To characterize in-stent restenosis after the implantation of sirolimus-eluting stents (SES), paclitaxel-eluting stents (PES), tacrolimus-eluting stents (TES), and zotarolimus-eluting stents (ZES), 25 patients treated with drug-eluting stents (DES; 9 PES, 10 SES, 4 TES, and 2 ZES) and 19 with bare-metal stents (BMS) underwent directional coronary atherectomy for in-stent restenosis 4 to 36 months after implantation. Restenosis after DES implantation was more frequently focal and associated with smaller specimens compared to that after BMS implantation. Light and confocal microscopy were used. Histologic features were similar in DES and BMS. In-stent restenotic lesions were composed mainly of neointima containing proteoglycan-rich smooth muscle cells and fibrolipidic regions. Small inflammatory infiltrates were observed, mostly in patients with unstable angina; CD18- and/or CD3+ cells were detected in patients with BMS and DES. Different smooth muscle cell phenotypes were observed: synthetic was more frequent with BMS and PES, intermediate with ZES, contractile or intermediate with SES, and contractile with TES. The mean proliferation index was low and comparable among stent types; cyclins B1 and D1 were expressed in all DES. In conclusion, intra-DES and intra-BMS restenotic tissue was composed mainly of smooth muscle cells with different phenotypes, proliferating at a low rate. The different smooth muscle cell phenotypes within the stent types might suggest different mechanisms of restenosis.

Drug-eluting stents (DES) have been shown to markedly reduce the need for repeat revascularization compared to bare-metal stents in patients with stable coronary artery disease. The benefit of DES in patients with acute coronary syndromes (ACS) is unclear. This analysis was undertaken to determine if DES have similar advantages over bare-metal stents in patients with ACS. A cohort of 3,771 patients underwent percutaneous coronary intervention with stent implantation in native coronary arteries. Patients presenting for primary angioplasty or rescue angioplasty were excluded. Patients were classified as having stable or unstable symptoms on presentation and then further divided by stent type, DES or bare-metal stent. Although there was a difference in efficacy, with fewer major adverse cardiac events after DES implantation for the stable patients at 1 year (8.2% vs 13.2%, p = 0.008), this benefit was not found in patients with ACS (11.2% vs 12.0%, p = 0.6). A reduced need for repeat revascularization of the initially treated artery accounted for this difference (5.6% vs 11.4%, p <0.001). Stent thrombosis by 1 year was equally rare with each stent type. In conclusion, the reduction in the need for repeat revascularization associated with DES appears to be limited to patients who present with stable angina pectoris. This observation may reflect the more frequent presence of vulnerable plaques in patients with ACS.

Chronic kidney disease (CKD) is a risk factor for poor outcomes in patients with coronary artery disease (CAD), but it is unknown whether CKD influences the efficacy of alternative CAD treatment strategies. Thus, we compared outcomes in stable CAD patients with and without CKD randomized to percutaneous coronary intervention (PCI) and optimal medical therapy (OMT) or OMT alone in a post hoc analysis of the 2,287 patient COURAGE study. At baseline, 320 patients (14%) had CKD defined as a glomerular filtration rate of <60 mL/min/1.73 m2, as estimated by the abbreviated 4-variable Modification of Diet in Renal Disease equation. The patients with CKD were older (68 ± 9 vs 61 ± 10 years; p <0.001) and more often had diabetes mellitus (42% vs 33%; p = 0.002), hypertension (81% vs 65%; p <0.03), heart failure (13% vs 3.4%; p <001), and three-vessel CAD (37% vs 29%, p = 0.01). After adjustment for these differences, CKD remained an independent predictor of death or nonfatal myocardial infarction (hazard ratio 1.48, 95% confidence interval 1.15 to 1.90). PCI had no effect on these outcomes. Furthermore, at 36 months, a similar percentage of patients with CKD treated with OMT (70%) and PCI plus OMT (76%) were angina free compared to patients without CKD. In conclusion, CKD is an important determinant of clinical outcomes in patients with stable CAD, regardless of the treatment strategy. Although PCI did not reduce the risk of death or myocardial infarction when added to OMT for patients with CKD, it also was not associated with worse outcomes in this high-risk group.

Accelerated idioventricular rhythm (AIVR) has been considered a marker of successful reperfusion in fibrinolytic-treated patients. Evidence is limited regarding its significance in patients with ST-elevation myocardial infarction treated with primary percutaneous coronary intervention (PPCI). The purpose of the present study was to determine the prevalence and associated outcomes of arrhythmias and conduction disturbances occurring during PPCI. In 503 patients with ST-elevation myocardial infarction, the arrhythmias and conduction disturbances occurring from arrival at the catheterization laboratory to 90 minutes after PPCI were registered. Continuous ST-monitoring was performed to determine the interval from the first wire to complete ST resolution. The area at risk was evaluated in the acute phase and the final infarct size (FIS) after 1 month using myocardial perfusion imaging. Mortality was registered at a median follow-up of 2.9 years. The most common arrhythmias observed during PPCI were AIVR (42%), sinus bradycardia (28%), and nonsustained ventricular tachycardia (26%). The arrhythmias associated with the FIS included AIVR (unstandardized regression coefficient [B] = 5.27, p <0.001), sustained ventricular tachycardia (B = 15.7, p <0.001), and sinus bradycardia (B = −4.12, p = 0.001). Right bundle branch block was the only conduction disturbance associated with FIS (B = 7.17, p = 0.001). Patients with AIVR less often achieved spontaneous ST resolution before PPCI (13% vs 36%, p <0.001), less often had Thrombolysis In Myocardial Infarction flow 3 on admission (3% vs 33%, p <0.001), had a larger area at risk (35% vs 23% of the left ventricle, p <0.001), had a longer time to complete ST resolution (39 vs 21 minutes, p <0.001), had a larger FIS (13% vs 5% of the left ventricle, p <0.001) but had similar mortality (8.6% and 6.5%, p = 0.39) compared to patients without AIVR. In conclusion, AIVR is the most frequent arrhythmia occurring during PPCI in patients with ST-elevation myocardial infarction. However, it is not a marker of successful reperfusion but is associated with extensive myocardial damage and delayed microvascular reperfusion.

