Hs-CRP is a strong predictor of adverse cardiovascular events in patients with chest pain

Background Evidence showing that inflammation is a major pathophysiological driver of atherosclerosis has shifted scientific focus towards the prognostic value of downstream biomarkers such as high-sensitivity C-reactive protein (hs-CRP). Hs-CRP was recently proven to identify individuals with coronary artery disease and high inflammatory burden in the stable setting potentially benefiting from anti-inflammatory treatment irrespective of standard modifiable cardiovascular risk factors (SMuRFs), i.e. low-density cholesterol. The prognostic role of hs-CRP as a surrogate marker of inflammation in patients presenting with acute chest pain to the emergency department remains to be determined. Purpose We therefore sought to investigate the prognostic utility of hs-CRP in patients with suspected myocardial infarction. Methods Hs-CRP was measured in stored blood samples that were collected directly at admission from consecutive patients enrolled in the ongoing Biomarkers in Acute Cardiac Care (BACC) cohort study, who presented to the emergency department of a German tertiary hospital with chest pain. For follow-up, the first 6 years after index admission were considered to assess overall death and major adverse cardiovascular events (MACE) defined as a composite of cardiovascular death, myocardial infarction, revascularization and cardiac rehospitalization. Tertiles of hs-CRP concentrations were calculated to investigate their predictive utility for (i) all-cause death and (ii) MACE using Kaplan-Meier curves and risk factor-adjusted Cox regression analyses. Results Among 3149 patients with a median age of 63 (IQR 51-75) years, 35.9% were female. The prevalence of non-ST-elevation myocardial infarction was 12.7%. The median hs-CRP concentration was 2.5 mg/L (IQR 1.0-7.4 mg/L); hs-CRP tertiles were calculated as follows: 1st-hs-CRP <1.4 mg/L, 2nd-hs-CRP 1.4-4.7 mg/L, and 3rd-hs-CRP >4.7-160 mg/L. Patients with index hs-CRP concentrations in the highest tertile experienced significantly higher rates of all-cause death (median follow-up 5.2 years; 33.9% vs 8.6%, p<0.001) and MACE (median follow-up 4.9 years; 43.6% vs 28.5%, p<0.001) than those in the lowest tertile, respectively (Figure). After adjustment for age, sex, SMuRFs, and history of cardiovascular diseases, hs-CRP in the highest tertile remained a strong and independent predictor of all-cause death (HR 3.1, 95% CI 2.3-4.0, p<0.001), and with slightly attenuated effect magnitude, also of MACE (HR 1.3, 95% CI 1.1-1.6, p=0.002) as compared to the lowest tertile. Conclusion Hs-CRP, a marker of systemic inflammation, is an independent predictor of overall death and MACE in patients with symptoms suggestive of myocardial infarction. Identifying patients with elevated hs-CRP levels might potentially add to cardiovascular risk assessment and help to further elucidate the role of anti-inflammatory treatment in cardiovascular prevention beyond SMuRFs.