Weber K T, Brilla C G
Division of Cardiology, University of Missouri-Columbia.
Basic Res Cardiol. 1992;87 Suppl 1:291-301. doi: 10.1007/978-3-642-72474-9_25.
Myocardial fibrosis can be defined as an abnormal increase in collagen concentration of either ventricle. This accumulation of collagen, represented predominantly by fibrillar type I collagen, can occur a) on a reactive basis in the interstitial space and adventitia of intramyocardial coronary arteries and does not require myocyte necrosis, or b) as a replacement for necrotic myocytes, where it is considered a scar. Both forms can be found in the same ventricle. Various factors have been found to contribute to the reactive and reparative fibrosis that appears in both ventricles in acquired hypertension. In the case of microscopic scarring, myocyte necrosis is related to catecholamine or angiotensin II- mediated toxicity, reduced potassium stores that accompany chronic mineralocorticoid excess, and coronary vascular remodeling. Reactive fibrosis is associated with elevations in plasma aldosterone concentrations that are inappropriate relative to dietary sodium intake. These findings set the stage for additional in vivo and in vitro studies that may shed more light on our understanding of the factors that regulate the accumulation of fibrous tissue in the myocardium--a major determinant of pathologic structural remodeling which enhances its susceptibility to reentrant arrhythmias and ventricular dysfunction.
心肌纤维化可定义为任一心室中胶原蛋白浓度的异常增加。这种主要由I型纤维状胶原蛋白代表的胶原蛋白积累，可发生在以下两种情况：a）在反应性基础上，发生于心内膜下间隙和心肌内冠状动脉的外膜，且不需要心肌细胞坏死；b）作为坏死心肌细胞的替代物，此时被视为瘢痕。这两种形式可在同一心室中发现。已发现多种因素促成了后天性高血压患者两个心室中出现的反应性和修复性纤维化。在微观瘢痕形成的情况下，心肌细胞坏死与儿茶酚胺或血管紧张素II介导的毒性、慢性盐皮质激素过多伴随的钾储备减少以及冠状血管重塑有关。反应性纤维化与血浆醛固酮浓度升高有关，而这种升高相对于饮食钠摄入量而言是不适当的。这些发现为更多的体内和体外研究奠定了基础，这些研究可能会让我们对调节心肌纤维组织积累的因素有更深入的了解，而心肌纤维组织积累是病理性结构重塑的一个主要决定因素，会增加其对折返性心律失常和心室功能障碍的易感性。
