Structural remodeling in hypertensive heart disease and the role of hormones

Karl Weber, Yao Sun, Eduardo Guarda

Research output: Contribution to journalArticle

221 Citations (Scopus)

Abstract

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. Chronic elevations in circulating and/or local concentrations of stimulator hormones represent a wound-healing response that has gone awry, with adverse fibrosis the outcome in hypertensive heart disease.

Original languageEnglish (US)
Pages (from-to)869-877
Number of pages9
JournalHypertension
Volume23
Issue number6
DOIs
StatePublished - Jan 1 1994

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Heart Diseases
Fibrosis
Hormones
Adventitia
Bradykinin
Peptidyl-Dipeptidase A
Renin-Angiotensin System
Cardiac Myocytes
Angiotensin II
Myocardium
Collagen
Bradykinin Receptors
Fibrillar Collagens
Mineralocorticoid Receptors
Endothelin Receptors
Angiotensin Receptors
Endothelins
Heart Valves
Arterioles
Left Ventricular Hypertrophy

All Science Journal Classification (ASJC) codes

  • Internal Medicine

Cite this

Structural remodeling in hypertensive heart disease and the role of hormones. / Weber, Karl; Sun, Yao; Guarda, Eduardo.

In: Hypertension, Vol. 23, No. 6, 01.01.1994, p. 869-877.

Research output: Contribution to journalArticle

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