Background Acute coronary syndromes are characterised by a prothrombotic and pro-inflammatory state. Known biomarkers of thrombosis, such as platelet reactivity, and of inflammation, such as neutrophil to lymphocyte ratio (NLR) and high-sensitivity C-reactive protein (hs-CRP), can be used to quantify this state and predict cardiovascular outcomes. The relationship between these biomarkers and their combined use for risk stratification following ST-elevation myocardial infarction (STEMI), however, is not known. We aimed to assess the predictive value of these biomarkers, both alone and in combination, for short- and long-term clinical outcomes following STEMI.
Methods We prospectively collected blood samples from patients presenting with STEMI (n=541) upon arrival, before undergoing primary percutaneous coronary intervention (PPCI). Blood was tested for NLR, hs-CRP and platelet reactivity. The Global Thrombosis Test, a point-of-care assay situated in the cath lab, was used to assess platelet reactivity. The time taken to create an in vitro occlusive thrombus under high shear, reported as occlusion time (OT, sec), reflects platelet reactivity. Shorter occlusion time denotes higher platelet reactivity. Patients were followed up for 12 months for the 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 Significant but weak correlation was observed between hs-CRP and NLR (r=0.25, p<0.001), and hs-CRP and platelet reactivity (r=0.14, p=0.003). There was no correlation between platelet reactivity and NLR. A total of 42 patients experienced a MACE within the first 30 days, and 50 within 12 months. Optimal cut-points based on highest specificity and sensitivity from receiver operating characteristic analysis were: NLR 5.6, hs-CRP 8 mg/L and OT 302 sec. Platelet reactivity and hs-CRP were each only very 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, alone, was not predictive of MACE at either 30 days or 12 months (p=NS). Of the two-biomarker combinations, enhanced platelet reactivity and raised hs-CRP together 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). The combination of all three biomarkers, however, was the strongest overall predictor of MACE at 30 days (HR 2.58 [95% CI 1.78–3.75], p<0.001) and 12 months (HR 2.61 [95% CI 1.80–3.80], p<0.001) (Figure 1).
Conclusion In patients with STEMI undergoing PPCI, although individually, each biomarker was poorly predictive, in combination provide significant additive predictive value for the occurrence of MACE at 30 days and 12 months.
Conflict of Interest None
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