0338: C-reactive protein and mean platelet volume/platelet count ratio as predictors of ischemic stroke after acute myocardial infarction

Abstract

Stroke is a serious complication after acute myocardial infarction (AMI) and is associated with an increased risk of death. However, the increased use of evidence-based therapies (ASA, P2Y12 and statins) has reduced the risk of stroke during the last decade. Whereas the pathophysiological mechanisms are not exactly known, increased inflammation and platelet reactivity could play an important role in the occurrence of stroke during the acute phase of MI. We aimed to investigate the relationship between the mean platelet volume (MPV), a parameter of platelet function, the C-reactive protein (CRP), and the occurrence of in-hospital ischemic stroke (IHS) after AMI. Data were obtained from a French regional survey for AMI, including 5976 patients admitted in intensive care unit (ICU) between 2001 and 2010. Patients were divided in 2 groups according to the occurrence of IHS. MPV, platelet count and CRP were routinely measured from blood samples drawn at admission in ICU. 87 (1.4%) IHS were recorded during the hospitalization period after admission for AMI. After Cox multivariate regression, IHS was independently associated with history of stroke (OR: 2.26, 95% CI: 1.26-4.06, p=0.006), LVEF<40% (OR: 1.74, 95% CI: 1.08-2.81, p=0.002), glycemia (OR: 1.05, 95% CI:1.01-1.08, p=0.008), CRP>10 mg/l (OR: 2.56, 95% CI: 1,64-4.01, p<0.001), MPV/Platelet count ratio (OR 1.04, 95% CI: 1.01-1.08, p=0.03) and new onset atrial fibrillation (OR:1.91, 95% CI:1.12-3.24, p=0.02). Patients developing IHS had both an increased 30-day mortality (32.3% vs 8.3%, p<0.001) and 1-year mortality (44.4% vs 13.5%, p<0.001) (fig.1). This study describes predictive factors for IHS after AMI, with both higher short and long-term risk of death. At hospital admission, new biological parameters as high MPV/Platelet count ratio and high level of CRP might help to identify patients at increased risk of IHS. Moreover, these results provide new insights on the potential role played by increased inflammation and platelet reactivity underlying the occurrence of stroke after AMI. Abstract 0338 – Figure