Key result
Admission serum endocan was elevated in patients with acute heart failure and cardiogenic shock compared to controls, and correlated with left ventricular ejection fraction impairment.
Why the study?
Endocan contributes to inflammation and endothelial dysfunction, but has been scarcely explored in human acute heart failure.
Cohort (n=70)
No
Serum endocan is significantly elevated in acute heart failure and cardiogenic shock, correlating with disease severity and prognostic scores, suggesting its potential as a biomarker for endothelitis.
Answers are grounded in this paper and cite their sources.
Endocan elevation was associated with acute HF and shock severity; leaves open its role as an endothelial biomarker pending validation.
Aims: Inflammation-driven endothelitis seems to be a hallmark of acute heart failure (AHF) and cardiogenic shock (CS). Endocan, a soluble proteoglycan secreted by the activated endothelium, contributes to inflammation and endothelial dysfunction, but has been scarcely explored in human AHF. We aimed to evaluate serum (S-Endocan) and urinary endocan (U-Endocan) profiles in AHF and CS patients and to correlate them with biomarkers/parameters of inflammation, endothelial activation, cardiovascular dysfunction and prognosis. Methods: Blood and spot urine were collected from patients with AHF ( n = 23) or CS ( n = 25) at days 1–2 (admission), 3-4 and 5-8 and from controls (blood donors, n = 22) at a single time point. S-Endocan, U-Endocan, serum IL-1β, IL-6, tumour necrosis factor-α (S-TNF-α), intercellular adhesion molecule-1 (S-ICAM-1), vascular cell adhesion molecule-1 (S-VCAM-1) and E-selectin were determined by ELISA or multiplex immunoassays. Serum C-reactive protein (S-CRP), plasma B-type natriuretic peptide (P-BNP) and high-sensitivity troponin I (P-hs-trop I), lactate, urea, creatinine and urinary proteins, as well as prognostic scores (APACHE II, SAPS II) and echocardiographic left ventricular ejection fraction (LVEF) were also evaluated. Results: Admission S-Endocan was higher in both patient groups, with CS presenting greater values than AHF (AHF and CS vs. Controls, p < 0.001; CS vs . AHF, p < 0.01). Admission U-Endocan was only higher in CS patients ( p < 0.01 vs . Controls). At admission, S-VCAM-1, S-IL-6 and S-TNF-α were also higher in both patient groups but there were no differences in S-E-selectin and S-IL-1β among the groups, nor in P-BNP, S-CRP or renal function between AHF and CS. Neither endocan nor other endothelial and inflammatory markers were reduced during hospitalization ( p > 0.05). S-Endocan positively correlated with S-VCAM-1, S-IL-6, S-CRP, APACHE II and SAPS II scores and was positively associated with P-BNP in multivariate analyses. Admission S-Endocan raised in line with LVEF impairment ( p = 0.008 for linear trend). Conclusion: Admission endocan significantly increases across AHF spectrum. The lack of reduction in endothelial and inflammatory markers throughout hospitalization suggests a perpetuation of endothelial dysfunction and inflammation. S-Endocan appears to be a biomarker of endothelitis and a putative therapeutic target in AHF and CS, given its association with LVEF impairment and P-BNP and its positive correlation with prognostic scores.
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Reina‐Couto et al. (2022) conducted a cohort in Acute heart failure and cardiogenic shock (n=70). Acute heart failure and cardiogenic shock vs. Healthy controls was evaluated on Admission serum endocan (S-Endocan) concentration (p=<0.001). Admission serum endocan was elevated in patients with acute heart failure and cardiogenic shock compared to controls, and correlated with left ventricular ejection fraction impairment.
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