At one year after stenting, most clinical restenosis reflected TLR, which was predicted by the same variables previously associated with an increased risk of angiographic restenosis. The lower absolute rate of clinical restenosis relative to angiographic restenosis was due to infrequent TLR in lesions with less severe (<60% DS) angiographic renarrowing.

Background-There are limited studies of stent thrombosis in the modern era of second-generation stents, high-pressure deployment, and current antithrombotic regimens. Methods and Results-Six recently completed coronary stent trials and associated nonrandomized registries that enrolled 6186 patients (6219 treated vessels) treated with Ն1 coronary stent followed by antiplatelet therapy with aspirin and ticlopidine were pooled for this analysis. Within 30 days, clinical stent thrombosis developed in 53 patients (0.9%). The variables most significantly associated with the probability of stent thrombosis were persistent dissection NHLBI grade B or higher after stenting (OR, 3.7; 95% CI, 1.9 to 7.7), total stent length (OR, 1.3; 95% CI, 1.2 to 1.5 per 10 mm), and final minimal lumen diameter within the stent (OR, 0.4; 95% CI, 0.2 to 0.7 per 1 mm). Stent thrombosis was documented by angiography in 45 patients (0.7%). Clinical consequences of angiographic stent thrombosis included 64.4% incidence of death or myocardial infarction at the time of stent thrombosis and 8.9% 6-month mortality. Conclusions-Stent thrombosis occurred in Ͻ1.0% of patients undergoing stenting of native coronary artery lesions and receiving routine antiplatelet therapy with aspirin plus ticlopidine. Procedure-related variables of persistent dissection, total stent length, and final lumen diameter were significantly associated with the probability of stent thrombosis. Continued efforts to eliminate this complication are warranted given the serious clinical consequences. (Circulation.

The cutting balloon (CB) is a specialized device designed to create discrete longitudinal incisions in the atherosclerotic target coronary segment during balloon inflation. Such controlled dilatation theoretically reduces the force needed to dilate an obstructive lesion compared with standard percutaneous transluminal coronary angioplasty (PTCA). We report a multicenter, randomized trial comparing the incidence of restenosis after CB angioplasty versus conventional balloon angioplasty in 1,238 patients. Six hundred seventeen patients were randomized to CB treatment, and 621 to PTCA. The mean reference vessel diameter was 2.86 ؎ 0.49 mm, mean lesion length 8.9 ؎ 4.3 mm, and prevalence of diabetes mellitus in patients was 13%. The primary end point, the 6-month binary angiographic restenosis rate, was 31.4% for CB and 30.4% for PTCA (p ‫؍‬ 0.75). Acute procedural success, defined as the attainment of <50% diameter stenosis without in-hospital major adverse cardiac events, was 92.9% for CB and 94.7% for PTCA (p ‫؍‬ 0.24). Freedom from target vessel revascularization was slightly higher in the CB arm (88.5% vs 84.6%, log-rank p ‫؍‬ 0.04). Five coronary perforations occurred in the CB arm only (0.8% vs 0%, p ‫؍‬ 0.03). At 270 days, rates of myocardial infarction, death, and total major adverse cardiac events for CB and PTCA were 4.7% versus 2.4% (p ‫؍‬ 0.03), 1.3% versus 0.3% (p ‫؍‬ 0.06), and 13.6% versus 15.1% (p ‫؍‬ 0.34), respectively. In summary, the proposed mechanism of controlled dilatation did not reduce the rate of angiographic restenosis for the CB compared with conventional balloon angioplasty. CB angioplasty should be reserved for difficult lesions in which controlled dilatation is believed to provide a better acute result compared with balloon angioplasty alone.

ompared with balloon angioplasty, implantation of coronary stents has significantly decreased restenosis, 1-5 but in-stent restenosis caused by neointimal hyperplasia can occur in 20-30% of cases following bare metal stent implantation [6][7][8][9][10] and clinical in-stent restenosis or ischemia-driven revascularization for significant restenosis (≥50%) occurs in 10-15% following implantation of bare metal stents. This process usually occurs within 1 year of the index procedure and is believed to have a benign presentation with recurrent angina and/or evidence of ischemia on a stress test. However, there is scant data of an acute event such as myocardial infarction (MI) presenting as clinical in-stent restenosis. We sought to determine the incidence and type of MI, as well as clinical and angiographic characteristics of patients presenting with clinical instent restenosis (namely, any recurrent ischemia occurring in the stented segment) from our single center experience. Methods Study PatientsOf 2,462 consecutive patients who underwent percutaneous coronary interventions (PCI) with bare metal stents between June 2001 and December 2002, 212 (8.6%) were found to have clinical in-stent restenosis, which was defined as angiographic stenosis >50% within 5 mm of the stented segment for patients presenting for an angiogram for clinical evidence of ischemia (viz. angina or positive stress test). Patients presenting within 30 days of index procedure, with recurrent in-stent restenosis or restenosis following balloon angioplasty only, and patients presenting with MI clearly attributable to non-restenotic lesion or vessel were excluded. The antiplatelet regimen after the initial stent deployment was aspirin 325 mg daily indefinitely, and clopidogrel 75 mg daily for 4 weeks following a loading dose of 300 mg on the day of the procedure. The average follow-up period was 205±23 days (median 124 days). Based on the presenting symptoms and findings, the patients were divided into 3 groups: ST elevation MI (STEMI), non-ST elevation MI (NSTEMI), and non-MI groups. Patients with elevation of creatinine kinase (CK) 2-fold more than the normal reference with elevated MB fraction were considered to have a MI. Patients with STEMI were to have >1 mm ST-segment elevation in ≥2 contiguous leads. The NSTEMI group had elevated cardiac enzymes as above, without ST-segment elevation on the ECG. Renal failure was defined as baseline serum creatinine >2.0 mg/dl. The angiographic pattern of instent restenosis was analyzed as classified by Mehran et al. 11 Clinical and angiographic characteristics were compared among the 3 groups. Informed consent was given by each patient and the study protocol was approval by the institutional review board. Statistical AnalysisQuantitative data are presented as mean value ±1 SD or