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Assessing the arterial-ventricular uncoupling in pulmonary arterial hypertension – is there a place for stroke volume index?
Session:
Sessão de Posters 06 - Hipertensão Pulmonar
Speaker:
João Mirinha Luz
Congress:
CPC 2024
Topic:
I. Hypertension
Theme:
21. Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure
Subtheme:
21.2 Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure – Epidemiology, Prognosis, Outcome
Session Type:
Cartazes
FP Number:
---
Authors:
João Mirinha Luz; Bárbara Ferreira; Filipa Ferreira; Sofia Alegria; Ana Cláudia Vieira; Rita Calé; Mariana Martinho; Débora Repolho; Sílvia Vitorino; Hélder Pereira; Ernesto Pereira
Abstract
<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong><u>Introduction and objective:</u></strong> Arterial-ventricular uncoupling (AVU) is a major factor in pulmonary arterial hypertension (PAH) pathophysiology, and the gold standard to measure AVU is obtained by conductance catheterization. As this tool is not widely available, multiple surrogates have been investigated, and the ratio of tricuspid annular plane systolic excursion to estimated pulmonary arterial systolic pressure (TAPSE/PASP) as emerged as one of the best validated. As stroke volume is integral to measure AVU, our goal was to investigate if stroke volume index (SVI) could be a feasible surrogate.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong><u>Methods:</u></strong> We performed a retrospective longitudinal analysis of a cohort with confirmed PAH between January 2010 and December 2022 in a PH certified centre. We assessed their SVI [by both Fick method and thermodilution method (TD)] and TAPSE/PSAP at the time of first evaluation in our centre, and evaluate possible correlations between them. Adverse events until November 2023 were also registered and defined as need for parenteral prostanoids, lung transplantation and death by any cause.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong><u>Results:</u></strong><strong> </strong>Seventy-nine (79) patients were included in this analysis. Mean age at time of evaluation was 51 years old. 73,4% of patients were female, and 67,1% were naïve of pulmonary vasodilators. About a quarter (24,7%) of patients had idiopathic PAH, and other quarter (23,4%) had PAH associated with congenital heart disease. Median SVI using TD was 31,04ml/m2, and with Fick method was 29,14mL/m2. Median TAPSE/PASP was 0,20 mm/mmHg<span style="font-size:8.0pt"> </span>. By using Tello <em>et al</em> TAPSE/PASP cutoff of 0.31 mm/mmHg, SVI by Fick was significantly lower (25,06 vs 33,09, p=0.008), and there was moderate to high correlation between TAPSE/PASP and SVI (Fick) regarding need for prostanoids (r = 0,637). By using ERS/ESC 2022 TAPSE/PASP cutoff of 0.19mm/mmHg, both TD and Fick SVI were significantly lower (26.29 vs 33.35, p=0.038; 22.34 vs 34.01, p<0.001), but no correlation was established between TAPSE/PASP and SVI regarding adverse events. In linear regression analysis, we have discovered association of SVI by Fick with TAPSE/PSAP, which for each increase of 0,1 mm/mmHg in TAPSE/PSAP, there was an estimated increase of 4,5 ml of SVI (p=0,05).</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong><u>Conclusion:</u></strong> Our study shows that SVI could be a potential surrogate for AVU, and it also has prognostic implications. The main limitation was the comparison with a non-invasive, although validated, surrogate, so comparison with the gold-standard is mandatory to corroborate this hypothesis.</span></span></p> <div> <p> </p> </div>
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