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PET/CT Assessment of Flow-Mediated Epicardial Vasodilation in Obesity and Severe Obesity.
Valenta, Ines; Upadhyaya, Anand; Jain, Sudhir; Schindler, Thomas H.
Afiliação
  • Valenta I; Cardiovascular Division, John T. Milliken Department of Internal Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, USA.
  • Upadhyaya A; Cardiovascular Division, John T. Milliken Department of Internal Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, USA.
  • Jain S; Division of Nuclear Medicine-Cardiovascular, Washington University in St. Louis School of Medicine, Mallinckrodt Institute of Radiology, St. Louis, Missouri, USA.
  • Schindler TH; Cardiovascular Division, John T. Milliken Department of Internal Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, USA.
JACC Adv ; 3(5): 100936, 2024 May.
Article em En | MEDLINE | ID: mdl-38939628
ABSTRACT

Background:

It is not known whether the transition from obesity and severe obesity, as 2 different metabolic disease entities, affect flow-mediated and, thus, endothelium-dependent epicardial vasodilation.

Objectives:

The purpose of this study was to investigate the effect of obesity and severe obesity on flow-mediated epicardial vasomotion with positron emission tomography/computed tomography-determined longitudinal decrease in myocardial blood flow (MBF) from the base-to-apex direction of the left ventricle or gradient.

Methods:

13N-ammonia positron emission tomography/computed tomography evaluated global MBF during pharmacologically induced hyperemia and at rest for assessment of coronary microvascular function. In addition, the Δ longitudinal MBF gradient (hyperemia minus rest) was determined. 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 = 29), obesity (OB) (BMI 30.0-39.9 kg/m2, n = 53), and severe obesity (morbid obesity BMI ≥40 kg/m2, n = 43).

Results:

Compared to NW, left ventricular Δ longitudinal MBF gradient progressively declined in OW and OB (0.04 ± 0.09 mL/g/min vs -0.11 ± 0.14 mL/g/min and -0.15 ± 0.11 mL/g/min; P ≤ 0.001, respectively) but not significantly in SOB (-0.01 ± 0.11 mL/g/min, P = 0.066). Regadenoson-induced global hyperemic MBF was lower in OB than in NW (1.88 ± 0.40 mL/g/min vs 2.35 ± 0.32 mL/g/min; P ≤ 0.001), while comparable between NW and SOB (2.35 ± 0.32 mL/g/min vs 2.26 ± 0.40 mL/g/min; P = 0.302). The BMI of the study population was associated with the Δ longitudinal MBF gradient in a U-turn fashion (r = 0.362, standard error of the estimate = 0.124; P < 0.001).

Conclusions:

Increased body weight associates with abnormalities in coronary circulatory function that advances from an impairment flow-mediated, epicardial vasodilation in overweight and obesity to coronary microvascular dysfunction in obesity, not observed in severe obesity. The U-turn of flow-mediated epicardial vasomotion outlines obesity and severe obesity to affect epicardial endothelial function differently.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: JACC Adv Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: JACC Adv Ano de publicação: 2024 Tipo de documento: Article