title: [Morphological problems in cardiac hypertrophy].
abstract: 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)
authors.affiliation: Research Laboratory for Cardiovascular Pathology, Juntendo University School of Medicine, Tokyo.
authors.forename: R
authors.initials: R
authors.lastname: Okada
mesh_terms: D006332:Cardiomegaly / Q000209:etiology / Q000473:pathology*; D006801:Humans; D009206:Myocardium / Q000473:pathology*