Long-Term Effects of Right Ventricular Pressure and Volume Overload: A Comparative Analysis in an Ovine Model.

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.