We studied both the time course and risk factors for adverse clinical events after percutaneous coronary intervention (PCI). Such information is critical to clinical decision-making, but scant quantitative data exist ...
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We studied both the time course and risk factors for adverse clinical events after percutaneous coronary intervention (PCI). Such information is critical to clinical decision-making, but scant quantitative data exist to describe the time course of these adverse outcomes. Patients enrolled in the Integrilin to Minimize Platelet Aggregation and Coronary Thrombosis-ii (IMPACT-II) trial were analyzed. Patients undergoing elective, urgent, or emergency PCI (n = 4,010) were randomized to receive either placebo or 1 of 2 eptifibatide regimens during intervention. We evaluated the time to the primary end point of the trial, the 30-day composite of death, myocardial infarction, repeat nonelective PCI, nonelective bypass surgery, or stenting for abrupt closure. Adverse events occurred in 407 patients (10.1%). Because the risk of events declined substantially between 6 and 9 hours (66% occurred within b hours), events were classified as occurring before or after 6 hours. Independent predictors of "early" events included dissection, pre- and postprocedural coronary blood flow, side-branch occlusion, procedural thrombolytic use, previous bypass, presentation with unstable angina, absence of diabetes, and hyperlipidemia. The predictors of "late" events included lower weight, increased baseline heart rate, coronary dissection, and procedural thrombolytic use. The risk of ischemic events were greatest immediately after PCI and rapidly declined, so that by 9 hours the hazard function plot was flat;66% of events occurred within 6 hours of PCI. Knowledge of the risk factors for early and late events help risk-stratify patients before and after intervention for myocardial ischemic events. (C) 2000 by Excerpta Medico, Inc.
OBJECTIVES The purpose of this study was to determine whether the elevated levels of hemostatic markers in the early phase of myocardial infarction may serve as risk factors for subsequent cardiac mortality. BACKGROUN...
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OBJECTIVES The purpose of this study was to determine whether the elevated levels of hemostatic markers in the early phase of myocardial infarction may serve as risk factors for subsequent cardiac mortality. BACKGROUND Increased plasma hemostatic markers were noted in acute myocardial infarction, indicating that the blood coagulation system is highly activated in those patients. However, there are few clinical data concerning the association between the elevated hemostatic markers and survival in patients with myocardial infarction. METHODS Blood samples were obtained from 63 patients (mean age 67 w+/- 11 years;49 male)with acute myocardial infarction within 12 h after the onset of symptoms and before the initiation of any antithrombotic treatment. We measured plasma concentrations of fibrinopeptide A (FPA), prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complex (TAT) using the enzyme-linked immunosorbent assay method, and examined the associations between the level of these markers and survival with Cox proportional hazards models. RESULTS The follow-up time was 27 +/- 17 months, and 19 patients died of cardiac causes during inr follow-up. Univariate survival analysis identified Killip class IV (hazard ratio 4.86;95% confidence interval [CI] 1.55-15.19), left ventricular ejection fraction (hazard ratio 0.94;95% CI 0.90-0.99), FPA (hazard ratio 1.54;95% CI 1.13-2.10), F1+2 (hazard ratio 2.03;95% CI 1.17-3.53) and TAT (hazard ratio 1.88;95% CI 1.27-2.79) as significant factors associated with cardiac mortality In multivariate analyses, only FPA level (hazard ratio 1.84;95% CI 1.03-3.30) and left ventricular ejection fraction (hazard ratio 0.93;95% CI 0.88-0.98) were independent predictors of cardiac mortality. CONCLUSIONS Elevated FPA in the early phase of myocardial infarction identifies patients with increased risk for subsequent cardiac death. This association appears to be independent of residual left ventricular function after infarction. (C) 1999 by
Background Heparins, both standard unfractionated heparin (SUFH) and low-molecular weight heparin, play a prominent role in the treatment of acute coronary syndromes. Enoxaparin has been shown in 2 trials to be superi...
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Background Heparins, both standard unfractionated heparin (SUFH) and low-molecular weight heparin, play a prominent role in the treatment of acute coronary syndromes. Enoxaparin has been shown in 2 trials to be superior to heparin but has not been compared with placebo or untreated control. Methods A putative enoxaparin versus placebo/control odds ratio (OR) was computed with a recently described statistical technique with the logarithm of the ORs of the pooled results of both the enoxaparin-SUFH trials and SUFH-placebo or controlled trials. Results The combined heparin versus control results show a 33% reduction in the risk of death or acute myocardial infarction (AMI), with an OR of 0.67 (95% confidence interval [CI], 0.45 to 0.99). At up to 12 weeks (data from only 4 trials), the combined results show a 21% reduction (OR, 0.79;95% CI, 0.54 to 1. 15;P = .23). The 2 enoxaparin trials show a nonsignificant 20% reduction in the risk of death or AMI during treatment (OR, 0.80;95% CI, 0.68 to 1.16;P = .24) and a significant reduction at 43 days (OR, 0.82;95% CI, 0.69 to 0.97;P = .022). With these pooled data, the putative OR for enoxaparin versus placebo/untreated control during treatment is 0.53 (95% CI, 0.31 to 0.92;P = .023). The data are consistent with a 47% reduction in the risk of death or AMI. The difference persists on longer term follow-up period (OR, 0.65;95% CI, 0.43 to 0.98;P = .04). The risk of bleeding is nonsignificantly increased (OR, 2.32;95% CI, 0.8 to 7.85;P = .51). Conclusion On the basis of this methodology, enoxaparin would appear to be more effective than placebo when added to aspirin in acute coronary syndromes. Moreover, the effect of enoxaparin is similar to the results of a metaanalysis of trials of other low-molecular weight heparins versus placebo/control.
Intracoronary stents have significantly advanced the treatment of coronary artery disease.(1-3) Early data with self-expanding stents, however, showed early stent thrombosis rates of 24%.(4) Aggressive antiplatelet an...
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Intracoronary stents have significantly advanced the treatment of coronary artery disease.(1-3) Early data with self-expanding stents, however, showed early stent thrombosis rates of 24%.(4) Aggressive antiplatelet and anticoagulation regimens of dextran, aspirin, dipyridamole, and warfarin led to a reduction in early stent thrombosis to 3% to 4%, but greatly increased the rate of bleeding and vascular complications to as high as 13%.(2) Combination antiplatelet therapy after intracoronary stenting with aspirin and ticlopidine became standard practice after several nonrandomized trials showed reduced complication rates in patients with stents.(5-7) More recently, randomized trials demonstrated that aspirin and ticlopidine had a significantly lower primary cardiac end point rate (0.5%) than aspirin alone (3.6%) or than aspirin and warfarin (2.7%) in patients with coronary stents.(8-10) Ticlopidine, however, carries the risk of severe neutropenia (0.8% of patients), and compliance may be limited by twice-a-day dosing and,gastrointestinal intolerance. Recently, a new thienopyridine in the same class as ticlopidine, clopidogrel (Plavix, Bristol-Myers-Squibb, Princeton, New Jersey), has been introduced which has the purported advantage of a reduced incidence of severe neutropenia (0.04%), once-a-day dosing, a better side-effect profile, and a more rapid onset of action.(11) This study evaluates the safety, in-hospital, and 30-day clinical outcome in patients treated with aspirin and a 2-week course of clopidogrel after coronary stenting.
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