The myocardium is composed of cardiac muscle fibers supported within a three-dimensional scaffolding of fibrillar collagen. Collagen fibers surround and group these muscle fibers. They also tether individual muscle fibersto one another and their neighboring vasculature. Fibrillar collagen represents morphologic correlates of in-series and in-parallel elastic elements described in classic concepts of cardiac muscle mechanics. The contractile behavior of the heart is imparted by cardiac myocytes; its extracellular matrix and myocytes impart cardiac tissue with recoil<sup>12 Robinson T.F., Factor S.M., Sonneblick E.H. The heart as a suction pump Sci Am 1986 ;  254 : 84  [cross-ref]

Cliccare qui per andare alla sezione Riferimenti</sup>, and viscoelastic behavior.

The hypertrophic growth of myocardium, similar to what occurs with exercise training or with pressure or volume overloads of one or both ventricles, involves muscular and nonmuscular compartments. In the athlete, hypertrophy is adaptive because each compartment grows in relative proportion to one another. In disease states, extracellular matrix growth can be disproportionate relative to myocyte hypertrophy. Collagen accumulation can occur in the absence of myocyte growth. In either case, an adverse accumulation of fibrillar collagen leads to pathologic remodeling of cardiac tissue with profound functional consequences.

This article reviews the normal fibrillar collagen network of the heart, its structural iterations in hypertensive heart disease and ischemic cardiomyopathy, functional consequences of an abnormal collagen network of the myocardium, and factors regulating matrix growth, which is expressed morphologically as cardiac fibrosis. Finally, concepts of cardioprotection and cardioreparation are reviewed together with accompanying evidence which suggests that such selective strategies can be used to respectively prevent or regress cardiac fibrosis.