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Pulmonary thromboembolism: is B-type natriuretic peptide an earlier risk marker?
Session:
Posters (Sessão 4 - Écran 8) - Doença Arterial Pulmonar - Foco na Embolia Pulmonar
Speaker:
Lisa Maria Ferraz
Congress:
CPC 2022
Topic:
F. Valvular, Myocardial, Pericardial, Pulmonary, Congenital Heart Disease
Theme:
21. Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure
Subtheme:
21.6 Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure – Clinical
Session Type:
Pósters Electrónicos
FP Number:
---
Authors:
Lisa Maria Ferraz; Simão Carvalho; Adriana Pacheco; Diana Carvalho; Pedro Carvalho; Ana Faustino; Andreia Fernandes; Ana Neves
Abstract
<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Introduction: Cardiac troponin I provide prognosis information in patients (P) with acute pulmonary embolism (PE), however the role of B-type natriuretic peptide (BNP) to guide treatment decisions is still uncertain.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Purpose: To evaluate the prognostic impact of BNP elevation in P with PE. </span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Methods: Retrospective study of 237 consecutive adult P admitted with PE since January 1, 2015 and December 31, 2020: 59,9% (n=142) women, 69,4 ± 1,1 years. Demographics, risk factors, clinical and laboratorial parameters, transthoracic echocardiogram variables and complications during hospitalization were evaluated. PE severity and risk of early death (PESR) was defined according to the 2019 European Society of Cardiology Guidelines on PE.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Results: At admission, 48,6% of P had BNP elevation and 26,6% had troponin I elevation. All P with troponin I elevation at admission, had also BNP elevation. 5,5% of P with BNP elevation and no troponin I elevation at admission <span style="color:black">had </span>troponin I elevation 2 ± 3 days later. PESR was classified as intermediate-high in 21,5% and high in 5,7% of P. During hospitalization occurred 20 (8,4%) in-hospital deaths and 18 P (17,6%) undergo fibrinolysis due to hemodynamic instability. <span style="background-color:white"><span style="color:black">On univariate analysis, BNP elevation at admission was predictor of </span></span>high or intermediate-high PESR (89,2 vs 35,9%; p=0,04), fibrinolysis (81,8 vs 45,6%; p=0,02) and in-hospital mortality (92,6 vs 42,9%; p<0,001). On <span style="background-color:white"><span style="color:black">multivariate analysis, elevated BNP at admission was an independent predictor of </span></span>in-hospital mortality (<span style="color:black">OR</span> 1,6; 95%CI 0,31-0,83;<span style="background-color:white"><span style="color:black"> p < 0,001). There was a trend for BNP value at admission being predictor of </span></span>fibrinolysis<span style="background-color:white"><span style="color:black"> (</span></span>438 ± 76 vs 305 ± 69 pg/mL, p=0,06), without association with high or intermediate-high PESR (571 ± 121 vs 480 ± 101 pg/mL, p= 0,25) or in-hospital mortality (893 ± 245 vs 577 ± 70 pg/mL; p=0,15).<span style="background-color:white"><span style="color:black"> Maximum BNP value during hospitalization was predictor of </span></span>fibrinolysis<span style="background-color:white"><span style="color:black"> (</span></span>669 ± 104 vs 410 ± 94 pg/mL, p=0,038) and <span style="background-color:white"><span style="color:black">showed a trend for association with </span></span>high or intermediate-high PESR (661 ± 157 vs 460 ± 106 pg/mL, p=0,052) and in-hospital mortality (1256 ± 290 vs 661 ± 92 pg/mL, p=0,056). </span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Conclusion: BNP elevation at admission is associated with greater risk of in-hospital mortality and is present earlier than other well-established risk-markers, suggesting that the elevation of this biomarker, more than the value itself, could be used to refine the currently used scheme for risk stratification of early death.</span></span></p>
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