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BACKGROUND: Patients with decreased kidney function and acute ST-elevation myocardial infarction (STEMI) and non-STEMI are less likely to receive reperfusion therapy and aggressive medical treatment. This undertreatment may contribute to the poor outcome of these patients. The prognostic value of kidney function in patients with STEMI and NSTEMI treated predominantly with percutaneous coronary intervention (PCI) and aggressive medical treatment is less known. STUDY DESIGN: Prospective cohort study. SETTING & PARTICIPANTS: 2 academic centers in Germany; 4,701 consecutive patients with acute myocardial infarction (AMI) from 1998 to 2006. PREDICTOR: Estimated creatinine clearance (eCCr) at admission. OUTCOMES & MEASUREMENTS: The primary end point was all-cause mortality during the first year after PCI for AMI (STEMI and NSTEMI) with a prespecified landmark at 30 days (landmark analysis). Secondary end points were nonfatal myocardial infarction, stroke, and major bleeding. RESULTS: Patients were divided into quartiles according to eCCr less than 56, 56 to 76, 77 to 100, and greater than 100 mL/min. Patients had an increased risk of death with decreased eCCr both within 30 days (7.7%, 3.1%, 1.4%, and 0.7% for the 4 quartiles; P < 0.001) and after 30 days (12.1%, 4.8%, 1.9%, and 1.2%; P < 0.001). The association of eCCr with mortality was similar in patients younger and older than 70 years. Major bleeding within 30 days and incidence of stroke also were more frequent with reduced eCCr. However, recurrent myocardial infarction was not associated with eCCr. After adjustment for additional baseline characteristics, kidney function based on eCCr at admission remained a strong independent predictor of mortality at 1 year after AMI (hazard ratio, 1.21 per 10-mL/min decrease; 95% confidence interval, 1.13 to 1.30). LIMITATIONS: Single assessment of eCCr. CONCLUSIONS: In patients with AMI treated with primary PCI for STEMI and early PCI for NSTEMI, eCCr at admission remains a powerful independent predictor of short- and long-term mortality. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to assess the efficacy of a rapamycin plus 17-beta-estradiol-eluting stent versus a rapamycin-eluting stent in patients with coronary artery disease. Background: Estradiol promotes rapid re-endothelialization of coronary stents in animal models, but it is not known whether combining this drug with rapamycin represents an improved drug-eluting stent technology in terms of reduced lumen renarrowing. Methods: In this randomized study, we enrolled 502 patients with de novo lesions in native coronary arteries who were randomly assigned to receive either a polymer-free, estradiol plus rapamycin-eluting stent (ERES) (n = 252) or a polymer-free, rapamycin-eluting stent (RES) (n = 250). The primary end point was in-stent late lumen loss in the follow-up angiography. Secondary end points were binary angiographic restenosis, target lesion revascularization, combined incidence of death and myocardial infarction, and incidence of stent thrombosis during 1 year after randomization. The study was designed to test for the superiority of the ERES compared with the RES with respect to in-stent late lumen loss. Results: Late lumen loss (0.52 +/- 0.58 mm vs. 0.51 +/- 0.58 mm, p = 0.83), the incidence of binary angiographic restenosis (17.6% vs. 16.9%, p = 0.85), the incidence of target lesion revascularization (14.3% vs. 13.2%, p = 0.72), the combined incidence of death and myocardial infarction (7.9% vs. 8.0%, p = 0.98), and the incidence of stent thrombosis (0.8% vs. 1.2%, p = 0.99) were not significantly different between the ERES group and the RES group. Conclusions: No apparent beneficial effect is obtained by adding estradiol to a polymer-free rapamycin-eluting stent during the first year after the procedure. (The ISAR-PEACE trial; http://clinicaltrials.gov/ct/show/NCT00402636?order=1; NCT00402636). [ABSTRACT FROM AUTHOR]

