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Rex N. MacAlpin, MD

JAMA. 1978;240(5):461-462.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The magnitude of systolic shortening of cardiac muscle is related directly to the diastolic length of the muscle and to its contractile state, and inversely to the force against which it must shorten (afterload). The normal heart in diastole operates on a compliant part of its tension-length curve, ie, a small increase in distending force (filling pressure or preload) stretches the muscle a relatively large amount and causes a relatively great increase in diastolic volume. If the afterload remains unchanged, this distended ventricle will in systole eject an increased stroke volume. This is a means whereby the normal heart can increase its stroke output in response to an increase in input without resorting to an increase in heart rate or basic contractile state. By the same mechanism it can also maintain its stroke volume in the face of an increased afterload at the expense of a small increase in diastolic . . . [Full Text PDF of this Article]

Author Affiliations
University of California at Los Angeles School of Medicine Los Angeles

Footnotes
Address editorial communications to the Editor, 535 N Dearborn St, Chicago, IL 60610.

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