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) a...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2025-10-01
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| Series: | International Journal of Cardiology: Heart & Vasculature |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2352906725001885 |
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| Summary: | 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. |
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| ISSN: | 2352-9067 |