Restenosis of a segment of diseased coronary artery following metallic stenting is a common clinical problem and a major limitation of the procedure. Systemic pharmacologic interventions to deal with this problem have met with little success. Several small studies suggest that cilostazol, a phosphodiesterase III inhibitor whose pharmacologic properties include antiplatelet, antithrombotic, and vasodilatory effects; a beneficial effect on serum lipids; and in vitro inhibition of smooth muscle cell proliferation, may help prevent platelet aggregation and impede the accumulation of new intimal tissue in the stented artery. The Cilostazol for RESTenosis (CREST) trial will aim to evaluate more definitively the ability of cilostazol to prevent restenosis following uncomplicated stent implantation for de novo coronary artery stenosis. In this randomized, double-blind, multicenter study, 700 patients will receive clopidogrel, aspirin, and either cilostazol or placebo after successful intracoronary stent implantation. The primary endpoint is minimal luminal diameter (MLD) of the first lesion stented after 6 months; secondary endpoints include MLD in all lesions, mean percent diameter stenosis, target lesion revascularization, and major angiographic endpoints. Safety endpoints are abnormal complete blood count and liver function tests at 1, 3, and 6 months. The trial has been initiated, and enrollment is anticipated to be concluded in 2003. Cilostazol has properties that may reduce or avert in-stent coronary restenosis. The CREST trial is a large, rigorously conducted trial that may corroborate the favorable effects of cilostazol on coronary stent restenosis suggested by earlier studies.
After an unsuccessful left internal mammary artery (LIMA) to left anterior descending percutaneous coronary intervention (PCI) in an outside hospital, a patient presented with ST-segment elevation myocardial infarction. The patient was found to have LIMA occlusion and underwent a second PCI. However, there was a residual disruption of LIMA, subsequently, the patient was found to have complete LIMA recanalization, which emphasized the self-reparative nature of LIMA. (Level of Difficulty: Intermediate.).
Objectives: This study investigated the relationship between low wall shear stress (WSS) and severe endothelial dysfunction (EDFx).
Background: Local hemodynamic forces such as WSS play an important role in atherogenesis through their effect on endothelial cells. The study hypothesized that low WSS independently predicts severe EDFx in patients with coronary artery disease (CAD).
Methods: Forty-four patients with CAD underwent coronary angiography, fractional flow reserve, and endothelial function testing. Segments with >10% vasoconstriction after acetylcholine (Ach) infusion were defined as having severe EDFx. WSS, calculated using 3-dimensional angiography, velocity measurements, and computational fluid dynamics, was defined as low (<1 Pa), intermediate (1 to 2.5 Pa), or high (>2.5 Pa).
Results: Median age was 52 years, 73% were women. Mean fractional flow reserve was 0.94 ± 0.06. In 4,510 coronary segments, median WSS was 3.67 Pa. A total of 24% had severe EDFx. A higher proportion of segments with low WSS had severe EDFx (71%) compared with intermediate WSS (22%) or high WSS (23%) (p < 0.001). Segments with low WSS demonstrated greater vasoconstriction in response to Ach than did intermediate or high WSS segments (−10.7% vs. −2.5% vs. +1.3%, respectively; p < 0.001). In a multivariable logistic regression analysis, female sex (odds ratio [OR]: 2.44; p = 0.04), diabetes (OR: 5.01; p = 0.007), and low WSS (OR: 9.14; p < 0.001) were independent predictors of severe EDFx.
Conclusions: In patients with nonobstructive CAD, segments with low WSS demonstrated more vasoconstriction in response to Ach than did intermediate or high WSS segments. Low WSS was independently associated with severe EDFx.