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Hypertension, Vol 23, 869-877, Copyright © 1994 by American Heart Association
KT Weber, Y Sun and E Guarda
In hypertension, the risk of adverse cardiovascular events, including heart
failure, is increased in the presence of left ventricular hypertrophy.
Morphological studies suggest that it is not the quantity but rather the
quality, or structure, of myocardium that confers such risk. Iterations in
tissue structure that appear in hypertensive heart disease include a
remodeling of intramyocardial coronary arterioles, similar to that found in
systemic organs, and a disproportionate accumulation of fibrillar collagen
within their adventitia and neighboring interstitial space. Microscopic
scars replacing necrotic cardiac myocytes are also evident. These
expressions of fibrosis appear in the normotensive, nonhypertrophied right
and hypertensive, hypertrophied left ventricles and are linked to the
renin-angiotensin- aldosterone system. Cardiac myocyte growth, the major
determinant of myocardial mass, is related to ventricular loading.
Mechanisms responsible for the reactive and reparative fibrosis with renin-
angiotensin-aldosterone system activation are under investigation. In vitro
quantitative autoradiography has identified angiotensin II, aldosterone,
endothelin, and bradykinin receptors in the myocardium. A nonendothelial
tissue angiotensin-converting enzyme, whose binding density is marked in
the matrix of heart valves, adventitia, and sites of fibrosis, irrespective
of its pathogenic basis, has also been found. This angiotensin-converting
enzyme may be responsible for regulating local concentrations of
angiotensin II and bradykinin that govern fibroblast collagen turnover.
Based on a paradigm of discordant reciprocal regulation, in which a
relative abundance of stimulators (eg, angiotensin II, aldosterone, and
endothelins) of collagen synthesis exceeds inhibitors (eg, bradykinin,
prostaglandins, and glucocorticoids), fibrous tissue appears.(ABSTRACT
TRUNCATED AT 250 WORDS)
ARTICLES
Structural remodeling in hypertensive heart disease and the role of hormones
Department of Internal Medicine, University of Missouri Health Sciences Center, Columbia 65212.
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