Context: In unstable coronary syndromes, catheter intervention is frequently preceded by antithrombotic treatment to reduce periprocedural risk; however, evidence from clinical trials to support antithrombotic pretreatment is sparse.Objective: To test the hypothesis that prolonged antithrombotic pretreatment improves the outcome of catheter intervention in patients with acute unstable coronary syndromes compared with early intervention.Design, Setting, and Patients: Randomized controlled trial conducted from February 27, 2000, to April 8, 2002, and including patients admitted to 2 German tertiary care centers with symptoms of unstable angina plus either ST-segment depression or elevation of cardiac troponin T levels.Interventions: Patients were randomly allocated to antithrombotic pretreatment for 3 to 5 days or to early intervention after pretreatment for less than 6 hours. In both groups, antithrombotic pretreatment consisted of intravenous unfractionated heparin (60-U/kg bolus followed by infusion adjusted to maintain partial thromboplastin time of 60 to 85 seconds), aspirin (500-mg intravenous bolus followed by 100-mg twice-daily oral dose), oral clopidogrel (600-mg loading dose followed by 75-mg twice-daily dose), and intravenous tirofiban (10- microg/kg bolus followed by continuous infusion of 0.10 microg/kg per min).Main Outcome Measure: Composite 30-day incidence of large nonfatal myocardial infarction or death from any cause.Results: Of the 410 patients enrolled, 207 were allocated to receive prolonged antithrombotic pretreatment and 203 to receive early intervention. Elevated levels of cardiac troponin T were present in 274 patients (67%), while 268 (65%) had ST-segment depression. The antithrombotic pretreatment and the early intervention groups were well matched with respect to major baseline characteristics and definitive treatment (catheter revascularization: 133 [64.3%] vs 143 [70.4%], respectively; coronary artery bypass graft surgery: 16 [7.7%] vs 16 [7.9%]). The primary end point was reached in 11.6% (3 deaths, 21 infarctions) of the group receiving prolonged antithrombotic pretreatment and in 5.9% (no deaths, 12 infarctions) of the group receiving early intervention (relative risk, 1.96 [95% confidence interval, 1.01-3.82]; P =.04). This outcome was attributable to events occurring before catheterization; after catheterization, both groups incurred 11 events each (P =.92).Conclusion: In patients with unstable coronary syndromes, deferral of intervention for prolonged antithrombotic pretreatment does not improve the outcome compared with immediate intervention accompanied by intense antiplatelet treatment. [ABSTRACT FROM AUTHOR]

Objectives: We tested the hypothesis that patients with the DD genotype of the angiotensin I-converting enzyme (ACE) gene who are treated with ACE inhibitors are at a higher risk of restenosis after coronary stent placement than patients who do not receive ACE inhibitors.Background: Two recent studies with a limited series of patients carrying the DD genotype suggested an unfavorable impact of the use of ACE inhibitors on the restenotic process after implantation of stents in coronary arteries. Because these findings may question the use of ACE inhibitors after coronary stenting, we examined this important issue in a large series of patients.Methods: We determined the ACE gene I/D genotype of 2,222 consecutive patients with symptomatic coronary artery disease who underwent stent implantation. The patients with the DD genotype (n = 612) constituted the study population. The primary end point was in-stent restenosis, which was assessed as angiographic restenosis (> or =50% diameter stenosis at six-month follow-up) and clinical restenosis (need for target vessel revascularization due to symptoms or signs of ischemia in the presence of angiographic restenosis over one year after the intervention).Results: Of the 612 patients with the DD genotype, 403 (65.8%) were treated with ACE inhibitors and 209 (34.2%) did not receive ACE inhibitors. The angiographic and clinical restenosis rates were not significantly different between the group treated with ACE inhibitors and the group not receiving ACE inhibitors (p = 0.55). Continuous measures of restenosis, minimal lumen diameter, diameter stenosis, late lumen loss, and loss index were also similar in both groups (p > or = 0.55). In addition, one-year survival free of myocardial infarction was not significantly different between the two groups (p = 0.27).Conclusions: In contrast to previous reports, our study provides evidence that patients carrying the DD genotype are not exposed to an increased risk of restenosis after stent placement when treated with ACE inhibitors. [ABSTRACT FROM AUTHOR]

Objectives: We assessed the influence of statin therapy given after the procedure on one-year survival of patients treated with coronary artery stenting.Background: Coronary artery stenting is currently a common treatment option for patients with symptomatic coronary artery disease (CAD). Although several secondary prevention trials have demonstrated improved survival achieved with statin therapy in conservatively treated patients with CAD, it is not known whether this benefit can also be expected in patients undergoing percutaneous coronary interventions with intraluminal stenting.Methods: This study included 4,520 patients younger than 80 years who underwent coronary artery stenting and were discharged from the hospital in the period October 1995 through September 1999. We compared one-year mortality of 3,585 patients who received statins after stenting with that of 935 patients who did not.Results: The mortality rate at one year was 2.6% among patients who received statins and 5.6% among those who did not. Thus, statin therapy at discharge was associated with an unadjusted odds ratio (OR) of 0.46 (95% confidence interval [CI], 0.33 to 0.65), indicating a 54% reduction in the risk of death at one year. After adjusting for other covariates, the risk reduction associated with statin therapy was 49%, OR 0.51 (95% CI, 0.36 to 0.71). This reduction was observable in most of the subgroups of patients.Conclusions: The results of this nonrandomized study show that statin therapy improves survival after coronary artery stenting independent of patient characteristics recorded on the day of the intervention. [ABSTRACT FROM AUTHOR]

