Abstract 14599: Adverse Effects of Obesity, Hyperglycemia, and Insulin Resistance on Cardiac Mechanics
Introduction: Although obesity and insulin resistance are known risk factors for heart disease, including HF, their effects of on cardiac mechanics (systolic strain and diastolic tissue e’ velocities) are not well known. We hypothesized that markers of obesity and insulin resistance are each independently associated with abnormal cardiac mechanics.
Methods: We performed speckle-tracking analysis on echos from the HyperGEN study (N=1426). Global longitudinal, circumferential, and radial strain (GLS, GCS, and GRS), and e’ velocities were measured. We used mixed-effects linear regression (to account for subject relatedness) to determine whether BMI, fasting glucose, and HOMA-IR were each associated with abnormal cardiac mechanics. We also analyzed cardiac mechanics in a murine model of obesity and insulin resistance (db/db mice) and compared to wild type mice.
Results: The mean age of the cohort was 55±12 years, 58% were female, 35% were black, 73% were hypertensive, 50% were obese, 15% were diabetic, and 94% had normal EF (>50%). BMI, fasting glucose, and HOMA-IR were each associated with decreased GLS (P<0.0001). Hyperglycemia and increased HOMA-IR were each associated with reduced e’ velocity (P<0.001) whereas BMI was not. After adjusting for age, sex, study site, image quality, systolic BP, wall motion abnormalities, LV mass index, and EF, all 3 markers remained associated with GLS (Figure), and fasting glucose and HOMA-IR remained associated with reduced e’ velocity (P<0.001 for all associations). The observed associations persisted after excluding participants with diabetes (P<0.01 for all associations). Peak systolic strain and e’ velocity were both reduced in the db/db mouse compared to WT controls (Figure).
Conclusions: Obesity, hyperglycemia, and insulin resistance are associated with abnormal cardiac mechanics. Further study of cardiac mechanics in the db/db mouse may elucidate molecular mechanisms underlying these associations.
- © 2012 by American Heart Association, Inc.