Myocardial fibrosis and the renin-angiotensin-aldosterone system

• Published in: Journal of cardiovascular pharmacology Vol. 20 Suppl 1; p. S48
• Main Authors: Weber, K T, Brilla, C G
• Format: Journal Article
• Language: English
• Published: United States 1992
• Subjects: Aldosterone - blood; Angiotensin II - blood; Angiotensin-Converting Enzyme Inhibitors - therapeutic use; Animals; Cell Line; Endomyocardial Fibrosis - etiology; Endomyocardial Fibrosis - pathology; Female; Humans; Male; Myocardium - pathology; Peptidyl-Dipeptidase A - metabolism; Renin-Angiotensin System - physiology; RNA, Messenger - analysis
• ISSN: 0160-2446
• DOI: 10.1097/00005344-199212001-00010

In both men and women left ventricular hypertrophy (LVH) is the major risk factor associated with the appearance of diastolic and/or systolic myocardial failure. It is not the growth of cardiac myocytes, however, that is responsible for an abnormal structural remodeling of the hypertrophied myocardium in pathologic LVH, but instead, nonmyocyte cells whose behavior and growth are altered by chronic elevations in circulating hormones. Hormone-mediated cardiac fibroblast proliferation and/or enhanced collagen synthesis, for example, account for myocardial fibrosis. The signals mediating nonmyocyte cell involvement in LVH may also involve locally generated hormones having paracrine properties. Herein we review experimental findings pertaining to the reparative and reactive fibrosis of the myocardium seen in various forms of acquired and genetic arterial hypertension, where circulating or tissue renin-angiotensin-aldosterone systems are respectively activated. These hormonal systems determine whether myocardial structure will be altered in arterial hypertension and, accordingly, if myocardial failure ensues. The mechanisms by which these hormones lead to myocardial fibrosis remain to be elucidated and correspondingly will determine if fibrosis can be effectively prevented. At the same time, experimental strategies that regress excess collagen in LVH have been identified, but need to be developed further to determine if myocardial failure, caused by fibrosis, is indeed reversible in humans.