Abstract
Background: Fibrinogen is synthesized by hepatocytes. It is a precursor of fibrin and forms bridges between platelets during thrombus formation, but it is also a marker of ongoing inflammation. Neopterin is released by monocyte/ macrophage activation associated with atherosclerosis. Whether these markers interact or act independently among patients with suspected stable coronary heart disease has previously not been given much attention. Methods: We included 3526 patients undergoing elective coronary angiography at two university hospitals in Norway during 2000-2004, with a median follow-up of 7.3 years. Cox regression analysis was used to obtain hazard ratios (HR) and 95% confidence intervals (CI) for incident AMI of fibrinogen and neopterin levels in a crude model and a model adjusted for age, gender, diabetes, current smoking, hypertension and serum apoA1 and apoB. Potential effect modifications were investigated according to strata of fibrinogen or neopterin below or above the median, as well as across subgroups of age, gender, smoking status, diabetes, serum apoA1 and apoB. A p-value <0.05 was considered significant. Results: During follow-up, 580 patients experienced an AMI. In the unadjusted model, both fibrinogen and neopterin predicted future AMI [HR = 1.32; 95% CI 1.22-1.43; p<0.001 and HR = 1.31; 95% CI 1.23-1.40; p<0.001, respectively]. The estimates were only slightly attenuated in the multivariate model, and still associated with incident AMI when both biomarkers were added simultaneously [HR = 1.15; 95% CI 1.05-1.25; p<0.001 and HR = 1.20; 95% CI 1.12-1.28; p<0.001, respectively]. Baseline fibrinogen and neopterin levels were modestly correlated (Spearman’s rho = 0.18, p-value <0.001). There were no statistically significant interaction across subgroups (p for interaction fibrinogen and high/ low neopterin = 0.26, neopterin and high/low fibrinogen = 0.46, respectively). Conclusion: Patients with increased levels of fibrinogen or neopterin are at increased risk of future AMI. Neopterin levels did not significantly interact with the prognostic utility of fibrinogen. This suggests that circulating fibrinogen and neopterin may reflect different pathophysiological mechanisms.
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