Corrigan Minehan Heart Center, Cardiology Division, Massachusetts General Hospital, Boston, Massachusetts.
Corrigan Minehan Heart Center, Cardiology Division, Massachusetts General Hospital, Boston, Massachusetts; Cardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts.
J Card Fail. 2021 Jun;27(6):625-634. doi: 10.1016/j.cardfail.2021.02.011. Epub 2021 Feb 26.
Arterial stiffness is thought to contribute to the pathophysiology of heart failure with preserved ejection fraction (HFpEF). We sought to examine arterial stiffness in HFpEF and hypertension and investigate associations of arterial and left ventricular hemodynamic responses to exercise.
A total of 385 symptomatic individuals with an EF of ≥50% underwent upright cardiopulmonary exercise testing with invasive hemodynamic assessment of arterial stiffness and load (aortic augmentation pressure, augmentation index, systemic vascular resistance index, total arterial compliance index, effective arterial elastance index, and pulse pressure amplification) at rest and during incremental exercise. An abnormal hemodynamic response to exercise was defined as a steep increase in pulmonary capillary wedge pressure relative to cardiac output (∆PCWP/∆CO > 2 mm Hg/L/min). We compared rest and exercise measures between HFpEF and hypertension in multivariable analyses. Among 188 participants with HFpEF (mean age 61 ± 13 years, 56% women), resting arterial stiffness parameters were worse compared with 94 hypertensive participants (mean age 55 ± 15 years, 52% women); these differences were accentuated during exercise in HFpEF (all P ≤ .0001). Among all participants, exercise measures of arterial stiffness correlated with worse ∆PCWP/∆CO. Specifically, a 1 standard deviation higher exercise augmentation pressure was associated with 2.15-fold greater odds of abnormal LV hemodynamic response (95% confidence interval 1.52-3.05; P < .001). Further, exercise measures of systemic vascular resistance index, elastance index, and pulse pressure amplification correlated with a lower peak oxygen consumption.
Exercise accentuates the increased arterial stiffness found in HFpEF, which in turn correlates with left ventricular hemodynamic responses. Unfavorable ventricular-vascular interactions during exercise in HFpEF may contribute to exertional intolerance and inform future therapeutic interventions.
动脉僵硬被认为有助于射血分数保留的心力衰竭（HFpEF）的病理生理学。我们试图检查 HFpEF 和高血压中的动脉僵硬，并研究运动时动脉和左心室血液动力学反应的相关性。
共有 385 名 EF≥50%的有症状个体进行了直立心肺运动测试，对动脉僵硬和负荷（主动脉增强压、增强指数、全身血管阻力指数、总动脉顺应性指数、有效动脉弹性指数和脉搏压力放大）进行了侵入性血液动力学评估，在休息和递增运动期间。异常运动血液动力学反应定义为肺毛细血管楔压相对于心输出量的急剧增加（∆PCWP/∆CO>2mmHg/L/min）。我们在多变量分析中比较了 HFpEF 和高血压的休息和运动测量值。在 188 名 HFpEF 参与者（平均年龄 61±13 岁，56%为女性）中，与 94 名高血压参与者（平均年龄 55±15 岁，52%为女性）相比，静息动脉僵硬参数更差；在 HFpEF 中，这些差异在运动时更加明显（所有 P≤.0001）。在所有参与者中，动脉僵硬的运动测量值与更差的 ∆PCWP/∆CO 相关。具体而言，运动增强压力每增加 1 个标准差，异常左心室血液动力学反应的几率增加 2.15 倍（95%置信区间 1.52-3.05；P<.001）。此外，运动系统血管阻力指数、弹性指数和脉搏压力放大指数与峰值耗氧量降低相关。
运动加重了 HFpEF 中发现的动脉僵硬，这反过来又与左心室血液动力学反应相关。HFpEF 中运动时的不利心室血管相互作用可能导致运动不耐受，并为未来的治疗干预提供信息。
