Systemic inflammatory status is associated with increased platelet reactivity in the early period after acute coronary syndromes

Abstract

Systemic inflammation measured by high-sensitivity C reactive protein (CPR) is associated with increased risk of major adverse cardiovascular events (MACE). Recent clinical trials targeting CPR showed a reduction in MACE after an acute coronary syndrome (ACS). Inflammation could be linked to high platelet reactivity (HPR), which is an independent predictor of MACE in patients with ACS. We aimed to evaluate the impact of 1-month C-reactive Protein (CRP) levels on HPR in patients enrolled in the GEPRESS study. We measured CRP and platelet reactivity index (PRI) at 30 days follow-up. PRI was assessed with vasodilator stimulated phosphoprotein (VASP) phosphorylation assay at the same timepoint. HPR was defined as PRI >50%. Of the 1042 patients included in the GEPRESS study, 756 (75%) had both VASP and CRP data at 30 days follow-up. HPR was found in 61 (49.1%) patients with CRP >1 mg/L and 233 (36.4%) patients with CRP ≤1 mg/L, p = 0.012. After adjustment for covariates, we found a direct gradient of effect between CRP and HPR; the inclusion of CRP significantly increased the discrimination of HPR regression model. This is the first study showing that residual HPR is more likely to occur in patients with CRP >1 mg/L at 1 month after non-ST elevation-ACS and this may contribute to the unfavorable outcome observed in such patients.

Keywords: Acute coronary syndrome; C-reactive protein; inflammation; platelet reactivity.