OBJECTIVES: 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). BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
RCT Entities:
OBJECTIVES: 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). BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: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.
Authors: Jacek Kwiecinski; Evangelos Tzolos; Alexander J Fletcher; Jennifer Nash; Mohammed N Meah; Sebastien Cadet; Philip D Adamson; Kajetan Grodecki; Nikhil Joshi; Michelle C Williams; Edwin J R van Beek; Chi Lai; Adriana A S Tavares; Mark G MacAskill; Damini Dey; Andrew H Baker; Jonathon Leipsic; Daniel S Berman; Stephanie L Sellers; David E Newby; Marc R Dweck; Piotr J Slomka Journal: JACC Cardiovasc Imaging Date: 2022-02-16
Authors: Krishnaraj S Rathod; Anne-Marie Beirne; Richard Bogle; Sam Firoozi; Pitt Lim; Jonathan Hill; Miles C Dalby; Ajay K Jain; Iqbal S Malik; Anthony Mathur; Sundeep Singh Kalra; Ranil DeSilva; Simon Redwood; Philip A MacCarthy; Andrew Wragg; Elliot J Smith; Daniel A Jones Journal: J Am Heart Assoc Date: 2020-06-01 Impact factor: 5.501