Key result
This review discusses factors regulating the growth of myocardial compartments and signals promoting adverse remodeling of intramyocardial coronary arteries and arterioles by fibrous tissue.
This review highlights that the quality of the myocardium, specifically adverse remodeling by fibrous tissue, rather than just quantity, accounts for pathologic hypertrophy and increased risk of adverse cardiovascular events in hypertensive heart disease.
Adverse fibrous remodeling, not myocyte mass alone, drives hypertensive heart disease risk; extends mechanistic insights but leaves targeted therapies open.
The normal myocardium is composed of a variety of cells: cardiac myocytes and noncardiomyocytes, which include endothelial and vascular smooth muscle cells and fibroblasts. Hypertensive heart disease involves a structural remodeling of muscular and nonmuscular compartments. It is not the quantity but rather the quality of myocardium that accounts for pathologic hypertrophy and predisposes to ventricular dysfunction and arrhythmias, which, in turn, confer increased risk of adverse cardiovascular events. Herein, factors regulating growth of these compartments are reviewed and in particular signals involved in promoting adverse remodeling of intramyocardial coronary arteries and arterioles by fibrous tissue.
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Karl T. Weber (2000) conducted a review in Hypertensive heart disease. This review discusses factors regulating the growth of myocardial compartments and signals promoting adverse remodeling of intramyocardial coronary arteries and arterioles by fibrous tissue.
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