Pathophysiology of acute myocardial infarction

被引：155

作者：

Burke, Allen P. ^{[1
]}

Virmani, Renu ^{[1
]}

机构：

[1] CVPath Inst, 19 Firstfield Rd, Gaithersburg, MD 20878 USA

来源：

MEDICAL CLINICS OF NORTH AMERICA | 2007年 / 91卷 / 04期

关键词：

D O I：

10.1016/j.mcna.2007.03.005

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

More than 80% of acute myocardial infarcts are the result of coronary atherosclerosis with superimposed luminal thrombus. Uncommon causes of myocardial infarction include coronary spasm, coronary embolism, and thrombosis in nonatherosclerotic normal vessels. Additionally, concentric subendocardial necrosis may result from global ischemia and reperfusion in cases of prolonged cardiac arrest with resuscitation. Myocardial ischemia shares features with other types of myocyte necrosis, such as that caused by inflammation, but specific changes result from myocyte hypoxia that vary based on length of occlusion of the vessel, duration between occlusion and reperfusion, and presence of collateral circulation.

引用

页码：553 / 572

页数：20

共 70 条

[11] Impact of microvascular dysfunction on left ventricular remodeling and long-term clinical outcome after primary coronary angioplasty for acute myocardial infarction [J].

Bolognese, L ;

Carrabba, N ;

Parodi, G ;

Santoro, GM ;

Buonamici, P ;

Cerisano, G ;

Antoniucci, D .

CIRCULATION, 2004, 109 (09) :1121-1126

[12] Myocardial ischemia and reperfusion injury [J].

Buja, LM .

CARDIOVASCULAR PATHOLOGY, 2005, 14 (04) :170-175

[13] Doppler-derived mitral deceleration time - An early strong predictor of left ventricular remodeling after reperfused anterior acute myocardial infarction [J].

Cerisano, G ;

Bolognese, L ;

Carrabba, N ;

Buonamici, P ;

Santoro, GM ;

Antoniucci, D ;

Santini, A ;

Moschi, G ;

Fazzini, PF .

CIRCULATION, 1999, 99 (02) :230-236

[14] CELLULAR-RESPONSE OF THE EVOLVING MYOCARDIAL-INFARCTION AFTER THERAPEUTIC CORONARY-ARTERY REPERFUSION [J].

COWAN, MJ ;

REICHENBACH, D ;

TURNER, P ;

THOSTENSON, C .

HUMAN PATHOLOGY, 1991, 22 (02) :154-163

[15] Pinacidil but not nicorandil opens ATP-sensitive K+ channels and protects against simulated ischemia in rabbit myocytes [J].

Critz, SD ;

Liu, GS ;

Chujo, M ;

Downey, JM .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1997, 29 (04) :1123-1130

[16] INTRAMYOCARDIAL PLATELET-AGGREGATION IN PATIENTS WITH UNSTABLE ANGINA SUFFERING SUDDEN ISCHEMIC CARDIAC DEATH [J].

DAVIES, MJ ;

THOMAS, AC ;

KNAPMAN, PA ;

HANGARTNER, JR .

CIRCULATION, 1986, 73 (03) :418-427

[17] REGIONAL CARDIAC DILATATION AFTER ACUTE MYOCARDIAL-INFARCTION - RECOGNITION BY 2-DIMENSIONAL ECHOCARDIOGRAPHY [J].

EATON, LW ;

WEISS, JL ;

BULKLEY, BH ;

GARRISON, JB ;

WEISFELDT, ML .

NEW ENGLAND JOURNAL OF MEDICINE, 1979, 300 (02) :57-62

[18] THE RELEVANCE OF PLATELET AND FIBRIN THROMBOEMBOLISM OF THE CORONARY MICRO-CIRCULATION, WITH SPECIAL REFERENCE TO SUDDEN CARDIAC DEATH [J].

ELMARAGHI, N ;

GENTON, E .

CIRCULATION, 1980, 62 (05) :936-944

[19] Hibernating myocardium - An incomplete adaptation to ischemia [J].

Elsasser, A ;

Schlepper, M ;

Klovekorn, WP ;

Cai, WJ ;

Zimmermann, R ;

Muller, KD ;

Strasser, R ;

Kostin, S ;

Gagel, C ;

Munkel, B ;

Schaper, W ;

Schaper, J .

CIRCULATION, 1997, 96 (09) :2920-2931

[20]

ELSASSER A, 1995, BASIC RES CARDIOL, V90, P47

← 1 2 3 4 5 6 7 →