LAUSR

Inhibition of the interleukin-1β (IL-1β) innate immunity pathway is associated with anti-inflammatory effects and a reduced risk of recurrent cardiovascular events in stable patients with previous myocardial infarction (MI) and elevated high sensitivity C-reactive protein (hs-CRP). However, the prognosis value of IL-1β level in acute myocardial infarction patients has never been evaluated. We aim to assess the association between IL-1β level with all-cause mortality in patients with acute ST segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention and the interplay between IL-1β and hs-CRP concentrations on the risk of premature death. IL-1β concentration was measured among 1398 STEMI patients enrolled in a prospective cohort study. Crude and hazard ratios for all-cause and cardiovascular mortality were analyzed at 90-days and one-year using a multivariate-cox proportional regression analysis. Major cardiovascular events (MACE) were also analyzed. In a STEMI population, IL-1β concentration measured at admission was independently associated with all-cause mortality at 90 days (adjusted hazard ratio [adjHR], 1.43 per 1SD increase; 95% CI, 1.12 to 1.83; p<0.005). The relation was nonlinear, and we identified a threshold of IL-1β >10 pg/mL that was markedly associated with higher mortality rates at 90 days (adjHR: 2.80; 95% CI: 1.63–4.80, p=0.0002) and one-year (adjHR: 1.75; 95% CI: 1.09–2.78, p=0.019), regardless of the hs-CRP concentration. The relationship was even stronger when considering cardiovascular mortality and MACE at 90 days (adjHR: 2.31; 95% CI: 1.30–4.10, p=0.004 and 2.17; 95% CI: 1.24–3.80, p=0.006) and at one year (adjHR: 2.26; 95% CI: 1.31–3.87, p=0.03 and 2.25; 95% CI: 1.33–3.79, p=0.004). IL-1β measured at admission in acute MI patients is associated with the risk of mortality and recurrent major cardiovascular events, regardless of the CRP level. A threshold of 10 pg/mL identifies patients at higher risk of events. Survival Type of funding source: None