heart failurepatients underwent left heart catheterization (using a pressure-volume conductance catheter) and echocardiography at baseline and after a 2 mcg/kg bolus and 30-minute nesiritide infusion (0.01 mcg.kg.min). From invasive and noninvasive measurements, left ventricular (LV) systolic function indices were calculated, including ejection fraction, end-systolic elastance (E(es); single-beat invasive and noninvasive methods) and preload-recruitable stroke work (PRSW; noninvasive, single-beat method). The mean age was 60 +/- 11 years, 48% were male, 56% had coronary disease, and 64% had hypertension. Although nesiritide did not change LV ejection fraction, it did decrease contractility on pressure-volume analysis. Noninvasive E(es) decreased from 2.6 +/- 1.6 to 2.0 +/- 1.4 mm Hg/mL (P = .02). For those with reduced ejection fraction, E(es) decreased by invasive (P = .006) and noninvasive (P = .02) methods. PRSW decreased from 76 +/- 37 to 62 +/- 28 g/cm(2) (P = .003). On tissue Doppler imaging, nesiritide reduced the systolic annular tissue velocity of the mitral annulus from 8.0 +/- 1.9 to 6.9 +/- 1.3 cm/s (P = .04). CONCLUSIONS: Nesiritide infusion acutely decreases derived measures of contractility and systolic function in patients with chronic heart failure.