Hyperglycemia on admission predicts larger infarct size in patients undergoing percutaneous coronary intervention for acute ST-segment elevation myocardial infarction.

AIMS: To determine if hyperglycemia on admission correlates to infarct size measured by single-photon emission computed tomography (SPECT) in patients with acute ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). METHODS: We evaluated 347 STEMI patients who underwent primary PCI. Infarct size was determined by SPECT on Day 5. The population was divided into: hyperglycemia (glycemia on admission >11mmol/L) or non-hyperglycemia (

Association of leukocyte and neutrophil counts with infarct size, left ventricular function and outcomes after percutaneous coronary intervention for ST-elevation myocardial infarction.

Elevated leukocyte count during ST-segment elevation myocardial infarction is associated with adverse clinical outcomes. Whether increased leukocyte count after primary percutaneous coronary intervention (PCI) directly reflects larger infarct size and left ventricular impairment is not known. The aim of this study was to assess the relation between leukocyte and neutrophil counts with infarct size and the left ventricular ejection fraction (LVEF) after primary PCI. Three hundred sixty-three patients from the Evaluation of MCC-135 for Left Ventricular Salvage in Acute Myocardial Infarction (EVOLVE) study, a randomized, double-blind, placebo-controlled trial assessing the efficacy of intracellular calcium modulator as an adjunct to primary PCI in patients with first ST-segment elevation myocardial infarctions, were evaluated. Total and differential leukocyte counts were measured before and serially after PCI. Infarct size and the LVEF were assessed using single-photon emission computed tomography after 5 and 30 days, and patients were followed up to 180 days. Total leukocyte and neutrophil counts obtained 24 hours after PCI were significantly correlated with infarct size (r = 0.34 and 0.37, respectively, p <0.001) and inversely correlated with the LVEF (r = -0.20 and -0.22, respectively, p <0.001). Patients with elevated leukocyte and neutrophil counts had larger infarct sizes (12.5% vs 5% and 13.5% vs 5%, respectively, p <0.001). The highest neutrophil quartile was associated with increased 180-day composite cardiac events (19% vs 20% vs 23% vs 45%, log-rank p <0.001). Elevated leukocyte and neutrophil counts independently predicted adverse cardiac events (hazard ratios 2.5 and 2.2, respectively, p = 0.001). In conclusion, elevated leukocyte and neutrophil counts after primary PCI in patients with ST-segment elevation myocardial infarctions are directly related to myocardial infarct size and the LVEF and are independent predictors of cardiovascular outcomes.

Utility of cardiac biomarkers in predicting infarct size, left ventricular function, and clinical outcome after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction.

OBJECTIVES: We sought to determine the best cardiac biomarker to predict infarct size, left ventricular ejection fraction (LVEF), and clinical outcome in patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). BACKGROUND: The cardiac biomarkers, creatine kinase (CK), CK-MB, and troponins T and I are routinely measured after myocardial infarction. However, their correlation with functional and clinical outcomes after PCI for STEMI is not well established. METHODS: In the EVOLVE (EValuation Of MCC-135 for Left VEntricular Salvage in Acute Myocardial Infarction) trial, patients were randomized to receive intracellular calcium modulator as adjunct to primary PCI for first large STEMI. Cardiac biomarker levels were determined in 378 patients before PCI and serially up to 72 h. Single-photon emission computed tomography was performed after 5 and 30 days, and patients were monitored up to 180 days. RESULTS: All single time-point, peak, and area under time-concentration curve of CK, CK-MB, and troponins T and I after PCI significantly correlated with infarct size and LVEF. In particular, 72-h troponin I (TnI72h) correlated strongly with 5-day and 30-day infarct size (r > 0.70; p < 0.001). A TnI72h threshold >55 ng/ml was 90% sensitive for large infarct size (> or =10%) and low LVEF (< or =40%) with specificities of 70% and 52%, respectively (c = 0.88, 0.81; p < 0.001). The highest TnI72h tertile was associated with increased 180-day composite clinical events (23% vs. 23% vs. 42%; p = 0.001) and independently predicted adverse events (hazard ratio = 2.3; p = 0.01). CONCLUSIONS: Assessing TnI72h after primary PCI is a simple, effective method to estimate infarct size, LVEF, and potentially useful for risk stratification.

Randomized double-blind safety study of enoxaparin versus unfractionated heparin in patients with non-ST-segment elevation acute coronary syndromes treated with tirofiban and aspirin: the ACUTE II study. The Antithrombotic Combination Using Tirofiban and Enoxaparin.

BACKGROUND: In comparison with treatment with unfractionated heparin (UFH) and aspirin (ASA), both tirofiban administered with UFH and ASA, and enoxaparin plus ASA have shown superiority in reducing cardiac ischemic events in patients with unstable angina and non-ST-segment elevation myocardial infarction. Replacing UFH with enoxaparin when tirofiban is administered to patients may offer further therapeutic benefit, but could also increase bleeding. OBJECTIVE: Our objective was to provide estimates of the frequency of bleeding complications, as defined by means of the Thrombolysis In Myocardial Infarction(TIMI) group, and collect data on clinical efficacy of the combination of tirofiban with enoxaparin plus ASA. METHODS: Five hundred twenty-five patients with UA/NSTEMI were treated with tirofiban coadministered with ASA and randomized to receive either UFH (n = 210) or enoxaparin (n = 315). Therapy was administered for 24 to 96 hours. Bleeding incidences were assessed until 24 hours after trial therapy was discontinued; other clinical outcomes were assessed for as long as 30 days. RESULTS: The total bleeding rate (TIMI major + minor + loss-no-site) for the UFH group versus the enoxaparin group was 4.8% vs 3.5% (odds ratio [OR] 1.4, CI 0.6-3.4). The TIMI major and minor bleeding rates for the UFH versus the enoxaparin groups were 1.0% versus 0.3% (OR 3.0, CI 0.3-33.8) and 4.3% versus 2.5% (OR 1.7, CI 0.7-4.6). There was an increase in nuisance cutaneous and oral bleeds (<50 mL of blood loss) in the enoxaparin group. Death or myocardial infarction occurred with similar frequency in the 2 groups (9.0% vs 9.2%). However, refractory ischemia requiring urgent revascularization and rehospitalization because of unstable angina occurred more frequently in the UFH group (4.3% vs 0.6% and 7.1% vs 1.6%, respectively). CONCLUSIONS: Combination therapy with tirofiban plus enoxaparin appears safe, relative to therapy with tirofiban plus UFH.