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Abstract

The objective of this article was to present a review of the collagen tissue of the heart muscle as a function of age. The myocardial collagen matrix consists of a network of fibrillar collagen which is intimately connected to the myocyte. Most collagen fibers reside in parallel with myocytes. These fibers may have a wavy, taut or coiled appearance. Fibrillar collagen types I and III are the major components of the myocardial collagen matrix. Collagen type I has been found to represent nearly 80% of the total collagen protein, while type III collagen is present in lower proportions (approximately 11%). Cardiac fibroblasts are the cellular source of fibrillar collagen, cardiac myocytes expressing only mRNA for type IV collagen. Collagens types I and III exhibit a high tensile strength which plays an important role in the behavior of the ventricle during the cardiac cycle. The collagen concentration and the intermolecular cross-linking of collagen increase with age. Measurements of collagen content in myocardial tissue suggest that it is the type I collagen fibers that increase in number and thickness in the aged. At the same time, electron microscopic observations have shown an increase in the number of collagen fibrils with a large diameter in the aging heart. The mechanism responsible for the myocardial fibrosis in the senescent myocardium is unclear. The collagen deposition in the myocardium could be due to the regulation of collagen biosynthesis at pre-translational levels. It is possible that the regulatory elements involved in this process are growth factors such as TGF-beta 1 and hormones and neurotransmitters. Details of regulatory mechanism that may come into play during aging may be elucidated by further investigations. The accumulation of collagen within the myocardium increases muscle stiffness. Myocardial function is affected by this process; this is usually reflected by incomplete relaxation during early diastolic filling, and presumably account for the decrease in early left ventricular diastolic compliance.

Efeito do treinamento físico em alterações induzidas pelo envelhecimento no músculo papilar do rato

“…Collagen accumulation as a function of age was also observed in the human heart 11,12 . The mechanisms responsible for the loss of myocytes with areas of interstitial and replacement fibrosis in the myocardium are at present unknown 7 .…”

“…These results are similar to the findings obtained by others, which have shown a reduction in the total number of myocytes in the ventricles of rats from 4 to 12 months 7 and from 4 to 15 months 9 . According to Anversa et al 24 , a comparable phenomenon occurs in the human heart, as well 12,25,26 . It is possible that the myocyte hypertrophy that occurred in the aged heart was capable of compensating for the loss of these muscle cells.…”

“…However, Anversa et al 7 demonstrate that myocyte cellular hyperplasia also participates in the hypertrophic response of the myocardium during senescence 7 . The continued loss of myocytes in the ventricles can be expected to generate a greater workload on the remaining myocytes, which may function as a chronic mechanical stimulus for cellular growth 7,11,12,24,36 .…”

“…The papillary muscles are an integral part of the ventricles and play an important role in their geometry and systolic function [1][2][3][4] Previous studies of age-related variations in the papillary muscle [1][2][3]5 showed that the density of myocytes, connective tissue and capillaries as well as the crosssectional area of myocytes and the physical and biochemical characteristics of the papillary muscle are dependent upon age [6][7][8][9][10][11][12][13] . The most evident age-related effects on the papillary muscle are the loss of muscle cells and an increase in connective tissue 9,10 .…”

Association between Left Ventricular Diastolic Dysfunction and Renal Hemodynamic Change in Patients with Treated Essential Hypertension

“…LV diastolic dysfunction (abnormal relaxation) in hypertensive patients is induced not only by LV hypertrophy but also by cardiac fibrosis with an increase in myocardial collagen matrix. It has been shown that the number and thickness of type I collagen fibers and intermolecular cross-linking of collagen are increased in the aged (24). In an autopsy study, the percentage of focal and global glomerulosclerosis, the extent of interstitial fibrosis, and the extent of tubular atrophy were all increased with age (25).…”