Left Atrial Function Dynamics During Exercise in Heart Failure Pathophysiological Implications on the Right Heart and Exercise Ventilation Inefficiency

Left Atrial Function Dynamics During Exercise in Heart Failure Pathophysiological Implications on the Right Heart and Exercise Ventilation Inefficiency
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DOI:
10.1016/j.jcmg.2016.09.021
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发表时间:
2017-10-01
影响因子:
14
通讯作者:
Guazzi, Marco
Guazzi, Marco
中科院分区:
医学1区
文献类型:
--
作者:
Sugimoto, Tadafumi;Bandera, Francesco;Guazzi, Marco

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本研究的假设是,运动过程中左心房(LA)的动态损伤可能会触发右心室(RV)-肺循环(PC)解偶联和通气influenced.Background LA功能在射血分数降低的心力衰竭(HFrEF)和射血分数保留的心力衰竭(HFpEF)的血流动力学中起着关键作用。方法前瞻性纳入49例HFrEF患者、20例HFpEF患者和32例LA大小和储血功能正常的健康受试者(LA容积指数< 34 ml/m2,LA舒张期左房应变峰值> 23%)。他们进行了心肺运动试验和当代超声多普勒评估的LA应变和LA应变率和RV PC耦合(肺动脉收缩压/三尖瓣环收缩期峰值偏移比),在休息时,在40%的预测峰值耗氧量,并在recovery.Results在对照组,LA应变增加运动和恢复。HFpEF患者在运动和恢复过程中表现出一些LA应变增加,而HFrEF患者则无变化。对照组受试者的基线LA应变率更高;仅在该组中观察到恢复期间的显著增强。在HFpEF和HFrEF队列中,静息、运动和恢复时RV-PC解偶联和LA-应变与肺动脉收缩压/三尖瓣环收缩期峰值偏移以及通气量与二氧化碳斜率显著相关,在各组中呈连续性(对照组、HFpEF组、HFrEF组分别为r =-0.63和r =-0.59,r = -0.65和r =-0.50,r = -0.70和r = -0.53; p < 0.05)。结论在心力衰竭中,受损的LA-应变反应是RV-PC解偶联和运动通气无效的关键血液动力学触发因素,HFpEF和HFrEF表型之间有一些重叠。LA动力学的可逆性似乎是特定治疗干预的未达到目标。(C)2017年美国心脏病学院基金会。
OBJECTIVES The hypothesis of this study was that left atrial (LA) dynamic impairment during exercise may trigger right ventricular (RV)-to-pulmonary circulation (PC) uncoupling and ventilation inefficiency.BACKGROUND LA function plays a key role in the hemodynamics of heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). Extensive investigation of LA dynamics, however, has been performed exclusively at rest.METHODS A total of 49 patients with HFrEF, 20 patients with HFpEF, and 32 healthy subjects with normal LA size and reservoir function (LA volume index < 34 ml/m(2) and peak left atrial strain [LA-strain] during LA relaxation > 23%) were prospectively enrolled. They underwent cardiopulmonary exercise testing and contemporary echoDoppler assessment of LA-strain and LA-strain rate and of RV-to-PC coupling (pulmonary arterial systolic pressure/tricuspid annular peak systolic excursion ratio), measured at rest, at 40% of predicted peak oxygen consumption, and during recovery.RESULTS In control subjects, LA-strain increased during exercise and recovery. Patients with HFpEF exhibited some LA-strain increase during exercise and recovery, whereas no changes occurred in those with HFrEF. The baseline LA-strain rate was greater in control subjects; a significant enhancement during recovery was observed only in this group. In both the HFpEF and HFrEF cohorts, RV-to-PC uncoupling and LA-strain at rest, exercise, and recovery significantly correlated with pulmonary arterial systolic pressure/tricuspid annular peak systolic excursion, as well as ventilation versus carbon dioxide slope, in a continuous fashion across groups (r = -0.63 and r = -0.59, r = -0.65 and r = -0.50, and r = -0.70 and r = -0.53 for control subjects, HFpEF, and HFrEF, respectively; p < 0.05).CONCLUSIONS In heart failure, an impaired LA-strain response is a key hemodynamic trigger for RV-to-PC uncoupling and exercise ventilation inefficiency with some overlap between HFpEF and HFrEF phenotypes. Reversibility of LA dynamics seems to be an unmet target of specific therapeutic interventions. (C) 2017 by the American College of Cardiology Foundation.