Key result
Distinct electrocardiographic and echocardiographic patterns, along with progressive increases in plasma myosin light chain 3 and cardiac troponin I, were identified as useful non-invasive tools for monitoring pulmonary arterial hypertension progression.
Why the study?
With a main focus on invasive tools, echocardiography, electrocardiography, and biomarkers have been underutilized to non-invasively assess myocardial and pulmonary vascular changes during the course of pulmonary arterial hypertension.
Distinct non-invasive echocardiographic, electrocardiographic, and biomarker patterns correlate with invasive hemodynamics during PAH progression in a rat model, suggesting utility for early diagnosis and monitoring.
Suggests non-invasive biomarker and imaging panels may track pulmonary arterial hypertension progression; leaves open.
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.
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Zaky et al. (2021) studied Pulmonary arterial hypertension. SU5416 and hypoxia vs. Normoxia control was evaluated on Right ventricular systolic pressure (RVSP) and echocardiographic/biochemical markers. Distinct electrocardiographic and echocardiographic patterns, along with progressive increases in plasma myosin light chain 3 and cardiac troponin I, were identified as useful non-invasive tools for monitoring pulmonary arterial hypertension progression.
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