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Persistent Right Ventricular Dysfunction after Pulmonary Endarterectomy: Insights from Strain Imaging and Hemodynamic Correlation
Session:
Sessão de Comunicações Orais 07 – Para além do evento agudo: preditores e desfechos após lesão miocárdica
Speaker:
Liliana Brochado
Congress:
CPC 2026
Topic:
P. Other
Theme:
21. Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure
Subtheme:
21.4 Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure - Treatment
Session Type:
Comunicações Orais
FP Number:
---
Authors:
Liliana Brochado; João Mirinha Luz; Filipa Ferreira; Paula Fazendas; Sofia Alegria; Ana Cláudia Vieira; Bárbara Ferreira; Debora Repolho; Hélder Pereira
Abstract
<p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Background: </strong>Chronic thromboembolic pulmonary hypertension (CTEPH, Group 4 PH) is potentially curable by pulmonary endarterectomy (PEA). However, a substantial proportion of patients show persistent pulmonary hypertension (PH) and right ventricular (RV) dysfunction despite successful surgery. Echocardiographic strain analysis of the RV and right atrium (RA) enables the detection of subtle functional abnormalities and may provide additional insight beyond invasive hemodynamic assessment.</span></span></span></p> <p style="text-align:justify"> </p> <p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Methods:</strong> We performed a retrospective, single-centre study including all consecutive patients with CTEPH who underwent PEA. Postoperative echocardiograms were reviewed for RV and RA strain analysis. Patients with suboptimal image quality were excluded. Strain parameters were correlated with right heart catheterization (RHC) performed 6–12 months after surgery.</span></span></span></p> <p style="text-align:justify"> </p> <p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Results:</strong> Of 39 patients who underwent PEA, 20 met inclusion criteria (mean age 58.7 ± 15.4 years, 60% female). Residual PH was confirmed in 37% by RHC. Compared with patients without residual PH, those with residual PH showed significantly lower RV strain values: RV free-wall strain (StFW) 16.2 ± 6.6 vs 21.9 ± 5.2 %, p = 0.047; global RV strain (StRV) 14.8 ± 6.5 vs 19.5 ± 2.9 %, p=0.037; and basal segment strain 16.3 ± 7.7 vs 26.2 ± 8.5 %, p=0.025. No significant differences were observed in mid- or apical-segment strain or in RA strain values (RA reservoir 29.1 ± 9.8 vs 32.4 ± 8.6 %, p = ns). Overall, RV strain failed to recover in 55% of patients and RA strain in 15%. Non-recovery was associated with higher pulmonary pressures at follow-up RHC.</span></span></span></p> <p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Significant correlations were found between StFW and mean pulmonary artery pressure (r=0.52, p=0.02), right-ventricular diastolic pressure (r=0.46, p=0.04), pulmonary capillary wedge pressure (r=0.54, p=0.01), and cardiac output (r=0.52, p=0.02). Global RV strain correlated with pulmonary vascular resistance (r=0.62, p=0.003), systolic pulmonary artery pressure (r=0.61, p=0.004), mean pulmonary artery pressure (r = 0.78, p = 0.001), wedge pressure (r=0.66, p=0.02), transpulmonary gradient (r = 0.61, p=0.004), right-ventricular pressure (r=0.67, p=0.002), and right-ventricular tension (r=0.72, p=0.001).</span></span></span></p> <p style="text-align:justify"> </p> <p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Conclusion: </strong>After PEA, RV strain, particularly free-wall and basal-segment strain, remains impaired in more than half of patients, despite normalization of invasive hemodynamic indices. Strain parameters strongly correlate with catheterization data but frequently fail to normalize, suggesting incomplete or delayed myocardial recovery relative to hemodynamic improvement. Chronic pressure overload may result in irreversible structural remodeling or fibrosis. RV strain therefore emerges as a sensitive, non-invasive marker of persistent RV dysfunction and residual pulmonary hypertension after surgical treatment of CTEPH.</span></span></span></p>
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