OBJECTIVES: Liver enzyme elevations occur with ST-segment elevation myocardial infarction (STEMI); however, their significance in the modern era is not well-defined. The incidence of liver enzyme elevations in STEMI, temporal trends, correlations with creatine kinase-MB (CK-MB), and associations with clinical outcomes were evaluated. METHODS: The Complement Inhibition in Myocardial Infarction Treated with Angioplasty and Complement Inhibition in Myocardial Infarction Treated with Thrombolytics trials evaluated 1903 patients with STEMI. A core lab analyzed liver enzymes at baseline, days 1, 6, and 14, and CK-MB measured sequentially over 72 h. The GUSTO model for 30-day mortality was used to predict clinical endpoints. RESULTS:A total of 1783 patients were included in the analysis. Aspartate transaminase (AST) was elevated above the upper limit of normal in 85.6% and alanine transaminase (ALT) was elevated in 48.2% of patients at baseline or day 1. CK-MB area under the curve correlated with maximum AST (r=0.727) and maximum ALT (r=0.456). Both AST and ALT elevations were independent predictors of worse outcomes in multivariable adjusted analysis, even after adjustment for CK-MB. Hazard ratios and 95% confidence intervals of AST elevation were 1.12 (1.05-1.19) for all-cause mortality, and 1.08 (1.02-1.13) for the composite endpoint of death, congestive heart failure, shock, or stroke. Hazard ratios and 95% confidence intervals of ALT elevation were 1.15 (1.04-1.27) for mortality and 1.47 (1.10-1.98) for the composite endpoint. CONCLUSION: AST and ALT elevations are common in STEMI. Both markers are correlated with CK-MB area under the curve, but independently associated with worse mortality and clinical outcomes.
RCT Entities:
OBJECTIVES: Liver enzyme elevations occur with ST-segment elevation myocardial infarction (STEMI); however, their significance in the modern era is not well-defined. The incidence of liver enzyme elevations in STEMI, temporal trends, correlations with creatine kinase-MB (CK-MB), and associations with clinical outcomes were evaluated. METHODS: The Complement Inhibition in Myocardial Infarction Treated with Angioplasty and Complement Inhibition in Myocardial Infarction Treated with Thrombolytics trials evaluated 1903 patients with STEMI. A core lab analyzed liver enzymes at baseline, days 1, 6, and 14, and CK-MB measured sequentially over 72 h. The GUSTO model for 30-day mortality was used to predict clinical endpoints. RESULTS: A total of 1783 patients were included in the analysis. Aspartate transaminase (AST) was elevated above the upper limit of normal in 85.6% and alanine transaminase (ALT) was elevated in 48.2% of patients at baseline or day 1. CK-MB area under the curve correlated with maximum AST (r=0.727) and maximum ALT (r=0.456). Both AST and ALT elevations were independent predictors of worse outcomes in multivariable adjusted analysis, even after adjustment for CK-MB. Hazard ratios and 95% confidence intervals of AST elevation were 1.12 (1.05-1.19) for all-cause mortality, and 1.08 (1.02-1.13) for the composite endpoint of death, congestive heart failure, shock, or stroke. Hazard ratios and 95% confidence intervals of ALT elevation were 1.15 (1.04-1.27) for mortality and 1.47 (1.10-1.98) for the composite endpoint. CONCLUSION:AST and ALT elevations are common in STEMI. Both markers are correlated with CK-MB area under the curve, but independently associated with worse mortality and clinical outcomes.
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