Evidence Supporting the Existence of a Distinct Obese Phenotype of Heart Failure With Preserved Ejection Fraction.
Evidence Supporting the Existence of a Distinct Obese Phenotype of Heart Failure With Preserved Ejection Fraction.
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DOI：
10.1161/circulationaha.116.026807
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发表时间：
2017-07-04
期刊：
影响因子：
37.8
通讯作者：
Borlaug BA
中科院分区：
文献类型：
--
作者：
Obokata M;Reddy YNV;Pislaru SV;Melenovsky V;Borlaug BA
心力衰竭伴射血分数保留（HFpEF）是一种异质性综合征。将患者表型划分为病理生理同质组可能有助于更好地靶向治疗。肥胖在HFpEF中很常见，并且有许多心血管影响，这表明它可能是表型的可行候选者。我们比较了肥胖HFpEF、非肥胖HFpEF和对照组的心血管结构、功能和储备容量。肥胖HFpEF （BMI≥35kg/m2, n=99）、非肥胖HFpEF （BMI<30kg/m2, n=96）和无HF的非肥胖对照（n=71）进行了详细的临床评估、超声心动图和有创血流动力学运动试验。与非肥胖型HFpEF和对照组相比，肥胖型HFpEF患者血浆容量增加（3907 [3563,4333]vs. 2772[2555,3133]和2680 [2380,3006]ml, p<0.0001），左心室同心重构更多，右室扩张更大(基底34±7 vs. 31±6和30±6 mm， p=0.0005；长度66±7比61±7和61±7 mm， p<0.0001)，右室功能障碍加重，心外膜脂肪厚度增加（10±2比7±2和6±2 mm， p<0.0001），总心外膜心脏容积增大（945[831,1105]比797[643,979]和632 [517,768]ml, p<0.0001），尽管NT-proBNP水平较低。肥胖HFpEF组肺毛细血管楔压与体质量和血浆容量相关（r=0.22和0.27，p均<0.05），非肥胖HFpEF组无相关（p≥0.3）。肥胖HFpEF患者心脏容量的增加与心包约束和心室依赖性增强相关，表现为左右心充盈压比增加（0.64±0.17 vs 0.56±0.19和0.53±0.20,p=0.0004），肺静脉压相对于左心室跨壁压更高，左心室偏心率指数更高（1.10±0.19 vs 0.99±0.06和0.97±0.12,p<0.0001）。相关性随着肺动脉压力负荷的增加而增强（交互作用p<0.05）。与非肥胖HFpEF和对照组相比，肥胖HFpEF受试者表现出更差的运动能力（峰值耗氧量7.7±2.3 vs. 10.0±3.4和12.9±4.0 ml/min*kg, p<0.0001），运动时双心室充盈压升高，肺动脉血管扩张剂储备降低。肥胖相关的HFpEF是一种真正的心衰形式，也是一种可能需要特定治疗的临床相关表型。
Heart failure (HF) with preserved ejection fraction (HFpEF) is a heterogeneous syndrome. Phenotyping patients into pathophysiologically homogenous groups may enable better targeting of treatment. Obesity is common in HFpEF and has many cardiovascular effects, suggesting it may be a viable candidate for phenotyping. We compared cardiovascular structure, function, and reserve capacity in subjects with obese HFpEF, non-obese HFpEF, and controls. Subjects with obese HFpEF (BMI≥35kg/m2, n=99), non-obese HFpEF (BMI<30kg/m2, n=96), and non-obese controls free of HF (n=71) underwent detailed clinical assessment, echocardiography and invasive hemodynamic exercise testing. Compared to both non-obese HFpEF and controls, subjects with obese HFpEF displayed increased plasma volume (3907 [3563,4333] vs. 2772 [2555,3133] and 2680 [2380,3006] ml, p<0.0001), more concentric left ventricular remodeling, greater right ventricular dilatation (base 34±7 vs. 31±6 and 30±6 mm, p=0.0005; length 66±7 vs. 61±7 and 61±7 mm, p<0.0001), more right ventricular dysfunction, increased epicardial fat thickness (10±2 vs. 7±2 and 6±2 mm, p<0.0001), and greater total epicardial heart volume (945 [831,1105] vs. 797 [643,979] and 632 [517,768] ml, p<0.0001), despite lower NT-proBNP levels. Pulmonary capillary wedge pressure was correlated with body mass and plasma volume in obese HFpEF (r=0.22 and 0.27, both p<0.05), but not in non-obese HFpEF (p≥0.3). The increase in heart volumes in obese HFpEF was associated with greater pericardial restraint and heightened ventricular interdependence, reflected by increased ratio of right to left heart filling pressures (0.64±0.17 vs. 0.56±0.19 and 0.53±0.20, p=0.0004), higher pulmonary venous pressure relative to left ventricular transmural pressure, and greater left ventricular eccentricity index (1.10±0.19 vs 0.99±0.06 and 0.97±0.12, p<0.0001). Interdependence was enhanced as pulmonary artery pressure load increased (interaction p<0.05). As compared to non-obese HFpEF and controls, obese HFpEF subjects displayed worse exercise capacity (peak oxygen consumption 7.7±2.3 vs. 10.0±3.4 and12.9±4.0 ml/min*kg, p<0.0001), higher biventricular filling pressures with exercise and depressed pulmonary artery vasodilator reserve. Obesity-related HFpEF is a genuine form of cardiac failure and a clinically relevant phenotype that may require specific treatments.