Fibrosis and hypertensive heart disease

被引:247
作者
Weber, KT [1 ]
机构
[1] Univ Tennessee, Ctr Hlth Sci, Dept Med, Div Cardiovasc Dis,Dobbs Res Inst, Memphis, TN 38163 USA
关键词
D O I
10.1097/00001573-200007000-00010
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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. (C) 2000 Lippincott Williams & Wilkins, Inc.
引用
收藏
页码:264 / 272
页数:9
相关论文
共 63 条
[1]  
ABRAHAMS C, 1987, LAB INVEST, V56, P676
[2]   HISTO-PATHOLOGICAL TYPES OF CARDIAC FIBROSIS IN MYOCARDIAL-DISEASE [J].
ANDERSON, KR ;
SUTTON, MGS ;
LIE, JT .
JOURNAL OF PATHOLOGY, 1979, 128 (02) :79-&
[3]   Acute angiotensin-converting enzyme inhibition increases the plasma level of the natural stem cell regulator N-acetyl-seryl-aspartyl-lysyl-proline [J].
Azizi, M ;
Rousseau, A ;
Ezan, E ;
Guyene, TT ;
Michelet, S ;
Grognet, JM ;
Lenfant, M ;
Corvol, P ;
Menard, J .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (03) :839-844
[4]   ANTI-ALDOSTERONE TREATMENT AND THE PREVENTION OF MYOCARDIAL FIBROSIS IN PRIMARY AND SECONDARY HYPERALDOSTERONISM [J].
BRILLA, CG ;
MATSUBARA, LS ;
WEBER, KT .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1993, 25 (05) :563-575
[5]   Advanced hypertensive heart disease in spontaneously hypertensive rats - Lisinopril-mediated regression of myocardial fibrosis [J].
Brilla, CG ;
Matsubara, L ;
Weber, KT .
HYPERTENSION, 1996, 28 (02) :269-275
[6]   IMPAIRED DIASTOLIC FUNCTION AND CORONARY RESERVE IN GENETIC-HYPERTENSION - ROLE OF INTERSTITIAL FIBROSIS AND MEDIAL THICKENING OF INTRAMYOCARDIAL CORONARY-ARTERIES [J].
BRILLA, CG ;
JANICKI, JS ;
WEBER, KT .
CIRCULATION RESEARCH, 1991, 69 (01) :107-115
[7]   REMODELING OF THE RAT RIGHT-AND-LEFT-VENTRICLES IN EXPERIMENTAL-HYPERTENSION [J].
BRILLA, CG ;
PICK, R ;
TAN, LB ;
JANICKI, JS ;
WEBER, KT .
CIRCULATION RESEARCH, 1990, 67 (06) :1355-1364
[8]   TEMPORAL DIFFERENCES IN FIBROBLAST PROLIFERATION AND PHENOTYPE EXPRESSION IN RESPONSE TO CHRONIC ADMINISTRATION OF ANGIOTENSIN-II OR ALDOSTERONE [J].
CAMPBELL, SE ;
JANICKI, JS ;
WEBER, KT .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1995, 27 (08) :1545-1560
[9]   LEFT-VENTRICULAR HYPERTROPHY IS ASSOCIATED WITH WORSE SURVIVAL INDEPENDENT OF VENTRICULAR-FUNCTION AND NUMBER OF CORONARY-ARTERIES SEVERELY NARROWED [J].
COOPER, RS ;
SIMMONS, BE ;
CASTANER, A ;
SANTHANAM, V ;
GHALI, J ;
MAR, M .
AMERICAN JOURNAL OF CARDIOLOGY, 1990, 65 (07) :441-445
[10]  
DAVIS JAMES O., 1965, HANDBOOK PHYSIOL, V3, P2071