ATHEROGENESIS AND THROMBOSIS - MECHANISMS, PATHOGENESIS, AND THERAPEUTIC IMPLICATIONS

被引:7
作者
CLARK, LT
机构
[1] Department of Medicine, State University, New York Health Science Center at Brooklyn. N.Y., Brooklyn, NY
关键词
D O I
10.1016/0002-8703(92)91068-C
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Although the mortality rate from coronary heart disease (CHD) has declined by almost 50% during the past 25 years, CHD remains the leading cause of death in the United States and is responsible for more than 500,000 deaths annually. The underlying cause of CHD is coronary atherosclerosis. Although the intact intima is highly resistant to thrombus formation, when injury occurs, even superficial, a sequence of reactions is initiated-platelet aggregation, macrophage accumulation, intimal smooth muscle proliferation, fibrous tissue proliferation, and lipid accumulation-that result in the development of obstructive atheroma. Repeat intimal injury and cycling of this process lead to continued progression of the atheroma and coronary artery occlusion. Unstable angina and acute myocardial infarction appear to result from rupture of an atherosclerotic plaque, hemorrhage into the plaque, and luminal thrombosis. The cause of plaque rupture is unknown and may result from normal hemodynamic forces when the fibrous cap of an atheroma has become severely attenuated and fragile. Based on the pathogenesis of chronic atherosclerosis and acute rapid atheroma progression, several therapeutic options become evident. These include antiplatelet, anticoagulant, and thrombolytic therapies, as well as the possibility of arrest and reversal of atherosclerosis in some patients.
引用
收藏
页码:1106 / 1109
页数:4
相关论文
共 27 条
[1]   ANGIOGRAPHIC PROGRESSION OF CORONARY-ARTERY DISEASE AND THE DEVELOPMENT OF MYOCARDIAL-INFARCTION [J].
AMBROSE, JA ;
TANNENBAUM, MA ;
ALEXOPOULOS, D ;
HJEMDAHLMONSEN, CE ;
LEAVY, J ;
WEISS, M ;
BORRICO, S ;
GORLIN, R ;
FUSTER, V .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1988, 12 (01) :56-62
[2]  
[Anonymous], 1988, LANCET, V2, P349
[3]  
[Anonymous], 1986, LANCET, V1, P397
[4]   BENEFICIAL-EFFECTS OF COMBINED COLESTIPOL-NIACIN THERAPY ON CORONARY ATHEROSCLEROSIS AND CORONARY VENOUS BYPASS GRAFTS [J].
BLANKENHORN, DH ;
NESSIM, SA ;
JOHNSON, RL ;
SANMARCO, ME ;
AZEN, SP ;
CASHINHEMPHILL, L .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1987, 257 (23) :3233-3240
[5]   REGRESSION OF CORONARY-ARTERY DISEASE AS A RESULT OF INTENSIVE LIPID-LOWERING THERAPY IN MEN WITH HIGH-LEVELS OF APOLIPOPROTEIN-B [J].
BROWN, G ;
ALBERS, JJ ;
FISHER, LD ;
SCHAEFER, SM ;
LIN, JT ;
KAPLAN, C ;
ZHAO, XQ ;
BISSON, BD ;
FITZPATRICK, VF ;
DODGE, HT .
NEW ENGLAND JOURNAL OF MEDICINE, 1990, 323 (19) :1289-1298
[6]  
CARRYON P, 1987, J NATL MED ASSOC, V79, P265
[7]  
Clark LT, 1989, CLIN CARDIOL S4, V12, pIV13
[8]   SEVERITY OF CORONARY-ARTERY DISEASE AMONG BLACKS WITH ACUTE MYOCARDIAL-INFARCTION [J].
COOPER, R ;
CASTANER, A ;
CAMPO, A ;
ISLAM, N ;
SIMMONS, B .
AMERICAN JOURNAL OF CARDIOLOGY, 1989, 63 (12) :788-791
[9]   MORPHOLOGIC FEATURES OF UNSTABLE ATHEROTHROMBOTIC PLAQUES UNDERLYING ACUTE CORONARY SYNDROMES [J].
FALK, E .
AMERICAN JOURNAL OF CARDIOLOGY, 1989, 63 (10) :E114-E120
[10]   PLATELET-INHIBITOR DRUGS ROLE IN CORONARY-ARTERY DISEASE [J].
FUSTER, V ;
ADAMS, PC ;
BADIMON, JJ ;
CHESEBRO, JH .
PROGRESS IN CARDIOVASCULAR DISEASES, 1987, 29 (05) :325-346