Chen L, Théroux P, Lespérance J, Shabani F, Thibault B, De Guise P
Department of Medicine, Montreal Heart Institute, Quebec, Canada.
J Am Coll Cardiol. 1996 Nov 15;28(6):1493-9. doi: 10.1016/s0735-1097(96)00344-0.
The aim of the study was to compare the angiographic features of culprit coronary lesions located in grafts with those in native coronary arteries in patients with unstable angina and previous coronary artery bypass graft surgery (CABG).
Deterioration of angina in patients with previous CABG is usually due to progression of atherosclerosis in coronary arteries or in vein grafts, but the relative importance of graft versus native coronary artery disease as well as the morphologic features of the culprit lesions in unstable angina have not been systematically assessed.
Disease progression and angiographic features of vein grafts and ungrafted and grafted coronary arteries were assessed in 95 consecutive patients admitted with unstable angina or non-Q wave myocardial infarction with CABG > 6 months previously. All patients were receiving aspirin and heparin, and 46 had received streptokinase during the acute phase in a doubleblind, placebo-controlled study. Coronary and vein angiography was performed within 8 days after admission (mean [+/- SD] 5 +/- 2 days). The most recent angiogram served to assess disease progression by quantitative angiography.
The culprit lesion was located in a vein graft in 51 patients, an ungrafted coronary artery in 17 and a grafted artery (proximal and distal to the site of graft insertion) in 9 and was of undetermined site in the remaining 18. The proportion of grafts accounting for acute disease increased to 85% with CABG > or = 5 years. Total occlusion occurred in 25 vein grafts and 4 ungrafted coronary arteries (49% vs. 24%, p = 0.02). Intravessel thrombus was found in 18 culprit vein grafts but in only 2 ungrafted coronary arteries (37% vs. 12%, p = 0.04). Both intravessel thrombus and total occlusion were demonstrated in six culprit vein grafts but in none of the ungrafted coronary arteries (12% vs. 0%, p = NS). The prevalence of total occlusion and thrombus was not influenced by trial medication, streptokinase or placebo.
Unstable angina in patients with previous CABG is most often due to graft disease and is associated with more frequent thrombi that are more refractory to medical therapy.
本研究旨在比较不稳定型心绞痛且既往有冠状动脉旁路移植术(CABG)患者的移植血管与自身冠状动脉中罪犯冠状动脉病变的血管造影特征。
既往接受CABG患者的心绞痛恶化通常归因于冠状动脉或静脉移植血管中动脉粥样硬化的进展,但移植血管病变与自身冠状动脉病变的相对重要性以及不稳定型心绞痛中罪犯病变的形态学特征尚未得到系统评估。
对95例因不稳定型心绞痛或非Q波心肌梗死入院且既往CABG超过6个月的连续患者,评估其静脉移植血管、未移植冠状动脉以及移植冠状动脉的疾病进展和血管造影特征。所有患者均服用阿司匹林和肝素,在一项双盲、安慰剂对照研究中,46例患者在急性期接受了链激酶治疗。入院后8天内(平均[±标准差]5±2天)进行冠状动脉和静脉血管造影。通过定量血管造影利用最近的血管造影评估疾病进展。
51例患者的罪犯病变位于静脉移植血管,17例位于未移植的冠状动脉,9例位于移植动脉(移植部位近端和远端),其余18例病变部位未确定。CABG≥5年时,导致急性疾病的移植血管比例增至85%。25条静脉移植血管和4条未移植冠状动脉发生完全闭塞(49%对24%,p = 0.02)。在18条罪犯静脉移植血管中发现血管内血栓,而未移植冠状动脉中仅2条发现(37%对12%,p = 0.04)。6条罪犯静脉移植血管同时存在血管内血栓和完全闭塞,而未移植冠状动脉中均未出现(12%对0%,p =无显著性差异)。完全闭塞和血栓的发生率不受试验用药、链激酶或安慰剂的影响。
既往有CABG患者的不稳定型心绞痛最常归因于移植血管病变,且与更频繁的血栓形成相关,对药物治疗更具抵抗性。