Elevated IL-27 in patients with acute coronary syndrome is associated with adverse ventricular remodeling and increased risk of recurrent myocardial infarction and cardiovascular death.
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Grufman H, Yndigegn T, Gonçalves I, Nilsson J, Schiopu A
Cytokine 122 (-) 154208 [2019-10-00; online 2018-02-07]
IL-27 is an immunoregulatory cytokine belonging to the IL-6/IL-12 family that was found to be elevated in acute coronary syndrome (ACS) patients. We investigated whether IL-27 is related to post-ischemic cardiac remodeling and long-term prognosis in this patient group. We included 524 ACS patients, defined as acute myocardial infarction (AMI) or unstable angina (UA). A subgroup of 107 patients donated blood samples 6 weeks after the index event, and underwent a follow-up echocardiographical examination at 1 year. We measured plasma levels of IL-27, high sensitivity troponin T (hsTNT), C-reactive protein (hsCRP) and cystatin C at baseline and in the 6-week samples. The median follow-up period of the cohort was 2.2 years. The incidence of the combined end-point of AMI and cardiovascular death was higher in patients with plasma IL-27 within the top two tertiles both at baseline and after 6 weeks. After correction for cardiovascular risk factors, medication, hsTNT, hsCRP, and eGFR, patients with baseline IL-27 levels within the highest tertile had a significantly elevated risk for the combined end-point compared with the lowest tertile (hazard ratio 2.70, 95% CI 1.06-6.90, p = .038). Additionally, higher baseline IL-27 levels were associated with deleterious left ventricular remodeling and deterioration of systolic and diastolic function during the first year of follow-up. Elevated IL-27 at the time of an ACS is independently related to impaired cardiac function and worse long-term prognosis. Our data warrants further mechanistic studies to elucidate the involvement of IL-27 in cardiac repair and remodeling after ACS.
Affinity Proteomics Uppsala [Service]
PLA and Single Cell Proteomics [Service]
PubMed 29428559
DOI 10.1016/j.cyto.2017.11.002
Crossref 10.1016/j.cyto.2017.11.002
pii: S1043-4666(17)30344-7