Background:
Mechanical thrombectomy has emerged as an effective reperfusion strategy for intermediate-high-risk pulmonary embolism (PE). While improvements in right ventricular (RV) function and pulmonary haemodynamics have been demonstrated, the mechanisms underlying haemodynamic stabilization remain incompletely understood. We investigated whether mechanical thrombectomy improves left ventricular (LV) filling by reversing pathological ventricular interdependence.
Methods:
We retrospectively analysed 26 consecutive patients with CT-confirmed intermediate-high-risk PE treated with FlowTriever mechanical thrombectomy. Pre- and post-procedural assessments included invasive haemodynamics obtained by right heart catheterization, three-dimensional CT-based biventricular volumetry, quantification of interventricular septal curvature (SC) as a marker of ventricular interdependence, and echocardiographic indices of LV diastolic filling. Correlation and mediation analyses were performed to evaluate mechanistic relationships between RV afterload, septal geometry, and LV filling.
Results:
Mechanical thrombectomy significantly reduced systolic pulmonary artery pressure (64.4 ± 19.9 vs. 46.2 ± 17.2 mmHg, p<0.0001) and pulmonary capillary wedge pressure (21.7 ± 6.9 vs. 17.7 ± 6.4 mmHg, p<0.001). RV volumes and RV/LV ratios decreased, whereas LV volumes increased significantly. SC improved markedly after thrombectomy (p<0.0001) and demonstrated a strong inverse correlation with systolic pulmonary artery pressure (r = −0.84, p<0.001). Echocardiography revealed significant improvement in LV filling dynamics, including a reduction in E/e′ (p = 0.0002). E/e′ correlated positively with pulmonary artery pressure (r = 0.57, p = 0.009) and inversely with SC (r = −0.51, p = 0.02). Mediation analysis demonstrated that approximately 64% of the relationship between pulmonary artery pressure and LV filling pressure was mediated through changes in septal geometry.
Conclusions:
Mechanical thrombectomy in intermediate-high-risk PE improves LV filling by relieving RV pressure overload and reversing pathological ventricular interdependence. Interventricular septal curvature emerges as a novel imaging marker linking RV afterload to impaired LV filling and may represent a promising parameter for haemodynamic phenotyping and treatment monitoring in acute PE. These findings provide a mechanistic explanation for the haemodynamic benefits of catheter-based reperfusion.
