Key result
Chronic RV pressure overload reduces TAPSE/RVSP ratio ~43% versus volume overload in an ovine model.
Why the study?
Pressure overload and volume overload are important mechanisms underlying right ventricular failure, but long-term comparative data on their distinct pathophysiological consequences remain limited.
Does chronic pressure overload versus volume overload induce distinct pathophysiological consequences and remodeling patterns in a juvenile ovine model?
RCT (n=15)
Randomized
No
Does chronic pressure overload versus volume overload induce distinct pathophysiological consequences and remodeling patterns in a juvenile ovine model?
Absolute Event Rate: 0.17% vs 0.3%
p-value: p=0.0022
Chronic pressure and volume overload induce distinct phenotypes of right ventricular dysfunction and remodeling, with pressure overload causing more severe RV diastolic dysfunction and ventriculo-arterial uncoupling.
Supports distinct RV remodeling mechanisms in ovine models; leaves open translation to human pressure versus volume overload phenotypes.
Background/Objectives: Pressure overload (PO) and volume overload (VO) represent important mechanisms underlying right ventricular (RV) failure; however, long-term comparative data regarding their distinct pathophysiological consequences remain limited. This study aimed to compare the long-term effects of PO versus VO in a large animal model. Methods: Juvenile sheep were randomly assigned to either a PO group (n = 7) or a VO group (n = 8). PO was induced by pulmonary artery banding, whereas VO was induced by pulmonary leaflet perforation (n = 4) or transannular patch (TAP) reconstruction (n = 4). Both VO procedures resulted in moderate-to-severe pulmonary regurgitation with comparable acute hemodynamic profiles and were therefore analyzed as a single VO group for the long-term assessment. Six animals from each group completed the follow-up period. Animals were evaluated preoperatively and at one-year follow-up using invasive hemodynamic monitoring, blood gas analysis, and echocardiography, followed by postmortem histological analysis of the myocardium. Results: Both models resulted in significant reductions in stroke volume index, cardiac index, RV stroke work index, ScvO2 and tricuspid annular plane systolic excursion (TAPSE). Similarly, the TAPSE/RV systolic pressure (RVSP) ratio decreased in both groups but was significantly lower in the PO group than in the VO group (p = 0.0022). Moreover, PO showed more pronounced RV diastolic dysfunction, characterized by a significant increase in right atrial pressure from baseline (p = 0.0313) and higher RV diastolic pressure compared to VO (p = 0.0065). In contrast, VO showed a greater impact on left ventricular (LV) geometry and diastolic filling, evidenced by reduced transmitral filling (p = 0.0313) and a lower indexed LV internal diameter compared to PO (p = 0.0411). Histological analysis revealed myocardial hypertrophy and fibrosis in both groups, as well as clusters of multinucleated cardiomyocyte-like cells showing preferential ventricular distribution according to overload physiology. Conclusions: Chronic PO and VO induced distinct phenotypes of RV dysfunction with differential ventricular adaptation and remodelling patterns.
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Hussein et al. (2026) conducted an RCT in Right ventricular pressure and volume overload (n=15). Pressure overload (pulmonary artery banding) vs. Volume overload (pulmonary leaflet perforation or transannular patch) was evaluated on TAPSE/RVSP ratio at one-year follow-up (p=0.0022). Chronic right ventricular pressure overload resulted in a significantly lower TAPSE/RVSP ratio compared to volume overload (0.17 vs 0.30, p=0.0022) in an ovine model.
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