Abstract

Introduction: Obesity is associated with excess cardiovascular morbidity and mortality as well as structural and functional differences in left ventricular (LV) mass (LVM), end-diastolic volume (LVEDV), and stroke volume despite indexation. Hypothesis: We hypothesize that overweight and obesity impact LV structure and function in a healthy community dwelling cohort. Methods: Framingham Offspring study participants (N=678, 62%F; 65±9y) free of any history of hypertension, myocardial infarction, heart failure, or CMR wall-motion abnormality and underwent bSSFP CMR at 1.5T. They were stratified by sex and body mass index (BMI) category (normal weight =18.5 to 24.9; overweight =25.0 to 29.9; obese ≥30 kg/m 2 ). LVM was measured from contiguous short-axis images, then indexed to height (HT, m), body surface area (BSA, m 2 ), and weight (WT, kg). We calculated myocardial contraction fraction (MCF), a marker of LV myocardial shortening, as LV stroke volume divided by LV myocardial volume. The ratio of LVM/LVEDV was used as a measure of LV concentricity to evaluate LV structure. Results: The Table shows MCF, LV concentricity, and indexed LVM (LVMi) stratified by BMI. WT-indexation resulted in a declining LVMi with increasing BMI in both men and women. However, indexation to HT showed an increasing LVMi with higher BMI. BSA-indexation remained consistent across BMI categories in both men and women. MCF decreased and concentricity increased with increasing BMI in both sexes. Conclusion: The association of LVMi with BMI varies by indexation method. In a healthy, community-dwelling cohort, BSA yields “consistent” LVM indexation across BMI categories. However, MCF decreased, and concentricity increased with increasing categories of BMI. These adverse alterations of MCF and concentricity may provide insight into obesity-related LV remodeling, whereas consideration of LVM alone may not. These data lay the groundwork for further outcomes analyses in this population.

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