Cardioreparation in hypertensive heart disease.

Research output: Contribution to journalReview article

52 Citations (Scopus)

Abstract

The normal myocardium is composed of a variety of cells. Cardiac myocytes, tethered within an extracellular matrix of fibrillar collagen, represent one third of all cells; noncardiomyocytes account for the remaining two thirds. Ventricular hypertrophy involves myocyte growth. Hypertensive heart disease (HHD) includes myocyte and nonmyocyte growth that leads to an adverse structural remodeling of the intramural coronary vasculature and matrix. In HHD, it is not the quantity of myocardium but rather its quality that accounts for increased risk of adverse cardiovascular events. Structural homogeneity of cardiac tissue is governed by a balanced equilibrium existing between stimulator and inhibitor signals that regulate cell growth, apoptosis, phenotype, and matrix turnover. Stimulators (eg, angiotensin II, aldosterone, and endothelins) are normally counterbalanced by inhibitors (eg, bradykinin, NO, and prostaglandins) in a paradigm of reciprocal regulation. To reduce the risk of heart failure and sudden cardiac death that accompanies HHD, its adverse structural remodeling must be targeted for pharmacologic intervention. Cardioprotective agents counteract the imbalance between stimulators and inhibitors. They include ACE and endopeptidase inhibitors and respective receptor antagonists. Cardioreparative agents reverse the growth-promoting state and regress existing abnormalities in coronary vascular and matrix structure. ACE inhibition has achieved this outcome with favorable impact on vasomotor reactivity and tissue stiffness. Today's management of hypertension should not simply focus on a reduction in blood pressure, it must also target the adverse structural remodeling that begets HHD.

Original languageEnglish (US)
Pages (from-to)588-591
Number of pages4
JournalHypertension
Volume38
Issue number3 Pt 2
StatePublished - Jan 1 2001

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Heart Diseases
Growth
Muscle Cells
Myocardium
Fibrillar Collagens
Cardiotonic Agents
Endothelins
Sudden Cardiac Death
Bradykinin
Protease Inhibitors
Aldosterone
Angiotensin-Converting Enzyme Inhibitors
Cardiac Myocytes
Angiotensin II
Hypertrophy
Prostaglandins
Extracellular Matrix
Blood Vessels
Heart Failure
Apoptosis

All Science Journal Classification (ASJC) codes

  • Internal Medicine

Cite this

Cardioreparation in hypertensive heart disease. / Weber, Karl.

In: Hypertension, Vol. 38, No. 3 Pt 2, 01.01.2001, p. 588-591.

Research output: Contribution to journalReview article

Weber, K 2001, 'Cardioreparation in hypertensive heart disease.', Hypertension, vol. 38, no. 3 Pt 2, pp. 588-591.
Weber, Karl. / Cardioreparation in hypertensive heart disease. In: Hypertension. 2001 ; Vol. 38, No. 3 Pt 2. pp. 588-591.
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