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 ± 0.84 vs. 2.50 ± 0.67 and 2.33 ± 0.63; p ≤ 0.04 by ANOVA), while it increased again in MOB comparable to NW (2.51 ± 0.51 vs. 2.71 ± 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.