C-Reactive Protein Level and the Genetic Variant rs1130864 in the CRP Gene as Prognostic Factors for 10-Year Cardiovascular Outcome.

BACKGROUND: Cardiovascular disease (CVD) is the primary cause of premature death and disability worldwide. There is extensive evidence that inflammation represents an important pathogenetic mechanism in the development and prognosis of CVD. C-reactive protein (CRP) is a potential marker of vascular inflammation and plays a direct role in CVD by promoting vascular inflammation. The objective of this study (ClinTrials.gov identifier: NCT01045070) was to assess the prognostic impact of CRP protein levels and genetic variants of CRP gene events on cardiovascular (CV) outcome (10-year follow-up) in patients suffering from CVD. METHODS: CVD patients were prospectively included in this study (n = 1002) and followed up (10 years) regarding combined CV endpoint (CV death, death from stroke, myocardial infarction (MI), and stroke/transient ischemic attack (TIA)). CRP protein level (particle-enhanced immunological turbidity test) and genetic variants (rs1130864, rs1417938, rs1800947, rs3093077; polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) after DNA extraction from EDTA-blood) were evaluated. RESULTS: In survival analyses, increased CRP protein levels of ≥5 mg/L (log-rank test: p < 0.001, Cox regression: p = 0.002, hazard ratio = 1.49) and CT + TT genotype of rs1130864 (log-rank test: p = 0.041; Cox regression: p = 0.103, hazard ratio = 1.21) were associated with a weaker CV prognosis considering combined CV endpoint. CONCLUSIONS: Elevated CRP level and genetic variant (rs1130864) were proven to provide prognostic value for adverse outcome in CVD patients within the 10-year follow-up period.

C-reactive protein levels and genetic variants of CRP as prognostic markers for combined cardiovascular endpoint (cardiovascular death, death from stroke, myocardial infarction, and stroke/TIA).

BACKGROUND: The aim of this analysis was to evaluate the importance of C-reactive protein levels and genetic variants of CRP as prognostic markers for further cardiovascular (CV) events (3-year follow-up) in a cohort of in-patients with cardiovascular disease (CVD) patients. METHODS AND RESULTS: Patients with angiographic proven CVD (n=939) were prospectively included. The three-year CV outcome of the patients was evaluated considering the predefined, combined endpoint (CV death, death from stroke, myocardial infarction, and stroke/TIA). Polymorphisms rs1800947, rs1417938, rs1130864, rs3093077 were analysed. In Kaplan-Meier survival curve and Cox regression increased CRP levels of ⩾5mg/l (log-rank test: p=0.001, Cox regression: hazard ratio=1.77, 95% CI: 1.2-2.7) and the GG genotype of rs1800947 (log-rank test: p=0.01, Cox regression: hazard ratio=1.99, 95% CI: 1.1-3.6) were associated with the incidence of the combined endpoint. CONCLUSIONS: Both a CRP level ⩾5mg/l and SNP rs1800947 of the CRP gene were independent risk factors for further adverse CV events among patients with CVD within three years follow-up.