Relative spatial distributions of coronary artery bypass graft insertion and acute thrombosis: a model for protection from acute myocardial infarction.

BACKGROUND: Randomized trials have demonstrated coronary artery bypass surgery (CABG) to be superior to percutaneous coronary intervention with respect to long-term mortality and morbidity from myocardial infarction within specific high-risk cohorts. The purpose of this study was to analyze the spatial distribution of coronary artery bypass graft anastomoses relative to acute thromboses in native coronary arteries. We hypothesized that insertion sites of bypass grafts are located distal to sites of acute thrombosis and consequently decrease cardiac morbidity and mortality associated with plaque rupture. METHODS: We analyzed 168 patients with prior CABG and 208 patients with ST-segment elevation myocardial infarctions (STEMI) presenting to the Brigham and Women's Hospital who underwent coronary angiography. We constructed a spatial map of the coronary arterial bypass graft insertion sites and compared these locations to sites of acute thrombosis leading to STEMI. RESULTS: Graft insertion sites were consistently located distal to acute thrombosis sites (left anterior descending artery median graft insertion versus median thrombosis site = 72 versus 34 mm, right coronary artery 91 versus 42 mm, left circumflex artery 44 versus 37 mm). Greater than 97% of thrombosis sites were located proximal to 75% of graft insertion sites. CONCLUSIONS: Coronary arterial bypass grafts provide the coverage of anatomic zones at risk for STEMI. The superior performance of CABG in high risk patients may be attributed to targeting of proximal coronary locations where thrombosis risk is clustered.

Robustness of late lumen loss in discriminating drug-eluting stents across variable observational and randomized trials.

BACKGROUND: Binary angiographic and clinical restenosis rates can vary widely between clinical studies, even for the same stent, influenced heavily by case-mix covariates that differ among observational and randomized trials intended to assess a given stent system. We hypothesized that mean in-stent late loss might be a more stable estimator of restenosis propensity across such studies. METHODS AND RESULTS: In 46 trials of drug-eluting and bare-metal stenting, increasing mean late loss was associated with higher target lesion revascularization (TLR) rates (P<0.001). When the class of bare-metal stents was compared with the class of effective drug-eluting stents, late loss was more discriminating than TLR as measured by the high intraclass correlation coefficient (rho) (late loss, rho=0.71 versus TLR, rho=0.22; 95% CI of difference=0.33, 0.65). When the individual drug-eluting stents and bare-metal stents were compared, late loss was a better discriminator than TLR (0.68 versus 0.19; 95% CI of difference=0.24, 0.60). Greater adjustments of study covariates are needed to stabilize assessments of TLR compared with late loss because of greater influence of reference vessel diameter on TLR than on in-stent late loss. Optimization of late loss with the use of a novel method of standardization according to diabetes prevalence and mean lesion length resulted in minor adjustments in late loss (<0.08 mm for 90% of reported trials) and an ordered array of mean late loss values for the stent systems studied. CONCLUSIONS: Late loss is more reliable than restenosis rates for discriminating restenosis propensity between new drug-eluting stent platforms across studies and might be the optimum end point for evaluating drug-eluting stents in early, nonrandomized studies.