Acute Effects of Intravenous Nesiritide on Cardiac Contractility in Heart Failure |
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| Authors: | Sanjiv J. Shah Andrew D. Michaels |
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| Affiliation: | 1. Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL;2. Division of Cardiology, Department of Medicine, University of Utah, Salt Lake City, UT;1. Institut de Génétique Moléculaire de Montpellier, CNRS, UMR 5535, Montpellier, France;2. Université Montpellier 1, Montpellier, France;3. Université Montpellier 2, Montpellier, France;4. Department of Rheumatology, Montpellier I University and Lapeyronie Teaching Hospital, Montpellier, France;1. School of Immunity and Infection, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK;2. Department of Rheumatology, Sandwell and West Birmingham Hospitals NHS Trust, Birmingham B18 7QH, UK;3. Academic Medical Center, Division of Clinical Immunology & Rheumatology F4-105, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands;4. Clinical Unit Cambridge, GlaxoSmithKline, Addenbrooke’s Centre for Clinical Investigation, Box 128, Hills Road, Cambridge CB2 0GG, UK;1. Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada;2. Department of Physics, London Regional Cancer Program, London, Ontario, Canada;3. Department of Radiation Oncology, London Regional Cancer Program, London, Ontario, Canada |
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| Abstract: | BackgroundAlthough 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 ResultsTwenty-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 (Ees; 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 Ees decreased from 2.6 ± 1.6 to 2.0 ± 1.4 mm Hg/mL (P = .02). For those with reduced ejection fraction, Ees decreased by invasive (P = .006) and noninvasive (P = .02) methods. PRSW decreased from 76 ± 37 to 62 ± 28 g/cm2 (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).ConclusionsNesiritide infusion acutely decreases derived measures of contractility and systolic function in patients with chronic heart failure. |
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