Instantaneous force-velocity-length relations

Experimental findings and clinical correlates

Karl Weber, Joseph S. Janicki

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

The clinically failing heart and its response to various therapeutic interventions are discussed in terms of the shortening characteristics of the intact ventricular myocardium. The maximal wall force developed from any given initial fiber length is observed in the isovolumetrically beating heart and described by the linear isovolumetric force-length relation. Positive (norepinephrine-induced) or negative (propranolol-induced) shifts in contractile state, respectively, raise or lower the slope of the force-length relation. Moreover, this relation determines the end-systolic limits of fiber shortening for the ejecting ventricle: that is, regardless of the contractile state, the magnitude of systolic force and the course of the systolic force with respect to time, shortening will cease when the conditions of maximal (isovolumetric) force and length are matched. Thus the end-systolic and isovolumetric force-length relations are equivalent, with the slope of either relation providing an estimate of contractile state. A depression in contractility reduces the extent of shortening and thereby describes one mechanical characteristic of the failing heart. The rate and extent of shortening for any given contractile state are also determined by the interrelation of instantaneous force and length. An ejection force of increased magnitude (afterload excess) as seen in the enlarged or pressure-overloaded heart will restrict shortening and serves as another explanation of failure. These instantaneous relations are also fundamental to understanding of the therapeutic concept of unloading.

Original languageEnglish (US)
Pages (from-to)740-747
Number of pages8
JournalThe American journal of cardiology
Volume40
Issue number5
DOIs
StatePublished - Jan 1 1977
Externally publishedYes

Fingerprint

Propranolol
Myocardium
Norepinephrine
Pressure
Therapeutics

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Instantaneous force-velocity-length relations : Experimental findings and clinical correlates. / Weber, Karl; Janicki, Joseph S.

In: The American journal of cardiology, Vol. 40, No. 5, 01.01.1977, p. 740-747.

Research output: Contribution to journalArticle

@article{ef53ba743905420d9f68d68450ddbe42,
title = "Instantaneous force-velocity-length relations: Experimental findings and clinical correlates",
abstract = "The clinically failing heart and its response to various therapeutic interventions are discussed in terms of the shortening characteristics of the intact ventricular myocardium. The maximal wall force developed from any given initial fiber length is observed in the isovolumetrically beating heart and described by the linear isovolumetric force-length relation. Positive (norepinephrine-induced) or negative (propranolol-induced) shifts in contractile state, respectively, raise or lower the slope of the force-length relation. Moreover, this relation determines the end-systolic limits of fiber shortening for the ejecting ventricle: that is, regardless of the contractile state, the magnitude of systolic force and the course of the systolic force with respect to time, shortening will cease when the conditions of maximal (isovolumetric) force and length are matched. Thus the end-systolic and isovolumetric force-length relations are equivalent, with the slope of either relation providing an estimate of contractile state. A depression in contractility reduces the extent of shortening and thereby describes one mechanical characteristic of the failing heart. The rate and extent of shortening for any given contractile state are also determined by the interrelation of instantaneous force and length. An ejection force of increased magnitude (afterload excess) as seen in the enlarged or pressure-overloaded heart will restrict shortening and serves as another explanation of failure. These instantaneous relations are also fundamental to understanding of the therapeutic concept of unloading.",
author = "Karl Weber and Janicki, {Joseph S.}",
year = "1977",
month = "1",
day = "1",
doi = "10.1016/0002-9149(77)90191-6",
language = "English (US)",
volume = "40",
pages = "740--747",
journal = "American Journal of Cardiology",
issn = "0002-9149",
publisher = "Elsevier Inc.",
number = "5",

}

TY - JOUR

T1 - Instantaneous force-velocity-length relations

T2 - Experimental findings and clinical correlates

AU - Weber, Karl

AU - Janicki, Joseph S.

PY - 1977/1/1

Y1 - 1977/1/1

N2 - The clinically failing heart and its response to various therapeutic interventions are discussed in terms of the shortening characteristics of the intact ventricular myocardium. The maximal wall force developed from any given initial fiber length is observed in the isovolumetrically beating heart and described by the linear isovolumetric force-length relation. Positive (norepinephrine-induced) or negative (propranolol-induced) shifts in contractile state, respectively, raise or lower the slope of the force-length relation. Moreover, this relation determines the end-systolic limits of fiber shortening for the ejecting ventricle: that is, regardless of the contractile state, the magnitude of systolic force and the course of the systolic force with respect to time, shortening will cease when the conditions of maximal (isovolumetric) force and length are matched. Thus the end-systolic and isovolumetric force-length relations are equivalent, with the slope of either relation providing an estimate of contractile state. A depression in contractility reduces the extent of shortening and thereby describes one mechanical characteristic of the failing heart. The rate and extent of shortening for any given contractile state are also determined by the interrelation of instantaneous force and length. An ejection force of increased magnitude (afterload excess) as seen in the enlarged or pressure-overloaded heart will restrict shortening and serves as another explanation of failure. These instantaneous relations are also fundamental to understanding of the therapeutic concept of unloading.

AB - The clinically failing heart and its response to various therapeutic interventions are discussed in terms of the shortening characteristics of the intact ventricular myocardium. The maximal wall force developed from any given initial fiber length is observed in the isovolumetrically beating heart and described by the linear isovolumetric force-length relation. Positive (norepinephrine-induced) or negative (propranolol-induced) shifts in contractile state, respectively, raise or lower the slope of the force-length relation. Moreover, this relation determines the end-systolic limits of fiber shortening for the ejecting ventricle: that is, regardless of the contractile state, the magnitude of systolic force and the course of the systolic force with respect to time, shortening will cease when the conditions of maximal (isovolumetric) force and length are matched. Thus the end-systolic and isovolumetric force-length relations are equivalent, with the slope of either relation providing an estimate of contractile state. A depression in contractility reduces the extent of shortening and thereby describes one mechanical characteristic of the failing heart. The rate and extent of shortening for any given contractile state are also determined by the interrelation of instantaneous force and length. An ejection force of increased magnitude (afterload excess) as seen in the enlarged or pressure-overloaded heart will restrict shortening and serves as another explanation of failure. These instantaneous relations are also fundamental to understanding of the therapeutic concept of unloading.

UR - http://www.scopus.com/inward/record.url?scp=0017742949&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0017742949&partnerID=8YFLogxK

U2 - 10.1016/0002-9149(77)90191-6

DO - 10.1016/0002-9149(77)90191-6

M3 - Article

VL - 40

SP - 740

EP - 747

JO - American Journal of Cardiology

JF - American Journal of Cardiology

SN - 0002-9149

IS - 5

ER -