Okada R
Research Laboratory for Cardiovascular Pathology, Juntendo University School of Medicine, Tokyo.
J Cardiol. 1988 Jun;18(2):537-40.
Ventricular hypertrophy is categorized as (1) volume hypertrophy (eccentric hypertrophy or hypertrophy with dilatation), and (2) pressure hypertrophy (concentric hypertrophy or hypertrophy without dilatation). Hypertrophy per se is considered as a reaction to hemodynamic overload, both in occasions of excessive volume and of elevated pressure except in (idiopathic) cardiomyopathies. In patients with volume hypertrophy, some alteration of myocardial architecture is inevitable if the volume load exceeds a critical degree. Such alteration is characterized by deterioration of the median circular muscular layer of the ventricle resulting from over-stretching of the horizontally-coursing myocyte bundles. Hypertrophy of the inner oblique muscular layer of the left ventricle in cases with mitral regurgitation, and of the outer oblique muscular layer in cases with aortic regurgitation develops according to the changing configuration of the left ventricle; globular in the former, and elongated in the latter. In patients with pressure hypertrophy, there is some increase of the myocyte mass, with a disarrangement at the anterior triangle of the interventricular septum. The latter is physiologically situated at the anterior margin of the septum between the outer and median layers of both the ventricles. This seems to be a prelude to thickening of the septum and tends to hypertrophy of the free wall. A reduction in the deranged myocyte mass due to fibrosis or adiposis corresponds to arrest of the active hypertrophic process, and it may be the beginning of decompensation of cardiac function. Peculiar modes of dilatation and hypertrophy in cardiomyopathies have common denominators with those of known etiologies.(ABSTRACT TRUNCATED AT 250 WORDS)
(1)容量性肥大(离心性肥大或伴有扩张的肥大),以及(2)压力性肥大(向心性肥大或不伴有扩张的肥大)。肥大本身被认为是对血流动力学过载的一种反应,除了(特发性)心肌病外,在容量过多和压力升高的情况下均会出现。在容量性肥大的患者中,如果容量负荷超过临界程度,心肌结构的某些改变是不可避免的。这种改变的特征是水平走行的心肌束过度伸展导致心室中间环形肌层退化。二尖瓣反流患者左心室内斜肌层肥大,主动脉反流患者外斜肌层肥大,其发展与左心室形态的变化有关;前者呈球形,后者呈细长形。在压力性肥大的患者中,心肌细胞质量有所增加,室间隔前三角区出现排列紊乱。后者生理上位于两个心室外层和中间层之间的室间隔前缘。这似乎是室间隔增厚的前奏,并倾向于游离壁肥大。由于纤维化或脂肪变性导致紊乱的心肌细胞质量减少,对应于活跃肥大过程的停止,这可能是心功能失代偿的开始。心肌病中特有的扩张和肥大模式与已知病因的情况有共同特征。(摘要截断于250字)