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 (PϽ0.001). 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 () (late loss, ϭ0.71 versus TLR, ϭ0.22; 95% CI of differenceϭ0.33, 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 differenceϭ0.24, 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 (Ͻ0.08 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.

Patients with chronic kidney disease have high rates of myocardial infarction and death following an initial attack. Proximal location of coronary atherosclerotic lesions has been linked to the risk of acute myocardial infarction and to infarction-associated mortality. To examine if the spatial distribution of lesions differs in patients with and without chronic kidney disease, we used quantitative coronary angiography to measure this in patients with acute coronary thromboses who were having angiography following acute myocardial infarction. Multivariable linear regression was used to adjust for differences in baseline characteristics. Among 82 patients with stage 3 or higher chronic kidney disease, 55.6% of lesions were located within 30 mm and 87.7% were within 50 mm of the coronary ostia. This compared to 34.7 and 71.8%, respectively, among 299 patients without significant kidney disease. Chronic kidney disease was independently and significantly associated with a 7.0 mm decrease in the distance from the coronary ostia to the problem lesion. Our study suggests that a causal link between a more proximal culprit lesion location in patients with chronic kidney disease and their high mortality rates after myocardial infarct is possible and may have important implications for interventions to prevent infarction.

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BACKGROUND: Acute coronary occlusions occur most frequently as a result of rupture of an atherosclerotic plaque. Previous studies have found greater extent of atherosclerotic disease in the coronary arteries of diabetic patients. While the burden of disease is higher in diabetics, less is known about the spatial distribution of myocardial infarction in this population. METHODS: We sought to compare the spatial distribution of myocardial infarction (STEMI and Non-STEMI) in patients with diabetes mellitus and in those without, based on quantitative coronary and statistical analysis. We analyzed 756 patients with STEMI (n = 556) and NSTEMI (n=200), of which 175 patients comprised the diabetic cohort, and mapped the location of the acute coronary occlusion. RESULTS: Coronary occlusions were not uniformly distributed throughout each of the major epicardial coronary arteries but tended to cluster within the proximal third of each of the vessels in both cohorts. There was no difference in the distribution of occlusions in diabetics vs. non-diabetics in any of the vessels (left anterior descending artery, P=0.35; left circumflex artery; P=0.33 right coronary artery, P=0.20; Figure). CONCLUSIONS: Acute coronary occlusions leading to STEMI and NSTEMI in both diabetics and non-diabetics tend to cluster in predictable “hot spots” within the proximal third of the coronary arteries. Identification of these high-risk zones for acute coronary occlusions will lead to future advances in vulnerable plaque detection technology and potentially locally directed preventive strategies. Spatial distribution of myocardial infarction in diabetics vs. non-diabetics using distance to lesion from the ostium of the coronary artery.