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Hybrid therapeutic approach with specific drug therapy and balloon pulmonary angioplasty in patients with chronic thromboembolic pulmonary hypertension: Effects on pulmonary arterial compliance.
Session:
CO 17 - Interventional Cardiology-TEP
Speaker:
Rita Calé
Congress:
CPC 2021
Topic:
H. Interventional Cardiology and Cardiovascular Surgery
Theme:
25. Interventional Cardiology
Subtheme:
25.4 Interventional Cardiology - Other
Session Type:
Comunicações Orais
FP Number:
---
Authors:
Rita Calé; Ana Rita F. Pereira; Filipa Ferreira; Sofia Alegria; Débora Repolho; Pedro Santos; Sílvia Vitorino; Mariana Martinho; Daniel Sebaiti; Maria José Loureiro; Helder Pereira
Abstract
<p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Introduction:</strong> Pulmonary arterial compliance (C<sub>PA</sub>) is a measure of arterial distensibility <span style="color:black">and is directly related with right ventricular (RV) systolic overload and prognosis in pulmonary hypertension. The effects on </span><span style="color:black">C<sub>PA</sub></span><span style="color:black"> of a hybrid therapeutic approach with pulmonary vasodilators and balloon pulmonary angioplasty (BPA) in patients (pts) with chronic thromboembolic pulmonary hypertension (CTEPH) remain unclear.</span></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"><strong><span style="color:black">Purpose: </span></strong><span style="color:black">To determine the effect on </span><span style="color:black">C<sub>PA</sub></span><span style="color:black"> of a hybrid therapeutic approach with pulmonary vasodilators and BPA in CTEPH pts.</span></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"><strong>Methods:</strong> Prospective single-centre study that included all BPA sessions performed in <span style="color:black">CTEPH pts from 2017 to 2020. Right heart catheterization was performed at baseline before the start of pulmonary vasodilator therapy (N=13), just before the first BPA session (N=13) and at 6-months of follow-up (FUP) after the last BPA session (N=10, as </span><span style="color:black">3 pts did not complete the 6-months FUP). </span><span style="color:black">C<sub>PA</sub></span><span style="color:black"> was calculated as stroke volume/pulmonary arterial pulse pressure [systolic </span><span style="color:black">pulmonary artery pressure (PAP) – diastolic PAP], normal values 3.8-12 ml/mmHg, poor prognostic values < 2.5 ml/mmHg as previously described (Ann Am Thorac Soc. 2016;13(2): 276–284; Circulation. 2017;136:314–326).</span></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"><strong>Results:</strong> 69 BPA sessions were performed in 13 CTEPH pts: mean age 62.4<span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">14.9 years; 67% with inoperable disease. At baseline, mean value of </span><span style="color:black">C<sub>PA</sub></span><span style="color:black"> was severely decreased (1.4</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">0.8 ml/mmHg). Eleven pts (84.6%) were treated with specific vasodilator therapy (guanylate cyclase stimulators in 9; endothelin receptor antagonists in 6; phosphodiesterase type 5 inhibitors in 2, prostacyclin analogues in 3 and selexipag in 1). The number of pulmonary vasodilators decreased from 1.4</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">1.0 before BPA to 1.2</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">0.7 at FUP (p=0.082). Mean number of BPA sessions was 5.3</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">1.8 per pt (min 2-max 8) and mean number of total vascular segments treated 9.9</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">2.3 per pt (min 6-max 15).</span><span style="color:black"> BPA alone was associated with a significant reduction of diastolic PAP (</span><span style="color:black">23.8</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">7.6 versus 15.5</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">6.0 mmHg, </span><span style="color:black">p=</span><span style="color:black">0.039) </span><span style="color:black">and a tendency to reduction of mean pulmonary vascular resistance (PVR of </span><span style="color:black">5.3</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">3.1 versus 3.0</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">1.4, </span><span style="color:black">p=0.056), but did not significantly increase C<sub>PA </sub>(</span><span style="color:black">2.4</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">1.1 versus 2.7</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">1.0 ml/mmHg, </span><span style="color:black">p=0.564). However, a BPA strategy on top of pulmonary vasodilator therapy further improved mean PAP (</span><span style="color:black">45.1</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">11.4 versus 25.1</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">6.6 mmHg, </span><span style="color:black">p=0.002), PVR (</span><span style="color:black">10.2</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">4.5 versus 3.0</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">1.4 mmHg, </span><span style="color:black">p=0.001) and C<sub>PA</sub> (</span><span style="color:black">1.4</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">0.8 versus 2.7</span><span style="font-family:Symbol"><span style="color:black">±</span></span><span style="color:black">1.0 ml/mmHg, </span><span style="color:black">p=0.004) to values near normal at 6 months of follow-up (Table). An inversely significant correlation was found between decrease in PVR an increase in C<sub>PA</sub> (r=-0.82, p=0.004) leading to a reduce in RV systolic overload.</span></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"><strong>Conclusions: </strong><span style="color:black">BPA on top of pulmonary vasodilator therapy improves haemodynamic, including </span><span style="color:black">C<sub>PA</sub>, having an overall and consistent significant benefit</span><span style="color:black">. These data also suggest that the hybrid therapeutic approach decreases RV systolic afterload </span><span style="color:black">i</span><span style="color:black">n pts with inoperable CTEPH or </span><span style="color:black">residual/recurrent PH after </span><span style="color:black">surgery. </span></span></span></span></p> <p style="text-align:justify"> </p> <p style="text-align:justify"> </p>
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