Hyperfibrinogenemia and metabolic syndrome in type 2 diabetes: a population-based study

It has been hypothesized that fibrinogen clusters with several components of the metabolic syndrome, thus increasing its cardiovascular risk. The aims of the present study were to assess in a large population-based cohort of patients with type 2 diabetes (1) variables associated with fibrinogen and (2) the relationship between hyperfibrinogenemia, a number of components of the metabolic syndrome, and coronary heart disease (CHD).

We identified a cross-sectional, population-based cohort of 1574 patients with type 2 diabetes using multiple sources of ascertainment. Components of the metabolic syndrome were hypertension (systolic blood pressure > or = 160 mmHg and/or diastolic blood pressure > or = 95 mmHg and/or treatment with antihypertensive drugs), dyslipidemia (tryglicerides >2.82 mmol/l and/or HDL-cholesterol <1.03 mmol/l), hyperuricemia (uric acid >416 micromol/l) and increased albumin excretion rate (AER > or = 20 microg/min).

Fibrinogen increases with age, HbA(1c), smoking, hypertension and a number of components of the metabolic syndrome, even after adjustment for confounders. Prevalence of CHD increases linearly across quartiles of fibrinogen (from 26.1 to 40.6%, p=0.046). However, in logistic regression, after adjustment for both confounders and known risk factors for CHD, the role of fibrinogen is no more significant, whereas ORs for HbA(1c) between 6.8 and 8.8% and >8.8% vs values <6.8% are, respectively, 1.91 (95% CI 1.36-2.69) and 1.56 (1.07-2.27).

This population-based study shows that fibrinogen increases with age, HbA(1c), smoking, hypertension and a number of components of the metabolic syndrome, independent of major confounders. We also found that poor blood glucose control was associated with CHD.