P327Predictive value of platelet reactivity, neutrophil to lymphocyte ratio, and hs-CRP at presentation in patients with ST-elevation myocardial infarction treated with percutaneous coronary intervention

Background Patients with ST-elevation myocardial infarction (STEMI) exhibit enhanced platelet reactivity and a rise in inflammatory biomarkers such as neutrophil to lymphocyte ratio (NLR) and high-sensitivity C-reactive protein (hs-CRP). The extent of the prothrombotic and inflammatory state are predictive of adverse outcomes in patients with acute coronary syndromes. The relationship of these markers of inflammation and thrombosis in the hyperacute phase of STEMI and, whether together, they improve cardiovascular outcome prediction, is not known. Purpose The aim of this study was to assess the individual and combined predictive values of NLR, hs-CRP, and platelet reactivity for clinical outcomes in patients with STEMI. Method In a prospective study of 541 patients presenting with STEMI, acute admission bloods taken prior to emergency percutaneous coronary intervention, were analysed for NLR and hs-CRP. Platelet reactivity was measured using the point-of-care Global Thrombosis Test, which assesses platelet reactivity in native whole blood under high shear, and measures the occlusion time (OT, sec). Shorter occlusion time represents higher platelet reactivity. The study endpoint was occurrence of major adverse cardiovascular events (MACE, defined as composite of cardiovascular death [CVD], myocardial infarction [MI] or stroke [CVA]) at 30 days and 12 months. Results There was a weak, but significant, correlation between hs-CRP and NLR (r=0.25, p<0.001), and hs-CRP and platelet reactivity (r=0.14, p=0.003) on admission. There was no correlation between platelet reactivity and NLR. Amongst 541 patients, 42 patients experienced a MACE within the first 30 days, and 50 within 12 months. Cut-values associated with the highest specificity and sensitivity for 12-month MACE were NLR 5.6, hs-CRP 8 mg/L and OT 302 sec. Platelet reactivity and hs-CRP were each only weakly predictive of MACE at 30 days (platelet reactivity: hazard ratio [HR] 1.004 [95% confidence interval (CI) 1.002–1.006,] p<0.001; hs-CRP: HR 1.005 [95% CI 1.0009–1.009], p=0.016) and 12 months (platelet reactivity HR 1.004 (95% CI 1.002–1.006), p<0.001; hs-CRP HR 1.005 (95% CI 1.001–1.01), p=0.014). NLR was not predictive of MACE at either 30 days or 12 months (p=NS). When patients were divided into quartiles based on hs-CRP and platelet reactivity, patients in the highest quartile for both hs-CRP and platelet reactivity had an HR 3.46 (95% CI 1.81–6.63), p<0.001 compared to those in the lowest quartile for both (HR 0.04 (95% CI 0.005–0.27), p=0.001). The combination of enhanced platelet reactivity and raised hs-CRP was the strongest predictor of MACE at 30 days (HR 2.32 [95% CI 1.71–3.13], p<0.001) and 12 months (HR 2.31 [95% CI 1.71–3.11], p<0.001). Conclusion Both hs-CRP and platelet reactivity are very weakly predictive of MACE, but in combination provide a strong predictor of adverse outcome in STEMI.