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

Elgin Ozkan; Liya Dai; Farrokh Dehdashti; Kan Liu; Thomas H Schindler

doi:10.1016/j.ijcha.2025.101785

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

Int J Cardiol Heart Vasc. 2025 Aug 25:60:101785. doi: 10.1016/j.ijcha.2025.101785. eCollection 2025 Oct.

Authors

Elgin Ozkan¹, Liya Dai¹, Farrokh Dehdashti¹, Kan Liu², Thomas H Schindler^{1

2}

Affiliations

¹ Washington University in St. Louis School of Medicine, Mallinckrodt Institute of Radiology, Division of Nuclear Medicine - Cardiovascular, St. Louis, MO, USA.
² Washington University in St. Louis School of Medicine, John T. Milliken Department of Internal Medicine, Cardiovascular Division, St. Louis, MO, USA.

Abstract

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.

Keywords: Blood flow; Circulation; Coronary circulatory function; Coronary microvascular function; Left ventricular hypertrophy; Myocardial flow reserve; Myocardial perfusion; Obesity; PET; Vasomotion.