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J Am Coll Cardiol, 2008; 52:200-207, doi:10.1016/j.jacc.2008.02.083
© 2008 by the American College of Cardiology Foundation
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CLINICAL RESEARCH: HEART FAILURE

Sodium Nitroprusside for Advanced Low-Output Heart Failure

Wilfried Mullens, MD, Zuheir Abrahams, MD, PhD, Gary S. Francis, MD, FACC, Hadi N. Skouri, MD, Randall C. Starling, MD, MPH, FACC, James B. Young, MD, FACC, David O. Taylor, MD, FACC and W.H. Wilson Tang, MD, FACC*

Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Cleveland Clinic, Cleveland, Ohio.

Manuscript received November 15, 2007; revised manuscript received February 7, 2008, accepted February 12, 2008.

* Reprint requests and correspondence: Dr. W. H. Wilson Tang, Section of Heart Failure and Cardiac Transplantation Medicine, Department of Cardiovascular Medicine, Cleveland Clinic, 9500 Euclid Avenue, Desk F25, Cleveland, Ohio 44195. (Email: tangw{at}ccf.org).

Objectives: This study was designed to examine the safety and efficacy of sodium nitroprusside (SNP) for patients with acute decompensated heart failure (ADHF) and low-output states.

Background: Inotropic therapy has been predominantly used in the management of patients with ADHF presenting with low cardiac output.

Methods: We reviewed all consecutive patients with ADHF admitted between 2000 and 2005 with a cardiac index ≤2 l/min/m2 for intensive medical therapy including vasoactive drugs. Administration of SNP was chosen by the attending clinician, nonrandomized, and titrated to a target mean arterial pressure of 65 to 70 mm Hg.

Results: Compared with control patients (n = 97), cases treated with SNP (n = 78) had significantly higher mean central venous pressure (15 vs. 13 mm Hg; p = 0.001), pulmonary capillary wedge pressure (29 vs. 24 mm Hg; p = 0.001), but similar demographics, medications, and renal function at baseline. Use of SNP was not associated with higher rates of inotropic support or worsening renal function during hospitalization. Patients treated with SNP achieved greater improvement in hemodynamic measurements during hospitalization, had higher rates of oral vasodilator prescription at discharge, and had lower rates of all-cause mortality (29% vs. 44%; odds ratio: 0.48; p = 0.005; 95% confidence interval: 0.29 to 0.80) without increase in rehospitalization rates (58% vs. 56%; p = NS).

Conclusions: In patients with advanced, low-output heart failure, vasodilator therapy used in conjunction with optimal current medical therapy during hospitalization might be associated with favorable long-term clinical outcomes irrespective of inotropic support or renal dysfunction and remains an excellent therapeutic choice in hospitalized ADHF patients.

Key Words: heart failure • hemodynamics • cardiac output • inotropic agents • vasodilation

Abbreviations and Acronyms
  ADHF = acute decompensated heart failure
  LV = left ventricle/ventricular
  MAP = mean systemic arterial pressure
  mPAP = mean pulmonary arterial pressure
  PCWP = pulmonary capillary wedge pressure
  SNP = sodium nitroprusside


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Vasodilator Therapy for Decompensated Heart Failure
Clyde W. Yancy
J. Am. Coll. Cardiol. 2008 52: 208-210. [Full Text] [PDF]



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C. W. Yancy
Vasodilator therapy for decompensated heart failure.
J. Am. Coll. Cardiol., July 15, 2008; 52(3): 208 - 210.
[Full Text] [PDF]




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