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Residual Pulmonary Hypertension after PEA – An ill-defined problem
Session:
Sessão de Posters 02 - Embolia Pulmonar
Speaker:
Catarina Sena Silva
Congress:
CPC 2024
Topic:
F. Valvular, Myocardial, Pericardial, Pulmonary, Congenital Heart Disease
Theme:
21. Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure
Subtheme:
21.4 Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure - Treatment
Session Type:
Cartazes
FP Number:
---
Authors:
Catarina Sena Silva; Cláudia Jorge; Ana Beatriz Garcia; Catarina Simões de Oliveira; Ana Margarida Martins; Miguel Azaredo Raposo; Daniel Inácio Cazeiro; Marta Vilela; Tatiana Guimarães; Nuno Lousada; Fausto J. Pinto; Rui Plácido
Abstract
<p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Introduction</strong></span></span></span></p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Chronic thromboembolic pulmonary hypertension (CTEPH) is a complex disease, with a pathophysiology that goes beyond thrombus induced mechanical obstruction. Pulmonary endarterectomy (PEA) is the gold-standard treatment for all suitable patients (pts), however, many suffer from residual PH. </span></span></span></p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Balloon pulmonary angioplasty (BPA) and vasodilator therapy are therapeutic options for these pts. </span></span></span></p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Residual pulmonary hypertension (PH) after PEA is a complex and ill-defined reality. While PEA is the gold-standard treatment for CTEPH, many pts still suffers from incomplete clearance of the pulmonary tree and/or persistent microvasculopathy after surgery.</span></span></span></p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">This study aimed to retrospectively analyze a population who underwent PEA to determine the presence of residual PH and explore potential predictors of this condition.</span></span></span></p> <p> </p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Methods</strong></span></span></span></p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">This retrospective study collected clinical and laboratory parameters at baseline and follow-up (FUP), including the COMPERA 4-strata risk assessment. Hemodynamic data from right heart catheterization, intra-op surgical disease classification, and echocardiographic assessment were compared. Clinically significant residual PH was defined as a mean pulmonary artery pressure (mPAP) > 37 at 6-month post-PEA. Mean absolute differences before and after treatment were calculated, and logistical regression was conducted to search for predictors of residual PH.</span></span></span></p> <p> </p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Results</strong></span></span></span></p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">The study included 30 pts with a mean age of 58±14.9 years. The majority (57%) were female, and the mean follow-up (FUP) duration was 74.4±24 months. Eleven pts (37%) had residual PH at 6-month post-PEA and were enrolled in BPA program after optimized medical therapy including vasodilators. Univariate analysis identified pre-PEA tricuspid S', pre-PEA pulmonary vascular resistance, and mPAP evaluated in the OR post PEA as factors significantly related to residual PH at 6 months. However, multivariate analysis using logistic regression failed to predict residual PH.</span></span></span></p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">At FUP, 85.7% of pts achieved a low to intermediate-low risk on the 4 strata assessment, with 70% experiencing an improvement in World Health Organization (WHO) functional class. Among these, 44% reduced their WHO class by more than 1 level. The mean decrease in NTproBNP, a marker of cardiac strain, was 1688±1156 pg/ml. Although not statistically significant, there was a trend towards smaller improvement in all categories for pts with residual PH. During the FUP period, 5 pts died, all of whom had heart failure hospitalizations.</span></span></span></p> <p> </p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"> </span></span></span></p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Conclusions</strong></span></span></span></p> <p><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Residual PH affects a significant number of pts who undergo PEA for CTEPH. The pathophysiology of residual PH after PEA is complex, and there is a lack of appropriately powered studies to identify risk factors. However, multimodal management in referral centers may lead to favorable outcomes in terms of functional capacity improvement and overall risk reduction.</span></span></span></p>
Slides
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