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European Heart Journal 1991 12(Supplement C):2-7; doi:10.1093/eurheartj/12.suppl_C.2
Copyright © 1991 by the European Society of Cardiology.
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© 1991 The European Society of Cardiology

Time-constant adaptations in heart failure

R. Zelis, L.I. Sinoway, U. Leuenberger, B. S. Clemson and D. Davis

Division of Cardiology, The Milton S. Hershey Medical Centre, The Pennsylvania State University, College of Medicine Hershey, Pennsylvania 17033, U.S.A.

Address for correspondence and reprints: R. Zelis, Division of Cardiology. The Milton S. Hershey Medical Centre. The Pennsylvania State University. College of Medicine, P.O. Box 850. Hershey. Pennsylvania 17033. U S.A.

The circulatory compensatory mechanisms designed to cope quickly with physiological stress (e.g. sympathetic nervous system and the Frank–Starling mechanism) are less effective when there is chronic pathological stress, such as congestive heart failure (CHF). Other mechanisms come into play that operate over a longer time (e.g. activation of the renin–angiotensin–aldosterone system, myocardial hypertrophy and physiological deconditioning). Changes in blood vessels and skeletal muscle metabolism that result from inadequate delivery of oxygenated blood to working muscles belong to the group of mechanisms that develop slowly. When CHF therapy is successful, the abnormalities produced by this latter group of mechanisms will improve, but slowly. The concept that compensatory mechanisms have either short or long time constants for activation and reversal may explain why exercise tolerance improves much later than haemodynamics, which can be reversed acutely with vasodilator therapy.

Key Words: Vasoconstriction • sympathetic tone • exercise capacity • vasodilator therapy • metabolic vasodilation • afterload mismatch • myocardial hypertrophy • vasoactive hormones


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