Key result
Elevated mPAP independently predicts RV mechanical dyssynchrony in pre-capillary pulmonary hypertension.
Why the study?
Right ventricular mechanical dyssynchrony represents a maladaptive response to increased afterload in pulmonary hypertension, but its hemodynamic and biochemical determinants remain unclear.
What are the clinical, hemodynamic, and biochemical correlates of right ventricular mechanical dyssynchrony in patients with pre-capillary pulmonary hypertension?
Cross-Sectional (n=30)
What are the clinical, hemodynamic, and biochemical correlates of right ventricular mechanical dyssynchrony in patients with pre-capillary pulmonary hypertension?
Effect estimate: β = 0.509 (95% CI 0.001-0.006)
p-value: p=0.004
Right ventricular mechanical dyssynchrony is independently associated with elevated mean pulmonary artery pressure in pre-capillary pulmonary hypertension, suggesting it reflects hemodynamic afterload rather than structural remodeling.
Small observational data link mPAP to RV dyssynchrony; leaves open clinical utility and requires larger validation.
Right ventricular (RV) mechanical dyssynchrony represents a maladaptive response to increased afterload in pulmonary hypertension (PH). However, its hemodynamic and biochemical determinants remain unclear. This study aimed to identify the clinical, hemodynamic, and biochemical correlates of RV dyssynchrony in patients with pre‐capillary PH. Thirty patients with pre‐capillary PH (83% female; age 56 ± 19 years), all without intraventricular conduction delay (QRS < 120 ms), underwent right heart catheterization, cardiac magnetic resonance imaging, and two‐dimensional speckle‐tracking echocardiography. RV dyssynchrony was quantified using the coefficient of variation of time‐to‐peak systolic strain in four mid‐basal RV segments (RV‐CV4) adjusted for heart rate. Mean pulmonary artery pressure (mPAP), pulmonary vascular resistance (PVR), and RV‐CV4 averaged 34.1 ± 11.2 mmHg, 522.3 (interquartile range, 289.4–692.6) dyn·s·cm −5 , and 0.134 ± 0.083, respectively, in a cohort with predominantly mild‐to‐moderate RV systolic dysfunction. RV dyssynchrony correlated significantly with mPAP ( β = 0.509) PVR ( β = 0.507), and RV‐pulmonary artery coupling ( β = −0.406) (all p < 0.05). In multivariate analysis, mPAP remained the sole independent predictor of RV dyssynchrony ( β = 0.509, 95% CI 0.001–0.006, p = 0.004), accounting for 26% of its variance. Neither RV end‐diastolic volume nor RV ejection fraction were independently associated with dyssynchrony. RV mechanical dyssynchrony reflects hemodynamic afterload, particularly elevated mPAP, rather than structural remodeling. Notably, dyssynchrony was evident even in mild‐to‐moderate RV dysfunction, indicating an early manifestation of pressure‐induced impairment. RV‐CV4 may serve as a noninvasive marker of pulmonary vascular load and highlight the importance of afterload reduction in optimizing RV mechanical coordination. Accordingly, RV dyssynchrony assessment may provide a practical echocardiographic surrogate for invasive hemodynamic evaluation in clinical practice.
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Igata et al. (2026) conducted a cross-sectional in Pre-capillary pulmonary hypertension (n=30). Elevated mean pulmonary artery pressure (mPAP) was evaluated on Right ventricular (RV) mechanical dyssynchrony (β = 0.509, 95% CI 0.001-0.006, p=0.004). Elevated mean pulmonary artery pressure was the sole independent predictor of right ventricular mechanical dyssynchrony (β = 0.509; 95% CI 0.001-0.006; p=0.004) in pre-capillary pulmonary hypertension.
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