Abstract
The effect of circulating biomarkers in predicting coronary artery disease (CAD) is not fully elucidated. This study aimed to determine the relationship with CAD and the predictive capacity of nine biomarkers of inflammation (TNF-α, IL-10, IL-6, MCP-1, CRP), oxidation (GHS-Px), and metabolism (adiponectin, leptin, and insulin). This was a case-cohort study, within the REGICOR population-cohorts (North-Eastern Spain), of 105 CAD cases and 638 individuals randomly selected from a cohort of 5,404 participants aged 35–74 years (mean follow-up = 6.1 years). Biomarkers’ hazard ratio (HR)/standard deviation was estimated with Cox models adjusted for age, sex, and classical risk factors. Discrimination improvement and reclassification were analyzed with the c-index and the Net reclassification index (NRI). GHS-Px (adjusted HRs = 0.77; 95%CI:0.60–0.99), insulin (1.46; 1.08–1.98), leptin (1.40; 1.03–1.90), IL-6 (1.34; 1.03–1.74), and TNF-α (1.80; 1.26–2.57) were significantly associated with CAD incidence. In the model adjusted for all biomarkers, TNF-α (1.87;1.31–2.66) and insulin (1.59;1.16–2.19) were independently associated with CAD. This final model, compared to a model without biomarkers, showed a c-index difference of 1.3% (−0.7, 3.2) and a continuous NRI of 33.7% (2.6, 61.9). TNF-α and insulin are independently associated with CAD incidence and they improve reclassification when added to a model including classical risk factors.
Highlights
Chronic inflammation in cardiovascular disease (CVD) appears to be associated with the oxidative/ anti-oxidative homeostasis, yielding an accumulation of oxidized low-density lipoproteins (LDL) in the arterial wall[5]
Baseline values of systemic GHS-Px, IL-6, insulin, leptin, and TNF-α were associated with 6-year incidence of coronary artery disease (CAD), independently of classical risk factors; this was not true for other well-known biomarkers
Insulin and TNF-α were independently associated with CAD incidence when considered together in fully adjusted models
Summary
Chronic inflammation in cardiovascular disease (CVD) appears to be associated with the oxidative/ anti-oxidative homeostasis, yielding an accumulation of oxidized low-density lipoproteins (LDL) in the arterial wall[5]. CRP activates the complement system that promotes phagocytosis which allows clearance of necrotic tissues in the atherosclerotic plaque and perpetuates the inflammatory response[3,7]. Within this inflammatory response, metabolism biomarkers–e.g., insulin, leptin, and adiponectin– play an important role. The objectives of the present study were: (1) to determine the individual and mutually adjusted relationship between the development of CAD events and systemic levels of a set of biomarkers of inflammation, oxidation, and metabolism and (2) to test the biomarkers’ incremental predictive capacity for CAD, beyond that of classical cardiovascular risk factors
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