Affiliations: [a] Department of Pathology, The University of Alabama at Birmingham, Birmingham, Alabama, USA | [b] Department of Physiology and Pharmacology, Auburn University, Auburn, Alabama, USA
Correspondence:
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Address correspondence to: Joseph S. Janicki, 106 Greene Hall, Auburn University, Auburn, Alabama 36849–5517, USA. Tel.: +1 334 844 3700; Fax: +1 334 844 3697.
Abstract: The extracellular collagen matrix of the myocardium plays an important role in maintaining muscle fiber and cardiac alignment and ventricular shape and size. It also influences tissue and ventricle stiffness. This network consists of an organized hierarchy of collagen that is intimately associated with individual and groups of myocyte and muscle fibers, as well as the coronary vasculature. In renovascular and genetic hypertension, the hypertrophic response of the myocardium includes an increase in collagen concentration, thickening of existing fibrillar collagen, and addition of newly synthesized collagen to all of the matrix components. The consequences of this remodeling are a stiffer myocardium and left ventricular diastolic dysfunction. With removal of less than half of the normal amount of collagen the opposite occurs. That is, the ventricle dilates and there is an increase in ventricular compliance. Thus an abnormal accumulation of collagen is a major distinguishing factor between physiologic and pathologic hypertrophy while an abrupt decrease in collagen concentration results in a ventricular remodeling similar to that of a heart in failure.