Background: Concern regarding the rate of delayed acute stent thrombosis associated with drug-eluting stent (DES) treatment has resulted in upward revision of the advised duration of dual antiplatelet therapy after DES implantation by both European and United States guideline writing committees. In fact, the corroboration of an increased rate of late thrombotic events remains outstanding, and these clinical practice guidelines are limited by an inadequate evidence base on which to ground their recommendations. Hypothesis: We postulate that a 6-month duration of clopidogrel therapy after DES implantation is associated with a clinical outcome that is not inferior to that of a 12-month therapy. Study Design: The Intracoronary Stenting and Antithrombotic Regimen: Safety And EFficacy of Six Months Dual Antiplatelet Therapy After Drug-Eluting Stenting (ISAR-SAFE) is a multinational, double-blind, placebo-controlled, randomized trial designed to examine the effects of a 6-month duration of clopidogrel therapy after DES implantation compared to that of 12 months. Patients on clopidogrel therapy at 6 months after DES implantation will be randomized in a 1:1 fashion to discontinuation of clopidogrel versus a further 6 months of treatment. The primary end point is a composite of death, myocardial infarction, stent thrombosis, stroke, or thrombolysis in myocardial infarction major bleeding. Clinical follow-up is scheduled at 9 months postrandomization (15 months postintervention). According to power calculations based on a noninferiority design, it is estimated that 6,000 patients are required to be enrolled. Summary: There is clinical equipoise on the issue of optimal duration of dual antiplatelet treatment after percutaneous intervention with DES. The ISAR-SAFE trial aims to assess whether discontinuation of clopidogrel 6 months after DES implantation is noninferior to routine prolongation of such therapy out to 1 year. [ABSTRACT FROM AUTHOR]

The ISAR-REACT 2 trial was designed to assess the effect of abciximab in patients with acute coronary syndromes undergoing percutaneous coronary intervention after a 600-mg loading dose of clopidogrel. The aim of the present study was to investigate the impact of abciximab on clinical and angiographic restenosis after coronary stenting in patients with acute coronary syndromes. The angiographic substudy included 1,544 patients from the ISAR-REACT 2 trial randomly assigned to abciximab (771 patients) or placebo (773 patients). All patients were scheduled for routine angiographic follow-up at 6 to 8 months after intervention. The primary end point was incidence of angiographic in-segment binary restenosis. The secondary end point was 1-year incidence of target-lesion revascularization. Binary restenosis was observed in 21.9% of patients in the abciximab group and 24.5% of patients in the placebo group (p=0.29). Percentages of in-stent (29+/-22% vs 33+/-24%; p=0.02) and in-segment (35+/-20% vs 38+/-21%; p=0.04) diameter stenoses were significantly lower in the abciximab group than the placebo group. There was a strong trend toward lower 1-year incidence of target-lesion revascularization in patients treated with abciximab than in patients treated with placebo (13.6% vs 16.8%; p=0.08). In conclusion, in patients with non-ST-segment elevation acute coronary syndromes undergoing early percutaneous coronary intervention with stenting after a 600-mg loading dose of clopidogrel, abciximab therapy may have a slight positive impact on the prevention of restenosis. [ABSTRACT FROM AUTHOR]

