Abstract

Abstract Funding Acknowledgements None. Background The rate of increase, i.e. the velocity, of circulating C-reactive protein (CRP) concentrations during myocardial infarction has been associated with left ventricular dysfunction. However, the prognostic yield of this biomarker as well as the underlying biological process that links high CRP velocity (CRPv) with increased myocardial injury are not clear. Therefore, we sought to determine the associations between CRPv early during STEMI with short- and long-term mortality and its correlation to myocardial necrosis. Methods We retrospectively examined 1,155 patients with the diagnosis of acute STEMI, who had at least two successive CRP measurements (up to 48 hours apart) and at least one echocardiographic evaluation, all within the first 96 hours of admission. We calculated CRPv and examined its correlation with myocardial injury, measured by cardiac troponin and overall mortality over a median follow-up period of 5.2 years [IQR 3.7-6.5]. Results Patients with high CRPv values (above 90th percentile, > 1 mg/L/h) had higher concentrations of cardiac troponin upon presentation regardless of their left ventricular systolic function (EF above or below 40%; Figure 1). Patients with high CRPv had increased 30-day and long-term mortality rates; OR= 4.6, 95% CI 2.3-9.2, p<0.001 for 30-day mortality and HR= 2.2, 95% CI 1.5-3.2, p<0.001 for long-term mortality. Furthermore, CRPv was associated with increased 30 –day and long term mortality rates even among patients with similar systolic function (EF above or below 40%; Figure 2). Conclusions High levels of CRPv early during STEMI are associated with increased mortality rates and elevated cardiac troponin release across all levels of left ventricular function. The higher mortality risk might be explained by an aggravated systemic inflammatory response to STEMI.CRP velocity and troponinCRP velocity and mortality

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