Echocardiographic, Biochemical, and Electrocardiographic Correlates Associated With Progressive Pulmonary Arterial Hypertension.
Echocardiographic, Biochemical, and Electrocardiographic Correlates Associated With Progressive Pulmonary Arterial Hypertension.
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DOI：
10.3389/fcvm.2021.705666
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发表时间：
2021
影响因子：
3.6
通讯作者：
Ahmad A
中科院分区：
文献类型：
--
作者：
Zaky A;Zafar I;Masjoan-Juncos JX;Husain M;Mariappan N;Morgan CJ;Hamid T;Frölich MA;Ahmad S;Ahmad A
背景：肺动脉高压(PAH)是一种进行性增生性血管病变，与机械和电学改变有关，最终导致血管阻力增加、右室衰竭和死亡。超声心动图、心电图学和生物标志物在无创评估PAH过程中心肌和肺血管结构和功能的变化方面一直未得到充分利用。方法：采用SU5416低氧大鼠模型建立PAH模型。在发病(0周)、进展(3周)和建立(5周)时用经胸二维(2D)超声心动图/多普勒(ECHO/多普勒)测量双室功能。同样，在0、3和5周时进行心电图检查。分别于0、3、5周进行有创性血流动力学检测和血浆心肌损伤标志物的检测。结果：PAH动物在0周、3周和5周时右室收缩压(RVSP)和等容压升降速度明显升高。EKG显示QT间期随PAH进展而稳定增加，而P波高度和RS宽度仅在PAH进展初期增加。超声心动图也确定了PAH进展和严重程度的标志物。观察到三种超声心动图类型：稳定期(0~5周)，回声参数随严重程度递增变化[下腔静脉(IVC)呼气直径和肺动脉加速时间(PAAT)]；早期(0~3周)，参数早期改变[右室面积变化分数(RV-FAC)、二尖瓣血流、左心室(LV)输出量、估测平均PA压、RV性能指数和LV收缩偏心指数]；晚期(3~5周)，PAH晚期仅有晚期升高(LV舒张期偏心指数)。RVSP与PAAT、PAAT/PA射血时间、下腔静脉内径、RV-FAC、三尖瓣收缩期离散度、LV收缩偏心率和心输出量、二尖瓣血流呈正相关。血浆肌球蛋白轻链(MYL-3)和心肌肌钙蛋白I(CTnI)在三个时间点均呈递增趋势。心肌肌钙蛋白T(CTnT)和脂肪酸结合蛋白-3(FABP-3)仅在5周时间点显著升高。结论：不同的心电图和超声心动图模式以及血浆生物标志物被认为是监测PAH进展的有用的无创性工具。
Background: Pulmonary arterial hypertension (PAH) is a progressive proliferative vasculopathy associated with mechanical and electrical changes, culminating in increased vascular resistance, right ventricular (RV) failure, and death. With a main focus on invasive tools, there has been an underutilization of echocardiography, electrocardiography, and biomarkers to non-invasively assess the changes in myocardial and pulmonary vascular structure and function during the course of PAH. Methods: A SU5416-hypoxia rat model was used for inducing PAH. Biventricular functions were measured using transthoracic two-dimensional (2D) echocardiography/Doppler (echo/Doppler) at disease onset (0 week), during progression (3 weeks), and establishment (5 weeks). Similarly, electrocardiography was performed at 0, 3, and 5 weeks. Invasive hemodynamic measurements and markers of cardiac injury in plasma were assessed at 0, 3, and 5 weeks. Results: Increased RV systolic pressure (RVSP) and rate of isovolumic pressure rise and decline were observed at 0, 3, and 5 weeks in PAH animals. EKG showed a steady increase in QT-interval with progression of PAH, whereas P-wave height and RS width were increased only during the initial stages of PAH progression. Echocardiographic markers of PAH progression and severity were also identified. Three echocardiographic patterns were observed: a steady pattern (0–5 weeks) in which echo parameter changed progressively with severity [inferior vena cava (IVC) expiratory diameter and pulmonary artery acceleration time (PAAT)], an early pattern (0–3 weeks) where there is an early change in parameters [RV fractional area change (RV-FAC), transmitral flow, left ventricle (LV) output, estimated mean PA pressure, RV performance index, and LV systolic eccentricity index], and a late pattern (3–5 weeks) in which there is only a late rise at advanced stages of PAH (LV diastolic eccentricity index). RVSP correlated with PAAT, PAAT/PA ejection times, IVC diameters, RV-FAC, tricuspid systolic excursion, LV systolic eccentricity and output, and transmitral flow. Plasma myosin light chain (Myl-3) and cardiac troponin I (cTnI) increased progressively across the three time points. Cardiac troponin T (cTnT) and fatty acid-binding protein-3 (FABP-3) were significantly elevated only at the 5-week time point. Conclusion: Distinct electrocardiographic and echocardiographic patterns along with plasma biomarkers were identified as useful non-invasive tools for monitoring PAH progression.