Campbell Duncan J, Somaratne Jithendra B, Prior David L, Yii Michael, Kenny James F, Newcomb Andrew E, Kelly Darren J, Black Mary Jane
St. Vincent's Institute of Medical Research, Fitzroy, Australia ; Department of Medicine, The University of Melbourne, St. Vincent's Health, Fitzroy, Australia.
PLoS One. 2013 Nov 29;8(11):e81798. doi: 10.1371/journal.pone.0081798. eCollection 2013.
Obesity is associated with diastolic dysfunction, lower maximal myocardial blood flow, impaired myocardial metabolism and increased risk of heart failure. We examined the association between obesity, left ventricular filling pressure and myocardial structure.
We performed histological analysis of non-ischemic myocardium from 57 patients (46 men and 11 women) undergoing coronary artery bypass graft surgery who did not have previous cardiac surgery, myocardial infarction, heart failure, atrial fibrillation or loop diuretic therapy.
Non-obese (body mass index, BMI, ≤ 30 kg/m(2), n=33) and obese patients (BMI >30 kg/m(2), n=24) did not differ with respect to myocardial total, interstitial or perivascular fibrosis, arteriolar dimensions, or cardiomyocyte width. Obese patients had lower capillary length density (1145 ± 239, mean ± SD, vs. 1371 ± 333 mm/mm(3), P=0.007) and higher diffusion radius (16.9 ± 1.5 vs. 15.6 ± 2.0 μm, P=0.012), in comparison with non-obese patients. However, the diffusion radius/cardiomyocyte width ratio of obese patients (0.73 ± 0.11 μm/μm) was not significantly different from that of non-obese patients (0.71 ± 0.11 μm/μm), suggesting that differences in cardiomyocyte width explained in part the differences in capillary length density and diffusion radius between non-obese and obese patients. Increased BMI was associated with increased pulmonary capillary wedge pressure (PCWP, P<0.0001), and lower capillary length density was associated with both increased BMI (P=0.043) and increased PCWP (P=0.016).
Obesity and its accompanying increase in left ventricular filling pressure were associated with lower coronary microvascular density, which may contribute to the lower maximal myocardial blood flow, impaired myocardial metabolism, diastolic dysfunction and higher risk of heart failure in obese individuals.
肥胖与舒张功能障碍、最大心肌血流量降低、心肌代谢受损以及心力衰竭风险增加相关。我们研究了肥胖、左心室充盈压与心肌结构之间的关联。
我们对57例接受冠状动脉搭桥手术且既往无心脏手术、心肌梗死、心力衰竭、心房颤动或袢利尿剂治疗的患者(46例男性和11例女性)的非缺血心肌进行了组织学分析。
非肥胖患者(体重指数,BMI,≤30kg/m²,n = 33)和肥胖患者(BMI>30kg/m²,n = 24)在心肌总纤维化、间质纤维化或血管周围纤维化、小动脉尺寸或心肌细胞宽度方面无差异。与非肥胖患者相比,肥胖患者的毛细血管长度密度较低(1145±239,平均值±标准差,vs. 1371±333mm/mm³,P = 0.007)且扩散半径较高(16.9±1.5 vs. 15.6±2.0μm,P = 0.012)。然而,肥胖患者的扩散半径/心肌细胞宽度比值(0.73±0.11μm/μm)与非肥胖患者(0.71±0.11μm/μm)无显著差异,这表明心肌细胞宽度的差异部分解释了非肥胖和肥胖患者之间毛细血管长度密度和扩散半径的差异。BMI增加与肺毛细血管楔压(PCWP)升高相关(P<0.0001),而较低的毛细血管长度密度与BMI增加(P = 0.043)和PCWP升高(P = 0.016)均相关。
肥胖及其伴随的左心室充盈压升高与较低的冠状动脉微血管密度相关,这可能导致肥胖个体的最大心肌血流量降低、心肌代谢受损、舒张功能障碍以及心力衰竭风险增加。