Chen L, Chester M R, Crook R, Kaski J C
Department of Cardiological Sciences, St. George's Hospital Medical School, London, England, United Kingdom.
J Am Coll Cardiol. 1996 Sep;28(3):597-603. doi: 10.1016/0735-1097(96)00203-3.
This study sought to compare the evolution of complex culprit stenoses in patients with stable and those with unstable angina pectoris.
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.
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 +/- 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 > or = 20% diameter reduction or new total occlusion.
At the first angiogram, 364 stenoses > or = 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 > or = 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.
A larger proportion of culprit complex stenoses progress in unstable angina than stable angina, and this is frequently associated with recurrence of coronary events.
本研究旨在比较稳定性心绞痛患者和不稳定性心绞痛患者复杂罪犯病变狭窄的演变情况。
复杂冠状动脉狭窄与不良临床及血管造影结果相关。然而,尚不清楚复杂狭窄在不稳定性心绞痛与稳定性心绞痛中的演变是否存在差异。
我们前瞻性评估了95例不稳定性心绞痛患者(1组),其心绞痛经药物治疗后稳定,以及200例稳定性心绞痛患者(2组)。诊断性血管造影后,所有患者被列入冠状动脉血管成形术等待名单,并在8±4(均值±标准差)个月后再次进行检查。在每位患者中,确定推测的罪犯病变狭窄并将其分类为复杂病变(边界不规则、边缘悬垂或有血栓)或光滑病变(无复杂特征)。通过计算机血管造影评估的狭窄进展定义为直径缩小≥20%或出现新的完全闭塞。
在首次血管造影时,识别出364处≥50%的狭窄和383处<50%的狭窄。复查时,29例1组患者中236处狭窄有36处(15%)进展,31例2组患者中502处狭窄有36处(7%)进展(p = 0.001)。进展的51处≥50%的狭窄中有45处(88%)以及21处<50%的狭窄中有6处(29%)发展为冠状动脉完全闭塞(p = 0.001)。1组中进展的罪犯病变狭窄比2组更多(p = 0.006),而两组中非罪犯病变狭窄的进展无显著差异。1组中罪犯复杂病变狭窄的进展比2组更频繁(p = 0.01)。随访期间,3例患者死亡(心肌梗死),51例发生非致命性冠状动脉事件。1组28例发生非致命性冠状动脉事件的患者中有15例(54%)罪犯病变狭窄进展,2组23例患者中有9例(39%)进展(p = 无显著性差异)。复杂形态(p < 0.001)和初次就诊时的不稳定性心绞痛(p < 0.01)是罪犯病变狭窄进展的预测因素。
与稳定性心绞痛相比,不稳定性心绞痛中更大比例的罪犯复杂病变狭窄会进展,且这常与冠状动脉事件复发相关。