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New Inotropic Drugs for Heart Failure
Irvin F. Goldenberg, MD;
Jay N. Cohn, MD
JAMA. 1987;258(4):493-496.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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DEPRESSION of myocardial contractility along with abnormalities in the peripheral circulation and the neuroendocrine system lead to the syndrome of congestive heart failure. Patients with heart failure have limited exercise tolerance because of breathlessness and/or fatigue. These symptoms are likely to be related to an exercise-induced rise in pulmonary capillary pressure and inadequate blood flow to exercising skeletal muscle. Optimal treatment of heart failure is based on manipulation of the three principal determinants of cardiac performance: preload, impedance, and contractility. Vasodilator therapy may reduce preload and/or impedance and improve cardiac function. This report will not deal with vasodilator treatment, which has been the subject of a recent review,1 but will focus on newer inotropic agents aimed at increasing myocardial contractility.
RATIONALE
The rationale for inotropic therapy is based on the observation that contractility of failing myocardium can be augmented.2 Studies in animal models with myocardial dysfunction and in
. . . [Full Text PDF of this Article]
Author Affiliations
From the Minneapolis Heart Institute (Dr Goldenberg) and the Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Minneapolis (Dr Cohn).
Footnotes
This article is one of a series sponsored by the American Heart Association.
Reprint requests to the Minneapolis Heart Institute, Suite 160, 920 E 28th St, Minneapolis, MN 55407 (Dr Goldenberg).
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