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: 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.