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

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