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- W4243980004 abstract "Hemodynamic impairment of cardiac function is not confined to restrictive cardiomyopathy and eosinophilic heart disease. Reviewing the hemodynamic signs of altered diastolic performance and their histological, immunohistochemical, molecular, and biochemical correlates in hypertensive hearts with severe fibrosis, this overview demonstrates that fibrosis must be differentiated between at least two forms: reactive fibrosis, which is regulated by the renin-angiotensin-aldosterone system; and reparative fibrosis, which is a scarring or replacement process that takes place after myocytolysis has occurred. Angiotensin-converting enzyme inhibition and aldosterone receptor blockade can be used therapeutically to reduce reactive fibrosis. In addition, these methods have made cardioreparation of the extracellular matrix a realistic therapeutic option in experimental renal hypertension, and have clinical importance for hypertension and endomyocardial fibrosis of unknown cause in humans. Classic concepts of eosinophilic heart disease are contrasted with the hypothesis that not all features of the disease are readily explained by toxic products from the eosinophil. Secondary immunopathogenesis may also play a role in the progression from the acute stage of eosinophilic and lymphocytic myocarditis to the terminal stage of endomyocardial fibrosis. Amyloid heart disease is revisited in the light of new biochemical methods of analysis of cardiac tissue containing amyloid. These new methods permit the characterization of transthyretin variants in the tissue. Recent reports on imaging methods for endomyocardial fibrosis are noted, with respect to the question of how to differentiate restrictive from constrictive disease." @default.
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- W4243980004 date "1993-05-01" @default.
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- W4243980004 title "Restrictive cardiomyopathy" @default.
- W4243980004 doi "https://doi.org/10.1097/00001573-199308030-00012" @default.
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