Structural basis for pathologic left ventricular hypertrophy

Karl Weber, Christian G. Brilla

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Left ventricular hypertrophy (LVH) is a major risk factor associated with the emergence of symptomatic congestive heart failure. Cardiac myocyte excitation‐contraction coupling has been the biochemical focus in the search for insights into the impaired contractility, relaxation, and stiffness of the hypertrophied myocardium. Although hypettrophied myocytes are the hallmark of LVH, other aspects of myocardial structure may be altered to impair pump function—specifically an abnormal accumulation of connective tissue (interstitial fibrosis). Cardiac fibroblasts, which are nonmyocyte cells of the cardiac interstitium, synthesize and degrade collagen and, therefore, represent an important determinant of pathologic LVH. Significantly, this reactive fibrosis has been found not only in the pressure‐overloaded hypertrophied left ventricle but also in the normotensive, nonhypertrophied right ventricle of animals with experimental hypertension. These findings suggest the involvement of a circulating substance that has access to the coronary circulation common to both ventricles. Based on in vivo studies that examined this hypothesis, it can be concluded that chronic elevation of circulating aldosterone, relative to sodium intake, is associated with myocardial fibrosis, which initially adversely alters diastolic function and ultimately systolic ventricular function. The mechanisms by which fibroblast collagen metabolism is invoked in this setting are under investigation. Elucidation of these mechanisms may prepare the way to the prevention as well as the reversal of myocardial fibrosis and, in turn, of pathologic LVH.

Original languageEnglish (US)
Pages (from-to)10-14
Number of pages5
JournalClinical Cardiology
Volume16
Issue number2 S
DOIs
StatePublished - Jan 1 1993

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Left Ventricular Hypertrophy
Fibrosis
Heart Ventricles
Collagen
Fibroblasts
Coronary Circulation
Ventricular Function
Aldosterone
Cardiac Myocytes
Connective Tissue
Muscle Cells
Myocardium
Heart Failure
Sodium
Hypertension

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Structural basis for pathologic left ventricular hypertrophy. / Weber, Karl; Brilla, Christian G.

In: Clinical Cardiology, Vol. 16, No. 2 S, 01.01.1993, p. 10-14.

Research output: Contribution to journalArticle

Weber, Karl ; Brilla, Christian G. / Structural basis for pathologic left ventricular hypertrophy. In: Clinical Cardiology. 1993 ; Vol. 16, No. 2 S. pp. 10-14.
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