December 21, 2019Medical Science MonitorOpen Access

C-Reactive Protein and All-Cause Mortality in Patients with Stable Coronary Artery Disease: A Secondary Analysis Based on a Retrospective Cohort Study

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Why the study?

The association between C-reactive protein (CRP) and all-cause mortality (ACM) in patients with stable coronary artery disease (CAD) was unclear.

Does elevated C-reactive protein predict all-cause mortality in patients with stable coronary artery disease?

Structured PICO

Does elevated C-reactive protein predict all-cause mortality in patients with stable coronary artery disease?

Population

196 patients aged 43 to 98 years with a first diagnosis of stable coronary artery disease (CAD)

Intervention

C-reactive protein (CRP) concentration (evaluated in quartiles: 0.01-0.03, 0.04-0.11, 0.12-0.33, and 0.34-9.20 mg/dL)

Outcome

All-cause mortality (ACM)hard clinical

Elevated C-reactive protein levels are associated with increased all-cause mortality in patients with stable coronary artery disease, with an optimal prognostic threshold of 0.345 mg/dL.

Implication

CRP elevation was associated with ACM in stable CAD; supports risk stratification but leaves open prospective validation.

Abstract

BACKGROUND The association between C-reactive protein (CRP) and all-cause mortality (ACM) in patients with stable coronary artery disease (CAD) is unclear. Therefore, the aim of the present study was to explore the correlation between CRP and ACM in stable CAD patients. MATERIAL AND METHODS This study was a secondary analysis. Between October 2014 and October 2017, 196 patients aged 43 to 98 years who had a first diagnosis of stable CAD were recruited into this study. We divided the patients into 4 groups (Quartile 1: 0.01-0.03 mg/dL; Quartile 2: 0.04-0.11 mg/dL; Quartile 3: 0.12-0.33 mg/dL; and Quartile 4: 0.34-9.20 mg/dL) according to the concentration of CRP. The indicator surveyed in this research was ACM. RESULTS During a median follow-up of 783 days, ACM occurred in 18 patients, with a mortality rate of 9.18% (18/196). Univariate analysis showed that elevated CRP was closely related to ACM in stable CAD patients (P<0.005). After controlling for potential confounding factors by multivariate logistic regression analysis, this relationship still existed. Pearson correlation analysis showed that elevated CRP log10 transform was associated with LVEF (r=-0.1936, P=0.0067). Receiver operating characteristic (ROC) curve analysis showed that the optimal concentration of CRP for the diagnosis of ACM was 0.345, and the area under the curve (AUC) was 0.735. CONCLUSIONS Elevated CRP is associated with ACM in stable CAD patients, and the best diagnostic threshold is 0.345.