To determine whether the incidence of nausea and vomiting in patients with acute myocardial infarction (AMI) varies with infarct location, we studied 180 patients who had been admitted to our hospital for ST-segment elevation AMI or AMI associated with left bundle branch block. The presenting symptoms (chest pain, nausea, and vomiting), initial electrocardiographic findings, and additional demographic, clinical, laboratory, and outcome data were extracted from the medical records and correlated with the infarct location. Of the 180 patients with AMI, 108 (60%) had inferior and 72 (40%) had anterior infarcts. Nausea was reported in almost 2/3 of all patients, and vomiting in nearly 1/3. Both nausea and vomiting showed a trend toward a greater incidence in patients with inferior than with anterior infarcts (69% vs 56% and 33% vs 26%, respectively). However, the differences were not statistically significant. In conclusion, nausea and vomiting are common presenting symptoms in patients with either inferior or anterior wall AMI, but their frequency is unrelated to the infarct location.

Electrocardiographic signs of a non–ST elevation myocardial infarction (NSTEMI) are nonspecific, and therefore the diagnosis of NSTEMI during acute coronary syndromes (ACS) depends mainly on cardiac biomarker levels. Fragmented QRS (fQRS) represents myocardial conduction abnormalities due to myocardial infarction (MI) scars in patients with coronary artery disease. However, the time of appearance of fQRS during ACS has not been investigated. It was postulated that in patients with ACS, fQRS on 12-lead electrocardiography occurs within 48 hours of presentation with NSTEMI as well as ST elevation MI and that fQRS predicts mortality. Serial electrocardiograms from 896 patients with ACS (mean age 62 ± 11 years, 98% men) who underwent cardiac catheterization were studied. Four hundred forty-one patients had MIs, including 337 patients with NSTEMIs, and 455 patients had unstable angina (the control group). Serial electrocardiograms were obtained every 6 to 8 hours during the first 24 hours after the diagnosis of MI and the next day (<48 hours). Fragmented QRS on 12-lead electrocardiography was defined by the presence of single or multiple notches in the R or S wave, without a typical bundle branch block, in ≥2 contiguous leads in 1 of the major coronary artery territories. Fragmented QRS developed in 224 patients (51%) in the MI group and only 17 (3.7%) in the control group (p <0.001). New Q waves developed in 122 (28%), 76 (23%), and 2 (0.4%) patients in the MI, NSTEMI, and control groups, respectively. The sensitivity values of fQRS for ST elevation MI and NSTEMI were 55% and 50%, respectively. The specificity of fQRS was 96%. Kaplan-Meier survival analysis revealed that patients with fQRS had significantly decreased times to death compared to those without fQRS. Fragmented QRS, T-wave inversion, and ST depression were independent predictors of mortality during a mean follow-up period of 34 ± 16 months. In conclusion, fQRS on 12-lead electrocardiography is a moderately sensitive but highly specific sign for ST elevation MI and NSTEMI. Fragmented QRS is an independent predictor of mortality in patients with ACS.

The currently available sudden cardiac death (SCD) risk prediction tools fail to identify most at-risk patients and cannot delineate a specific patient’s SCD risk. We sought to develop a tool to improve the risk stratification of patients with coronary artery disease. Clinical, demographic, and angiographic characteristics were evaluated among 37,258 patients who had undergone coronary angiography from January 1, 1985 to May 31, 2005, and who were found to have at least one native coronary artery stenosis of ≥75%. After a median follow-up of 6.2 years, SCD had occurred in 1,568 patients, 14,078 patients had died from other causes, and 21,612 patients remained alive. A Cox proportional hazards model identified 10 independent patient characteristic variables significantly associated with SCD. A simplified model accounting for 97% of the predictive capacity of the full model included the following 7 variables: depressed left ventricular ejection fraction, number of diseased coronary arteries, diabetes mellitus, hypertension, heart failure, cerebrovascular disease, and tobacco use. The Duke SCD risk score was created from the simplified model to predict the likelihood of SCD among patients with coronary artery disease. It was internally validated with bootstrapping (c-index = 0.75, chi-square = 1,220.8) and externally validated in patients with ischemic cardiomyopathy from the Sudden Cardiac Death Heart Failure Trial (SCD-HeFT) database (c-index = 0.64, chi-square = 14.1). In conclusion, the Duke SCD risk score represents a simple, validated method for predicting the risk of SCD among patients with coronary artery disease and might be useful for directing treatment strategies designed to mitigate the risk of SCD.