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J Am Coll Cardiol, 2002; 39:1623-1629 © 2002 by the American College of Cardiology Foundation |
* Brigham and Women’s Hospital, Cardiovascular Division, Harvard Medical School, Boston, Massachusetts, USA
Research Institute for Internal Medicine, University of Oslo, Oslo, Norway
Rijnland Hospital, Leiderdorp, Netherlands
University Hospital of Bergen, Department of Clinical Chemistry, Division of Endocrinology, Bergen, Norway
|| Toronto General Hospital, University of Toronto, Cardiology Division, Toronto, Canada
Manuscript received October 1, 2001; revised manuscript received February 13, 2002, accepted February 19, 2002.
* Reprint requests and correspondence: Dr. Lynne W. Stevenson, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis Street, Boston, Massachusetts 02115.
OBJECTIVES: This study was designed to determine whether therapy with vasodilators and diuretics, designed to normalize loading conditions in decompensated heart failure (HF), reduces neurohormonal activation in the short term.
BACKGROUND: Elevated vasoactive neurohormone levels in chronic HF have adverse prognostic impact and may be targeted by specific therapies.
METHODS: Endothelin-1, catecholamines, renin, aldosterone, angiotensin and atrial natriuretic peptides (ANP, N-ANP and BNP) were measured in 34 patients with advanced HF before and after hemodynamically guided therapy with vasodilators and diuretics. The therapy was designed to reduce filling pressures and systemic vascular resistance (SVR) without inotropic therapy. Blood was drawn before therapy (A), after initial diuretic and nitroprusside therapy to optimize hemodynamics (B, mean 1.4 days) and after transition to an oral regimen designed to maintain improved hemodynamics (C, mean 3.4 days).
RESULTS: Mean pulmonary wedge pressure fell from 31 to 18 mm Hg, right atrial pressure from 15 to 8 mm Hg, and SVR from 1,780 to 1,109 dynes/s/cm–5. Cardiac index increased from 1.7 to 2.6 l/min/m2 without intravenous inotropic agents (all p 
0.05). Average endothelin levels declined by 30%, from 7.7 to 5.5 pg/ml, and remained low at time point C, 5.2 pg/ml (p < 0.01). Norepinephrine was 858 at time A, 817 at time B, and fell by time C to 608 pg/ml (p 0.05). The mean plasma BNP level fell by 26% after only 1.4 days and by 53% at time C (p < 0.001).
CONCLUSIONS: Neurohormonal activation rapidly decreases after short-term therapy tailored to decrease severely elevated filling pressures and SVR without inotropic agents. Therapy designed to address neurohormonal activation should include therapy to improve severe resting hemodynamic compromise.
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