Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.
Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.
JACC Heart Fail. 2020 Aug;8(8):657-666. doi: 10.1016/j.jchf.2020.04.016. Epub 2020 Jul 8.
This study determined the impact of excess epicardial adipose tissue (EAT) in patients with the obese phenotype of heart failure with preserved ejection fraction (HFpEF).
Patients with HFpEF and an elevated body mass index differ from nonobese patients, but beyond generalized obesity, fat distribution may be more important. Increases in EAT are associated with excess visceral adiposity, inflammation, and cardiac fibrosis, and EAT has been speculated to play an important role in the pathophysiology of HFpEF, but no study has directly evaluated this question.
Patients with HFpEF and obesity (n = 169) underwent invasive hemodynamic exercise testing with expired gas analysis and echocardiography. Increased EAT was defined by echocardiography (EAT thickness ≥9 mm).
Compared with obese patients without increased EAT (HFpEF, n = 92), obese patients with HFpEF with increased EAT (HFpEF; n = 77) displayed a higher left ventricular eccentricity index, indicating increased pericardial restraint, but similar resting biventricular structure and function. In contrast, hemodynamics were more abnormal in patients with HFpEF, with higher right atrial, pulmonary artery, and pulmonary capillary wedge pressures at rest and during exercise compared with those of patients with HFpEF. Peak oxygen consumption (VO) was reduced in both groups but was 20% lower in patients with HFpEF (p < 0.01).
Among patients with the obese phenotype of HFpEF, the presence of increased EAT is associated with more profound hemodynamic derangements at rest and exercise, including greater elevation in cardiac filling pressures, more severe pulmonary hypertension, and greater pericardial restraint, culminating in poorer exercise capacity. Further study is needed to understand the biology and treatment of excessive EAT in patients with HFpEF.
本研究旨在探讨肥胖表型的射血分数保留心力衰竭（HFpEF）患者中，心外膜脂肪组织（EAT）过多的影响。
HFpEF 合并高体重指数的患者与非肥胖患者不同，但除了普遍肥胖外，脂肪分布可能更为重要。EAT 增加与内脏肥胖、炎症和心肌纤维化有关，并且 EAT 被推测在 HFpEF 的病理生理学中发挥重要作用，但尚无研究直接评估这一问题。
169 例 HFpEF 合并肥胖患者接受了有创血流动力学运动试验，包括呼气末气体分析和超声心动图检查。EAT 厚度≥9mm 定义为 EAT 增加。
与 EAT 不增加的肥胖 HFpEF 患者（HFpEF，n=92）相比，EAT 增加的肥胖 HFpEF 患者（HFpEF，n=77）的左心室偏心指数更高，表明心包约束增加，但静息时双心室结构和功能相似。相比之下，HFpEF 患者的血液动力学更为异常，静息和运动时右心房、肺动脉和肺毛细血管楔压均高于 HFpEF 患者。两组的峰值耗氧量（VO）均降低，但 HFpEF 患者降低了 20%（p<0.01）。
在肥胖表型的 HFpEF 患者中，EAT 增加与静息和运动时更严重的血液动力学紊乱相关，包括心腔充盈压升高更显著、肺动脉高压更严重以及心包约束更严重，最终导致运动能力更差。需要进一步研究以了解 HFpEF 患者过多 EAT 的生物学和治疗方法。
