■尚不清楚是否从肥胖和严重肥胖过渡,作为2种不同的代谢疾病实体,影响流量介导的,因此,内皮依赖性心外膜血管舒张。
■这项研究的目的是通过正电子发射断层扫描/计算机断层扫描确定的心肌血流(MBF)的纵向减少,研究肥胖和重度肥胖对血流介导的心外膜血管舒缩的影响。左心室或梯度的底部到顶点方向。
■13N-氨正电子发射断层扫描/计算机断层扫描评估了药理学诱导的充血和休息时的整体MBF,以评估冠状动脉微血管功能。此外,确定Δ纵向MBF梯度(充血减去休息)。然后根据体重指数(BMI)将患者分组为正常体重(NW)(BMI20.0-24.9kg/m2,n=27),超重(OW)(BMI25.0-29.9kg/m2,n=29),肥胖(OB)(BMI30.0-39.9kg/m2,n=53),和严重肥胖(病态肥胖:BMI≥40kg/m2,n=43)。
■与西北相比,左心室Δ纵向MBF梯度在OW和OB中逐渐下降(0.04±0.09mL/g/minvs-0.11±0.14mL/g/min和-0.15±0.11mL/g/min;P≤0.001),但在SOB中没有显着下降(-0.01±0.11mL/g/min,P=0.066)。在OB中,Regadenoson引起的整体充血MBF低于NW(1.88±0.40mL/g/minvs2.35±0.32mL/g/min;P≤0.001),NW和SOB之间具有可比性(2.35±0.32mL/g/minvs2.26±0.40mL/g/min;P=0.302)。研究人群的BMI与Δ纵向MBF梯度呈U型转弯(r=0.362,估计值的标准误差=0.124;P<0.001)。
■体重增加与冠状动脉循环功能异常有关,这种异常是由血流介导的损害引起的,超重和肥胖的心外膜血管舒张对肥胖的冠状动脉微血管功能障碍,在严重肥胖中未观察到。血流介导的心外膜血管舒缩的U型转弯概述了肥胖和严重肥胖对心外膜内皮功能的不同影响。
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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).
UNASSIGNED: 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).
UNASSIGNED: 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.