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31 December 1969

Connective tissue skeleton in the normal left ventricle and in hypertensiveleft ventricular hypertrophy and chronic chagasic myocarditis.

Marcos A Rossi

Med Sci Monit 2001; 7(4): RA820-832 :: ID: 421064

Abstract

Pictures certainly are worth a thousand words in the case of the structureof the connective tissue skeleton of normal and diseased myocardium. This report reviews the connectivetissue matrix of the normal human myocardial tissue and the pathological myocardial fibrosis in leftventricular hypertrophy due to chronic arterial hypertension in humans and in human chronic chagasicmyocarditis. The myocardial connective tissue matrix was studied employing a cell-maceration method thatremoves the myocardial tissue non-fibrous elements, and leaves behind a non-collapsed matrix, thus allowinga better three-dimensional view. Such information extends our knowledge of the expression of interstitialmyocardial fibrous tissue in normal hearts and in hypertensive left ventricular hypertrophy and chronicchagasic myocarditis. The progressive accumulation of interstitial collagen fibers in both chronic cardiacdiseases may be expected to decrease myocardial compliance and disrupt synchronous contractions of theventricles during systole, contributing to a spectrum of ventricular dysfunction that involve eitherthe diastolic or systolic phase of the cardiac cycle or both. In hypertensive heart disease myocardialfibrosis can be also implicated in the genesis of ventricular dysrhythmias, possible causes of suddendeath among chronic hypertensive patients. Regarding chronic chagasic myocarditis, myocardial fibrosisis probably implicated in the genesis of malignant ventricular tachyarrhythmias (ventricular tachycardiaand ventricular fibrillation), major causes of sudden death among patients with chronic Chagas' heartdisease. The collagen distribution could interfere on the electrical properties of the myocardium. Fibrosiscan block the cardiac impulse that may recycle (re-entry) through an alternative route and could slowconduction. In addition, the thick collagenous septa encompassing muscle fiber bundles could interferewith lateral impulse conduction, which would favor re-entry. Moreover, the methodology used is a usefultool to study the spatial organization of the collagen fibrils of the myocardium under normal and pathologicalconditions.

Keywords: Myocardium, connective tissue matrix, left ventricular hypertrophy, hypertensive heart disease,, left ventricular hypertrophy, chronic chagasic myocarditis, cell-maceration

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