Coronary vasodilator capacity in obesity and morbid obesity - divergent flow responses with left ventricular hypertrophy

Background: To investigate the relationship between coronary vasodilator capacity, left ventricular hypertrophy, and regional myocardial function in two different disease entities of obese (OB) and morbidly obese (MOB) individuals. Methods: 13N-ammonia PET/CT determined myocardial blood flow (MBF) at rest and during pharmacologically induced hyperemia, and corresponding myocardial flow reserve (MFR) with 13N-ammonia PET/CT. Left ventricular mass (LVM), early diastolic flow (E), relaxation (e') velocities, and global longitudinal strain (GLS) were acquired with 2D, trans-mitral Doppler and tissue Doppler, and speckle tracking echocardiography, respectively. Patients were then grouped according to the body mass index (BMI) into normal weight (NW: BMI 20.0-24.9 kg/ m2, n = 27), overweight (OW: BMI 25.0-29.9 kg/ m2, n = 31), obesity (OB: BMI 30.0-39.9 kg/m2, n = 71), and morbid obesity (MOB: BMI >= 40 kg/m2, n = 97). Results: MFR progressively decreased from NW, OW, to OB (2.71 f 0.84 vs. 2.50 f 0.67 and 2.33 f 0.63; p <= 0.04 by ANOVA), while it increased again in MOB comparable to NW (2.51 f 0.51 vs. 2.71 f 0.84, p = 0.70). In OB and MOB, MFR was inversely correlated with E velocity (cm/s), respectively (r = 0.32, SEE = 0.58, p = 0.02; and r = 0.29, SEE = 0.47, p = 0.02). Conversely, LVM, and GLS associated significantly and inversely with the MFR in OB (r = 0.27, SEE = 0.59, p = 0.05; and r = 0.31, SEE = 0.61, p = 0.04), but not in MOB, respectively (r = 0.13, SEE = 0.49, p = 0.27; and r = 0.05, SEE = 0.54, p = 0.73). Notably, GLS, E-velocity, and LVM remained independent predictors of MFR. Conclusion: Divergent associations of coronary vasodilator capacity with left ventricular mass and early myocardial contractile dysfunction outline OB and MOB to affect left ventricular remodeling differently.