Clinicopathological Study on the Thickening of Parietal Endocardium in the Adult Heart

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Macroscopical and microscopical examination of 117 unselected autopsied hearts revealed various degrees of pathological parietal endocardial thickening in 74% of them. The physiological thickening of the normal parietal endocardium was determined as 20μ at the outflow tract and papillary muscles of the left ventricle, as 10μ at the inflow tract of the left ventricle, the outflow tract and papillary muscles of the right ventricle, as 7μ at the inflow tract of the right ventricle, as 300μ at the posterior wall of the left atrium and as 100μ at the posterior wall of the right atrium. The parietal endocardium had a tendency to increase its thickness with age.A new classification of the pathological thickening of parietal endocardium which was made on the morphological and causal-genetic basis was proposed: A. Morphological classification. 1. structureless fibrosis. 2, fibroelstosis. 3. thickening of subendothelial layer. 4. thickening of all of the 5 layers. 5. thickening of subendocardial layer. 6. (false thickening.) B. Causal-genetic classification. I. thrombogenic type. II. hypertrophic and/or hyperplastic type. III. exudative, edematous or deposited type. IV. congenital type. The correlation between these 2 types of classification revealed the following evidences: (1) The endocardial fibrosis resulted from mechanical stimulation of the blood stream consisted of the jet lesion and the friction zone. The former was divided into 2 types and was commonly of thrombogenic origin. The impact of strong jet stream with vertical direction to the wall caused the structureless endocardial scar. On the other hand, the impact of jet stream with oblique direction caused the endocardial pocket or subendothelial fibrosis. The friction zone preserved all of the 5 layers of endocardium, but they were markedly hypertrophied and hyperplastic (Elastomyofibrosis). The pathogenesis of the friction zone was concerned with friction effect ofthe blood stream directed parallel to the wall and was related strictly with the persistent hypertension. (2) The endocardial change due to general metabolic disturbance, exhibited the subendocardial edema or fibrosis (endocardosis), and the degree of this change correlated with the lowering of serum albumin level. (3) The endocardial fibrosis due to endocarditis showed various histological types, and was mainly circumscribed fibrosis. Subendothelial fibrosis, subendocardial fibrosis or structureless fibrosis were frequently observed. They showed characteristically the irregular arrangement of collagen fibers with chronic inflammatory process. (4) The myocardial infarction was frequently accompanied with the structureless endocardial scar (reparative fibrosis). (5) The acquired endocardial fibroelastosis was developed from the fibrosis which lost the primary structure under a certain condition that consisted of mechanical distention and sufficiently long clinical course of more than 6 months. (6) There was apparent relationship between the grade of endocardial thickening and that of myocardial fibrosis. (7) The geographical distribution of the endocardial thickening showed commonly the preponderance at the outflow tract of both ventricles. However, some of the endocardosis had a tendency to be preponderant to the inflow tract of both ventricles. (8) Increase in the heart weight, the grade of cardiac dilatation and the grade of coronary sclerosis was incompatible with the normal endocardium, if they increased more than a certain limit.
International Heart Journal刊行会の論文

著者

OKADA Ryozo
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo

Clinicopathological Study on the Thickening of Parietal Endocardium in the Adult Heart

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