• Robert M Minutello, Luke Kim, Smita Aggarwal, Linda J Cuomo, Dmitriy N Feldman, and S Chiu Wong.
• Department of Medicine, Division of Cardiology, Weill Cornell Medical College, New York, New York 10065, USA. RMM2002@med.cornell.edu
• Tex Heart Inst J. 2010 Jan 1;37(2):161-5.

AbstractReduced door-to-balloon time in primary percutaneous coronary intervention for the treatment of ST-elevation myocardial infarction has been associated with lower cardiac mortality rates. However, it remains unclear whether door-to-balloon time is predominantly a surrogate for overall peri-myocardial infarction care and is not independently predictive of outcomes, particularly when differences in door-to-balloon time have narrowed and previous studies have contained myocardial infarction-selection bias.We analyzed 179 consecutive patients who presented emergently at our cardiac catheterization laboratory with ST-elevation myocardial infarction within 12 hours of symptom onset and who underwent primary percutaneous coronary intervention within 3 hours of presentation. Our curve estimation regression model used the natural logarithm (ln) of area under the curve (AUC) of creatine kinase to evaluate the effect of door-to-balloon time on cardiac biomarker levels. We correlated ln (AUC-creatine kinase) with improvement of left ventricular ejection fraction at follow-up and with the intermediate-term mortality rate.Median door-to-balloon time was 87 minutes (interquartile range, 65-113 min). The ln (AUC-creatine kinase) correlated significantly with door-to-balloon time (r=0.2, P=0.02). Upon propensity-score analysis, door-to-balloon time remained a significant independent predictor of ln (AUC-creatine kinase) (beta=0.15, P=0.03). Upon use of a Cox regression model, ln (AUC-creatine kinase) independently predicted death (P=0.04) and recovery of left ventricular function (P=0.001) at follow-up (mean, 14 mo).Longer door-to-balloon time independently predicts increased myocardial cell damage, and ln (AUC-creatine kinase) predicts improvement in left ventricular systolic function and intermediate-term death after ST-elevation myocardial infarction.

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