Revisiting the culprit lesion in non-Q-wave myocardial infarction: Results from the VANQWISH trial angiographic core laboratory

被引:113
作者
Kerensky, RA [1 ]
Wade, M
Deedwania, P
Boden, WE
Pepine, CJ
机构
[1] Malcom Randall Vet Affairs Med Ctr, Gainesville, FL USA
[2] Univ Florida, Coll Med, Div Cardiol Med, Gainesville, FL USA
[3] Vet Affairs Med Ctr, Syracuse, NY USA
[4] SUNY, Hlth Sci Ctr, Syracuse, NY USA
[5] Vet Affairs Med Ctr, Fresno, CA USA
[6] Hartford Hosp, Div Cardiol, Hartford, CT USA
关键词
D O I
10.1016/S0735-1097(02)01770-9
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVES We sought to determine the underlying coronary anatomy and characterize the Culprit lesion after non-Q-wave myocardial infarction (NQWMI). BACKGROUND Although the culprit lesion and infarct-related artery often are easily identified with coronary angiography after Q-wave MI, the culprit lesion after NQWMI has not been well, characterized. Small retrospective studies have suggested that the absence of Q-waves on an electrocardiogram is due to incomplete occlusion of the infarct-related artery. METHODS Coronary angiograms from 350 patients randomized to the earl., invasive strategy in the Veterans Affairs Non-Q-Wave Infarction Strategies in-Hospital (VANQWISH) trial were systematically analyzed in an angiographic core laboratory. A consensus panel identified the culprit lesion and the infarct-related artery using prespecified criteria for complex lesion morphology and acute versus chronic occlusions. Severity of angiographic disease and left ventricular function also were analyzed. Patients with a single identified culprit lesion were compared with those who had multiple apparent culprits and those without all identifiable culprit lesion. RESULTS A single culprit lesion was identified in only 49% of patients undergoing early angiography after NQWMI. The majority of patients either had no identifiable culprit (37%) or multiple apparent culprit lesions (14%). A single incomplete occlusion of the infarct-related artery was found in only 36% of patients, and an isolated acute Occlusion of the infarct-related artery occurred in 13%. Patients without,in identifiable culprit lesion had severe coronary disease (obstructive coronary artery disease [CAD] in 84%) but no complex lesion morphology. There was no difference in angiographic severity of disease comparing patients with and without identifiable culprit lesions. Patients with a single incomplete occlusion of the infarct-related artery were more likely to undergo percutaneous transluminal coronary angioplasty than other patients, whereas patients with multiple Culprit lesions were more frequently treated with coronary artery bypass grafting, CONCLUSIONS Coronary angiography early after NQWMI frequently identifies severe obstructive CAD, but a sincle identifiable culprit lesion was identified in <50% of patients. Multiple culprit lesions were seen in 14% of patients. An angiographic culprit lesion could not be identified in more than one-third of patients undergoing coronary angiography as part of an invasive strategy. (C) 2002 by the American College of Cardiology, Foundation.
引用
收藏
页码:1456 / 1463
页数:8
相关论文
共 30 条
[1]   ANGIOGRAPHIC MORPHOLOGY AND THE PATHOGENESIS OF UNSTABLE ANGINA-PECTORIS [J].
AMBROSE, JA ;
WINTERS, SL ;
STERN, A ;
ENG, A ;
TEICHHOLZ, LE ;
GORLIN, R ;
FUSTER, V .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1985, 5 (03) :609-616
[2]   ANGIOGRAPHIC EVOLUTION OF CORONARY-ARTERY MORPHOLOGY IN UNSTABLE ANGINA [J].
AMBROSE, JA ;
WINTERS, SL ;
ARORA, RR ;
ENG, A ;
RICCIO, A ;
GORLIN, R ;
FUSTER, V .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1986, 7 (03) :472-478
[3]   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
[4]   CORONARY ANGIOGRAPHIC MORPHOLOGY IN MYOCARDIAL-INFARCTION - A LINK BETWEEN THE PATHOGENESIS OF UNSTABLE ANGINA AND MYOCARDIAL-INFARCTION [J].
AMBROSE, JA ;
WINTERS, SL ;
ARORA, RR ;
HAFT, JI ;
GOLDSTEIN, J ;
RENTROP, KP ;
GORLIN, R ;
FUSTER, V .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1985, 6 (06) :1233-1238
[5]  
[Anonymous], 1994, Circulation, V89, P1545
[6]   Outcomes in patients with acute non-Q-wave myocardial infarction randomly assigned to an invasive as compared with a conservative management strategy [J].
Boden, WE ;
O'Rourke, RA ;
Crawford, MH ;
Blaustein, AS ;
Deedwania, PC ;
Zoble, RG ;
Wexler, LF ;
Kleiger, RE ;
Pepine, CJ ;
Ferry, DR ;
Chow, BK ;
Lavori, PW .
NEW ENGLAND JOURNAL OF MEDICINE, 1998, 338 (25) :1785-1792
[7]  
BRAUNWALD E, 1993, CIRCULATION, V87, P38
[8]   INCOMPLETE LYSIS OF THROMBUS IN THE MODERATE UNDERLYING ATHEROSCLEROTIC LESION DURING INTRACORONARY INFUSION OF STREPTOKINASE FOR ACUTE MYOCARDIAL-INFARCTION - QUANTITATIVE ANGIOGRAPHIC OBSERVATIONS [J].
BROWN, BG ;
GALLERY, CA ;
BADGER, RS ;
KENNEDY, JW ;
MATHEY, D ;
BOLSON, EL ;
DODGE, HT .
CIRCULATION, 1986, 73 (04) :653-661
[9]   Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. [J].
Cannon, CP ;
Weintraub, WS ;
Demopoulos, LA ;
Vicari, R ;
Frey, MJ ;
Lakkis, N ;
Neumann, FJ ;
Robertson, DH ;
DeLucca, PT ;
DiBattiste, PM ;
Gibson, CM ;
Braunwald, E .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (25) :1879-1887
[10]   Differential progression of complex culprit stenoses in patients with stable and unstable angina pectoris [J].
Chen, LJ ;
Chester, MR ;
Crook, R ;
Kaski, JC .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1996, 28 (03) :597-603