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Published on: November 26, 2018
Right Ventricular Mechanical Dyssynchrony Reflects Hemodynamic Load in Pre-Capillary Pulmonary Hypertension
Sachiyo Igata1,2, Nobuhiro Tahara1, Atsuko Tahara1
1Department of Medicine, Division of Cardiovascular Medicine Kurume University School of Medicine Kurume Fukuoka Japan.
Pulmonary Circulation
|June 25, 2026
Summary
Right ventricular mechanical dyssynchrony in pulmonary hypertension is linked to elevated pulmonary artery pressure. This early sign of impairment highlights the importance of afterload reduction for RV function.
Area of Science:
- Cardiology
- Pulmonary Hypertension Research
- Cardiac Mechanics
Background:
- Right ventricular (RV) mechanical dyssynchrony is a response to increased afterload in pulmonary hypertension (PH).
- The hemodynamic and biochemical factors driving RV dyssynchrony are not fully understood.
- Understanding these determinants is crucial for managing PH and RV dysfunction.
Purpose of the Study:
- To identify clinical, hemodynamic, and biochemical correlates of RV dyssynchrony in patients with pre-capillary PH.
- To investigate the relationship between RV dyssynchrony and hemodynamic parameters like mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR).
- To determine if RV dyssynchrony is an early indicator of RV impairment in PH.
Main Methods:
- Thirty patients with pre-capillary PH (QRS < 120ms) underwent right heart catheterization, cardiac MRI, and echocardiography.
- RV dyssynchrony was quantified using RV-CV4, the coefficient of variation of time-to-peak systolic strain in four mid-basal RV segments, adjusted for heart rate.
- Statistical analyses, including multivariate analysis, were performed to identify independent predictors of RV dyssynchrony.
Main Results:
- RV dyssynchrony (RV-CV4) correlated significantly with mPAP and PVR.
- In multivariate analysis, mPAP was the sole independent predictor of RV dyssynchrony, explaining 26% of its variance.
- RV dyssynchrony was present even with mild-to-moderate RV systolic dysfunction, and was not associated with RV end-diastolic volume or ejection fraction.
Conclusions:
- RV mechanical dyssynchrony primarily reflects hemodynamic afterload (mPAP) rather than structural RV remodeling.
- RV dyssynchrony is an early manifestation of pressure-induced RV impairment in PH.
- RV-CV4 may serve as a noninvasive marker of pulmonary vascular load, supporting the importance of afterload reduction and potentially replacing invasive hemodynamic evaluation.
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