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ENDOCAN - A POTENTIAL NEW BIOMARKER OF INFLAMMATION-DRIVEN “ENDOTHELITIS” IN HUMAN ACUTE HEART FAILURE AND CARDIOGENIC SHOCK
Session:
CO 22- Insuficiência cardíaca aguda
Speaker:
MARTA FERNANDA REINA COUTO
Congress:
CPC 2021
Topic:
D. Heart Failure
Theme:
11. Acute Heart Failure
Subtheme:
11.1 Acute Heart Failure – Pathophysiology and Mechanisms
Session Type:
Comunicações Orais
FP Number:
---
Authors:
Marta Reina-Couto; Carolina Silva-Pereira; Patrícia Pereira-Terra; Janete Quelhas-Santos; João Bessa; Catarina Marques; Paula Serrão; Joana Afonso; Sandra Martins; Roberto Roncon-Albuquerque; José Artur Paiva; António Albino-Teixeira; Teresa Sousa
Abstract
<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:"Times New Roman",serif">Inflammation-driven “endothelitis” appears to contribute to acute heart failure (AHF). Endocan has recently emerged as a novel biomarker of endothelial dysfunction and inflammation. However, its role in human AHF has not been explored yet. This study aimed at evaluating the serum and urinary endocan profile in patients with AHF or with cardiogenic shock (CS). Furthermore, their correlation with biomarkers of inflammatory status, endothelial activation, cardiac dysfunction, systolic (SBP) and diastolic (DBP) blood pressure and prognostic scores was also analysed. </span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:"Times New Roman",serif">This study was approved by the Health Ethics Committee of our hospital. Patients with the diagnosis of AHF (n=23) or CS (n=25) were included and blood samples were collected at days 1-2, 3-4 and 5-8. Blood donors were used as controls (n=22). Endocan, myeloperoxidase (MPO), urinary isoprostanes (U-Isop) and IL-10 were determined by ELISA kits. Serum IL-6, tumour necrosis factor-α (TNF-α) and vascular cell adhesion molecule-1 (VCAM-1) were determined using multiplex immunoassays. C-reactive protein (CRP), differential leukocyte count, B-type natriuretic peptide (BNP), high-sensitivity troponin I (hs-trop I) were evaluated using automated analyzers. Prognostic scores (APACHE II, SAPS II), echocardiographic parameters, SBP and DBP were also evaluated. </span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:"Times New Roman",serif">At admission, serum endocan was significantly higher in AHF and even higher in CS (p<0.001 for linear trend). Urinary endocan values were significantly higher in CS patients (p<0.01 vs controls). During hospitalization, there was no reduction in endocan values or in other inflammatory or endothelial biomarkers in both patients’ groups. Within patients, serum endocan was inversely correlated with SBP and DBP and positively correlated with IL-6, IL-10, BNP, hs-trop I and with APACHE II and SAPS II scores. Urinary endocan was inversely correlated with lymphocytes and albumin and positively correlated with serum endocan, IL-6, IL-10, TNF-α, VCAM-1, MPO, U-Isop, hs-trop I and CRP. Furthermore, when patients were stratified according to echocardiographic ejection fraction (EF), serum endocan significantly increased in line with the degree of ejection fraction impairment (p for linear trend =0.0089). </span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:"Times New Roman",serif">Serum and urinary endocan are increased in AHF and CS patients and positively correlated with proinflammatory status and endothelial biomarkers. There is no reduction of their values during hospitalization which suggests that present hospital treatment is not sufficient to counteract inflammation-driven “endothelitis” which might contribute to the prognosis of acute heart failure. Additionally, serum endocan appears to be a potential novel biomarker in AHF since it is significantly associated with the deterioration of ventricular function, cardiac injury biomarkers and with prognostic scores.</span></span></p> <p style="text-align:justify"><span style="font-size:11.0pt"><span style="font-family:"Times New Roman",serif">Funded by FCT/FEDER (COMPETE, Portugal 2020), PTDC/MEC-CAR/32188/2017.</span></span></p>
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