Role of vasoconstrictor mechanisms in the control of left ventricular performance of the normal and damaged heart

Jay N Cohn, FACC Iwao Mashiro, T. Barry Levine, Jawahar Mehta

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

The effect on the left ventricle of changes in the state of the arterial vasculature is best identified by utilizing calculations of pulsatile rather than steady flow phenomena. Impedance is the most satisfactory term to describe this effect. The normal ventricle compensates for changes in impedance largely by changes in preload, but the damaged heart loses this compensatory ability and its stroke volume becomes inversely related to outflow resistance. Patients with heart failure behave in a similar fashion and pharmacologic vasodilation may induce marked improvement in left ventricular pump function. Inappropriate vasoconstriction in heart failure may result from stimulation of the sympathetic or renin-angiotensin system. Early experience with converting enzyme inhibitors suggests that blockade of the formation of angiotensin II may be a useful means of treating some patients with heart failure.

Original languageEnglish (US)
Pages (from-to)1019-1022
Number of pages4
JournalThe American journal of cardiology
Volume44
Issue number5
DOIs
StatePublished - Oct 22 1979

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Vasoconstrictor Agents
Heart Failure
Electric Impedance
Enzyme Inhibitors
Renin-Angiotensin System
Vasoconstriction
Left Ventricular Function
Vasodilation
Angiotensin II
Stroke Volume
Heart Ventricles

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Role of vasoconstrictor mechanisms in the control of left ventricular performance of the normal and damaged heart. / Cohn, Jay N; Mashiro, FACC Iwao; Levine, T. Barry; Mehta, Jawahar.

In: The American journal of cardiology, Vol. 44, No. 5, 22.10.1979, p. 1019-1022.

Research output: Contribution to journalArticle

Cohn, Jay N ; Mashiro, FACC Iwao ; Levine, T. Barry ; Mehta, Jawahar. / Role of vasoconstrictor mechanisms in the control of left ventricular performance of the normal and damaged heart. In: The American journal of cardiology. 1979 ; Vol. 44, No. 5. pp. 1019-1022.
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