Differential progression of complex culprit stenoses in patients with stable and unstable angina pectoris

被引:33
|
作者
Chen, LJ [1 ]
Chester, MR [1 ]
Crook, R [1 ]
Kaski, JC [1 ]
机构
[1] UNIV LONDON ST GEORGES HOSP,SCH MED,DEPT CARDIOL SCI,CORONARY ARTERY DIS RES GRP,LONDON SW17 0RE,ENGLAND
关键词
D O I
10.1016/0735-1097(96)00203-3
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives. This study sought to compare the evolution of complex culprit stenoses in patients with stable and those with unstable angina pectoris. Background. Complex coronary stenoses are associated with adverse clinical and angiographic outcomes. However, it is not known whether the evolution of complex stenoses differs in unstable angina versus stable angina pectoris. Methods. We prospectively assessed stenosis progression in 95 patients with unstable angina whose angina stabilized with medical therapy (Group 1) and 200 patients presenting with stable angina (Group 2). After diagnostic angiography, all patients were placed on a waiting list for coronary angioplasty and restudied at 8 +/- 4 (mean a SD) months later. In each patient the presumed culprit stenosis was identified and classified as complex (irregular borders, overhanging edges or thrombus) or smooth (absence of complex features). Stenosis progression, as assessed by computerized angiography, was defined as greater than or equal to 20% diameter reduction or new total occlusion. Results. At the first angiogram, 364 stenoses greater than or equal to 50% and 383 stenoses <50% were identified. At restudy, 36 (15%) of 236 stenoses progressed in 29 Group 1 patients and 36 (7%) of 502 stenoses in 31 Group 2 patients (p = 0.001). Forty-five (88%) of 51 stenoses greater than or equal to 50% and 6 (29%) of 21 stenoses <50% that progressed developed to total coronary occlusion (p = 0.001). More culprit stenoses progressed in Group 1 than in Group 2 (p = 0.006), whereas progression of nonculprit stenoses was not significantly different in both groups. Culprit complex stenoses progressed more frequently in Group 1 than in Group 2 (p = 0.01). During follow-up, 3 patients died (myocardial infarction), and 51 had a nonfatal coronary event. Culprit stenoses progressed in 15 (54%) of the 28 patients with a nonfatal coronary event in Group 1 and in 9 (39%) of 23 patients in Group 2 (p = NS). Complex morphology (p < 0.001) and unstable angina at initial presentation (p < 0.01) were predictive factors for progression of culprit stenoses. Conclusions. A larger proportion of culprit complex stenoses progress in unstable angina than stable angina, and this is frequently associated with recurrence of coronary events.
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收藏
页码:597 / 603
页数:7
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