Gopal Deepa M, Santhanakrishnan Rajalakshmi, Wang Yi-Chih, Ayalon Nir, Donohue Courtney, Rahban Youssef, Perez Alejandro J, Downing Jill, Liang Chang-seng, Gokce Noyan, Colucci Wilson S, Ho Jennifer E
Cardiology Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (D.M.G.).
Cardiovascular Medicine Section, Boston University School of Medicine, Boston, MA (R.S., N.A., C.D., A.J.P., J.D., C.L., N.G., W.S.C., J.E.H.).
J Am Heart Assoc. 2015 Mar 10;4(3):e001597. doi: 10.1161/JAHA.114.001597.
Metabolic disease can lead to intrinsic pulmonary hypertension in experimental models. The contributions of metabolic syndrome (MetS) and obesity to pulmonary hypertension and right ventricular dysfunction in humans remain unclear. We investigated the association of MetS and obesity with right ventricular structure and function in patients without cardiovascular disease.
A total of 156 patients with MetS (mean age 44 years, 71% women, mean body mass index 40 kg/m(2)), 45 similarly obese persons without MetS, and 45 nonobese controls underwent echocardiography, including pulsed wave Doppler measurement of pulmonary artery acceleration time (PAAT) and ejection time. Pulmonary artery systolic pressure was estimated from PAAT using validated equations. MetS was associated with lower tricuspid valve e' (right ventricular diastolic function parameter), shorter PAAT, shorter ejection time, and larger pulmonary artery diameter compared with controls (P<0.05 for all). Estimated pulmonary artery systolic pressure based on PAAT was 42±12 mm Hg in participants with MetS compared with 32±9 and 32±10 mm Hg in obese and nonobese controls (P for ANOVA <0.0001). After adjustment for age, sex, hypertension, diabetes, body mass index, and triglycerides, MetS remained associated with a 20-ms-shorter PAAT (β=-20.4, SE=6.5, P=0.002 versus obese). This association persisted after accounting for left ventricular structure and function and after exclusion of participants with obstructive sleep apnea.
MetS is associated with abnormal right ventricular and pulmonary artery hemodynamics, as shown by shorter PAAT and subclinical right ventricular diastolic dysfunction. Estimated pulmonary artery systolic pressures are higher in MetS and preclinical metabolic heart disease and raise the possibility that pulmonary hypertension contributes to the pathophysiology of metabolic heart disease.
在实验模型中，代谢性疾病可导致特发性肺动脉高压。代谢综合征（MetS）和肥胖对人类肺动脉高压及右心室功能障碍的影响仍不明确。我们研究了无心血管疾病患者中MetS和肥胖与右心室结构及功能的关系。
共纳入156例MetS患者（平均年龄44岁，71%为女性，平均体重指数40kg/m²）、45例同样肥胖但无MetS的个体以及45例非肥胖对照者，进行超声心动图检查，包括用脉冲波多普勒测量肺动脉加速时间（PAAT）和射血时间。使用经过验证的公式根据PAAT估算肺动脉收缩压。与对照组相比，MetS与较低的三尖瓣e'（右心室舒张功能参数）、较短的PAAT、较短的射血时间及较大的肺动脉直径相关（所有P<0.05）。基于PAAT估算的MetS参与者肺动脉收缩压为42±12mmHg，而肥胖和非肥胖对照者分别为32±9mmHg和32±10mmHg（方差分析P<0.0001）。在调整年龄、性别、高血压、糖尿病、体重指数和甘油三酯后，MetS仍与PAAT缩短20ms相关（β=-20.4，标准误=6.5，与肥胖者相比P=0.002）。在考虑左心室结构和功能后以及排除阻塞性睡眠呼吸暂停参与者后，这种关联仍然存在。
MetS与右心室和肺动脉血流动力学异常相关，表现为PAAT缩短和亚临床右心室舒张功能障碍。MetS和临床前代谢性心脏病患者的估算肺动脉收缩压较高，提示肺动脉高压可能参与了代谢性心脏病的病理生理过程。
