MYOCARDIAL FIBROSIS IN HYPERTENSIVE HEART-DISEASE - AN OVERVIEW OF POTENTIAL REGULATORY MECHANISMS

Myocardial fibrosis in hypertensive heart disease (HHD) can present as a reactive process involving intramyocardial coronary arteries and ar terioles with extensions of collagen into the neighbouring interstitia l space, and as a replacement for necrotic cardiac myocytes. Fibrosis adversely affects myocardial stiffness and therefore regulatory mechan isms are of considerable interest. Mechanisms responsible for scarring (reparative fibrosis) are based on factors that adversely influence m yocyte survival. This topic is not covered in this brief review. Mecha nisms responsible for the perivascular/interstitial fibrosis that appe ar in both the normotensive, non-hypertrophied right and the pressure overloaded hypertrophied left ventricle in HHD are addressed herein. T hey include (a) angiotensin II (Ang II)- mediated coronary vascular hy perpermeability with subsequent fibrosis; (b) direct hormonal regulati on of fibroblast collagen turnover, whereby Ang II aldosterone and/or endothelins may be involved; (c) arecoline and paracrine signalling be tween fibroblasts and/or endothelial cells that alters collagen synthe sis and degradation and which includes an angiotensin converting enzym e found in fibrous tissue. Collagen turnover in the myocardium is a dy namic process and fibrous tissue is anything but inert.