Hausleiter J, Kastrati A, Mehilli J, Schühlen H, Pache J, Dotzer F, Glatthor C, Siebert S, Dirschinger J, Schömig A for the ISAR-SMART-2 investigators (Klinik an der TU München and Technische Universität, Munich; and Medizinische Klinik I des Klinikums Garmisch-Partenkirchen, Germany) A randomized trial comparing phosphorylcholine-coated stenting with balloon angioplasty as well as abciximab with placebo for restenosis reduction in small coronary arteries.J Intern Med2004;256:388–397.The objective of this randomized trial was to assess the antirestenotic effects of phosphorylcholine (PC)-coated stents as well as of abciximab in small coronary arteries when compared with percutaneous transluminal coronary angioplasty (PTCA) and placebo respectively.Stent coating with PC has been shown to reduce protein absorption and platelet activation which may reduce the risk of restenosis. Furthermore, on the basis of nondedicated studies abciximab is believed to reduce the risk of restenosis after coronary interventions.A total of 502 patients with lesions situated in small coronary arteries (vessel diameter≤2.5 mm) were randomly assigned to be treated with either PC-coated stents (n = 253) or PTCA (n = 249) and with either abciximab (n = 251) or placebo (n = 251) with the use of a 2 × 2 factorial design. All patients were pretreated with 600 mg clopidogrel. The primary end-point was the incidence of angiographic restenosis (≥50% diameter stenosis) at follow-up; death or myocardial infarction, and target vessel revascularization (TVR), were assessed as secondary end-points.Angiographic restenosis did not differ between patients treated with PC-coated stents or with PTCA (39.0% vs. 34.2%;P = 0.30) and between patients receiving abciximab or placebo (39.3% vs. 34.3%;P = 0.29). Similarly, the need for TVR at 1-year follow-up did not differ between patients receiving PC-coated stents or PTCA (20.2% vs. 20.5%;P = 0.98) as well as between patients treated with abciximab or placebo (18.7% vs. 21.9%;P = 0.44).PC-coated stents and abciximab failed to reduce the incidence of angiographic restenosis after percutaneous coronary intervention of small coronary arteries. These data strengthen the belief that future studies on prevention of restenosis in small coronary arteries should focus on drug-eluting stents. [ABSTRACT FROM AUTHOR]

Background In cardiogenic shock (CS) the Impella CP® device provides a fast available left ventricular circulatory support of up to 4.0 L/min. However, the use of the Impella CP® device was not systematically analysed yet. Methods We performed a retrospective analysis of 28 consecutive patients suffering from severe therapy refractory CS treated with Impella CP®. Mortality was estimated using the SAPS II-Score. Primary outcome was 30-day survival. We compared the different aetiologies of CS and the effect of additional extracorporeal life support (ECLS). Results Aetiology of CS was acute coronary syndrome (ACS) in 15 patients, 9 patients received additional therapy with ECLS. SAPS II was 73 ± 14, representing an estimated mortality of 87.1%. 18 patients deceased representing a 30-day survival of 36%. Comparing the different aetiologies, ACS-CS patients show a trend towards better survival. Additional therapy with ECLS did not change 30-day survival. In 3 cases, vascular complication needing surgical treatment occurred. All other patients showed no relevant complications except for the commonly seen haemolysis with consecutive need of transfusion. Conclusion Our data could demonstrate that the Impella CP ® application in these severely diseased patients is feasible and safe. Compared to the estimated mortality, the 30-day survival seems to be improved. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Mild therapeutic hypothermia (TH) is standard of care after cardiac arrest of any cause. However, its impact on on-treatment platelet reactivity and clinical outcome in patients with acute myocardial infarction (AMI) complicated by cardiogenic shock and undergoing PCI with P2Y12 receptor inhibitor treatment is less clear. METHODS AND RESULTS: For the ISAR-SHOCK registry, 145 patients with AMI, cardiogenic shock and primary PCI in two centers (Deutsches Herzzentrum München and Klinikum rechts der Isar, Technical University Munich) between January 2009-May 2012 were analysed. Of these, 64 (44%) patients received TH treatment. The median [IQR] ADP-induced platelet aggregation following thienopyridine loading dose administration (clopidogrel in 95 and prasugrel in 50 patients) did not differ between the two groups (419 [283-684] for TH vs. 355 [207-710] AU x min for non-TH patients, P=0.22). After 30days follow-up, no significant differences were observed between both groups for mortality (42 vs. 44 %, HR: 0.93, 95% CI [0.56-1.53], p=0.77), MI (6 vs. 6%, HR: 0.99 95% CI [0.27-3.7], p=0.99) and TIMI minor bleedings (17 vs. 17%, HR 0.99 95% CI [0.45-2.18], p=0.98). TIMI major bleedings were numerically higher in the TH vs. non-TH cohort (25 % vs. 12 %, HR: 2.1 95% CI [0.95-4.63], p=0.07). Three definite stent thrombosis (ST) were observed in this registry and all STs occurred in the TH group of patients (p=0.09). CONCLUSION: Results of this registry suggest that TH does not negatively impact on platelet reactivity in shock patients receiving either clopidogrel or prasugrel. The numerically higher rate of major bleedings and the clustering of STs in the TH cohort warrant further investigation. [ABSTRACT FROM AUTHOR]