Relationship Between Myocardial Function, Body Mass Index, and Outcome After ST-Segment-Elevation Myocardial Infarction.

Abstract

Better survival for overweight and obese patients after ST-segment-elevation myocardial infarction (STEMI) has been demonstrated. The association between body mass index (BMI), outcome, and left ventricular (LV) structure and function after STEMI, including LV longitudinal strain (global longitudinal strain), was evaluated. First patients with STEMI undergoing primary percutaneous coronary intervention (n=1604; mean age, 61±12 years; 75% men) had BMI measured on admission, and 2-dimensional transthoracic echocardiography performed within 48 hours. Patients were categorized based on standard criteria (normal/underweight, BMI<25 kg/m2 [n=486]; overweight, 25≤BMI<30 kg/m2 [n=820]; obese, BMI≥30 kg/m2 [n=298]). LV global longitudinal strain was measured using speckle-tracking analysis. Primary outcome measure was all-cause mortality. Compared with normal/underweight patients, obese patients were younger and more likely to have diabetes mellitus, hypertension, and hyperlipidemia and have higher discharge blood pressures. Despite no significant differences in infarct size, obese patients had significantly more impaired LV global longitudinal strain (-13.7±3.8 versus -15.0±4.2% and -15.0±4.1%; P<0.001) compared with normal/underweight and overweight patients, respectively. Although normal/underweight patients had the worst overall survival (log-rank P=0.04) after STEMI during a median follow-up of 5.2 (3.6, 6.9) years on Kaplan-Meier analysis, a significant nonlinear association between BMI and all-cause mortality across the range of BMI was seen, persisting after adjustment for age and sex. Obese patients demonstrate greater adverse LV remodeling and more impaired LV deformation after STEMI compared with those with normal BMI, amid similar infarct characteristics. Normal weight patients continue to demonstrate the worst survival, suggesting that the potential nonadverse effect of higher BMI in this population is independent of LV function.