Multimodality Deep Phenotyping Methods to Assess Mechanisms of Poor Right Ventricular-Pulmonary Artery Coupling.
Multimodality Deep Phenotyping Methods to Assess Mechanisms of Poor Right Ventricular-Pulmonary Artery Coupling.
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多模式的深度表型方法评估右心 - 肺动脉偶联较差的机制。
DOI：
10.1093/function/zqac022
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发表时间：
2022
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多模式诊断运动干预对肺动脉高压（PH）的深度表型分析可导致早期集中治疗干预。在此，我们报告了在运动过程中同时评估肺阻抗、双心室心肌应变差和右心室：肺动脉（RV：PA）解偶联的方法，我们在疑似PH的受试者中进行了试验。作为概念验证，我们显示了四名不同诊断的受试者[肺动脉高压（PAH）;慢性血栓栓塞性疾病（CTEPH）;射血分数保留的心力衰竭所致PH]。（PH-HFpEF）和非心源性呼吸困难（NCD）]对运动的反应模式不同。RV：PA偶联评估与运动的顺序为PAH > CTEPH > PH-HFpEF > NCD。运动输入阻抗（Z 0）在毛细血管前PH（PAH，CTEPH）中最高，其次是PH-HFpEF和NCD。除PH-HFpEF受试者外，特征阻抗（ZC）倾向于随运动而下降（中等工作负荷时初始Zc增加，随后在较高工作负荷时降低，心输出量增加）。PAH、CTEPH和NCD受试者的室间隔差异心肌应变正常，PH-HFpEF受试者的室间隔差异心肌应变较低。这些指标的组合允许对RV：PA解偶联机制的新见解。例如，虽然PH-HFpEF受试者在静息时的血流动力学与NCD受试者相当，但运动偶联急剧下降，这可归因于（通过室间隔心肌应变降低）左心室（LV）的支持较差。我们的结论是，这种深度表型分析方法可以区分后负荷敏感与LV依赖性机制的RV：PA解偶联在PH，这可能会导致新的治疗相关的见解。中心人物：搏动和稳态负荷（肺阻抗）和心室相互依赖性（局部心肌应变）对右心室的影响：从静息到运动的肺动脉耦合
Deep phenotyping of pulmonary hypertension (PH) with multimodal diagnostic exercise interventions can lead to early focused therapeutic interventions. Herein, we report methods to simultaneously assess pulmonary impedance, differential biventricular myocardial strain, and right ventricular:pulmonary arterial (RV:PA) uncoupling during exercise, which we pilot in subjects with suspected PH. As proof-of-concept, we show that four subjects with different diagnoses [pulmonary arterial hypertension (PAH); chronic thromboembolic disease (CTEPH); PH due to heart failure with preserved ejection fraction (PH-HFpEF); and noncardiac dyspnea (NCD)] have distinct patterns of response to exercise. RV:PA coupling assessment with exercise was highest-to-lowest in this order: PAH > CTEPH > PH-HFpEF > NCD. Input impedance (Z0) with exercise was highest in precapillary PH (PAH, CTEPH), followed by PH-HFpEF and NCD. Characteristic impedance (ZC) tended to decline with exercise, except for the PH-HFpEF subject (initial Zc increase at moderate workload with subsequent decrease at higher workload with augmentation in cardiac output). Differential myocardial strain was normal in PAH, CTEPH, and NCD subjects and lower in the PH-HFpEF subject in the interventricular septum. The combination of these metrics allowed novel insights into mechanisms of RV:PA uncoupling. For example, while the PH-HFpEF subject had hemodynamics comparable to the NCD subject at rest, with exercise coupling dropped precipitously, which can be attributed (by decreased myocardial strain of interventricular septum) to poor support from the left ventricle (LV). We conclude that this deep phenotyping approach may distinguish afterload sensitive vs. LV-dependent mechanisms of RV:PA uncoupling in PH, which may lead to novel therapeutically relevant insights. Central Figure: Impact of pulsatile and steady load (pulmonary impedance) and ventricular interdependence (regional myocardial strain) on right ventricular: pulmonary arterial coupling from rest-to-exercise