Soluble IL-1 receptor 2 is associated with left ventricular remodelling in patients with ST-elevation myocardial infarction
Permanent lenke
https://hdl.handle.net/10037/14395Dato
2018-05-28Type
Journal articleTidsskriftartikkel
Peer reviewed
Forfatter
Orrem, Hilde Lang; Shetelig, Christian; Ueland, Thor; Limalanathan, Shanmuganathan; Nilsson, Per; Husebye, Trygve Guttorm; Aukrust, Pål; Seljeflot, Ingebjørg; Hoffmann, Pavel; Eritsland, Jan; Mollnes, Tom Eirik; Andersen, Geir Øystein; Yndestad, ArneSammendrag
Background: The inflammatory response following myocardial infarction (MI) is prerequisite for proper healing of infarcted tissue, but can also have detrimental effects on cardiac function. Interleukin (IL)-1α and IL-1β are potent inflammatory mediators and their bioactivity is tightly regulated by IL-1 receptor antagonist (IL-1ra) and soluble (s) IL-1 receptors (R). We aimed to examine whether levels of soluble regulators of IL-1 signalling are changed during ST-elevation MI (STEMI) and their associations with parameters of cardiac injury and ventricular remodelling.
Methods: Plasma levels of IL-1Ra, sIL-1R1, sIL-1R2 and sIL-1R accessory protein (sIL-1RAcP) were measured by immunoassays in repeated samples from patients with STEMI (n = 255) and compared to healthy controls (n = 65).
Results: IL-1Ra, sIL-1R1 and sIL-1R2 levels were all significantly elevated after STEMI, while levels of sIL-1RAcP were lower compared to controls. sIL-1R2 levels (at different time points) correlated positively with C-reactive protein, myocardial infarct size and change in indexed left ventricular end-diastolic and end-systolic volume (LVEDVi and LVESVi) measured by cardiac MR acutely and after 4 months, and negatively with LV ejection fraction. Patients with >median levels of sIL-1R2 in the acute phase were more likely to have increased change in LVEDVi and LVESVi. Importantly, sIL-1R2 remained significantly associated with change in LVEDVi and LVESVi also after adjustment for clinical covariates.
Conclusion: Levels of sIL-1R2 are independently associated with parameters of LV adverse remodelling following STEMI.