Background: Previous reports have suggested an association between elevated fibrinogen and CAD. Few studies have so far investigated the impact of diabetes on fibrinogen levels and its association with coronary artery disease (CAD) and platelet reactivity in diabetic patients that are therefore the aims of the current study. Methods: We measured fibrinogen in 3280 consecutive patients undergoing coronary angiography. Samples were collected at admission for fibrinogen levels assessment. Coronary disease was defined for at least 1 vessel stenosis > 50% as evaluated by QCA. Results: Diabetes was observed in 1201 out of 3280 patients. Diabetic patients were older with more hypercholesterolemia, hypertension, higher BMI, more renal failure, previous MI or coronary revascularization (p < 0.001, respectively) and smoking (p = 0.001). Diabetic patients were more often on ACE-inhibitors, ARBs, b-blockers, calcium-antagonists, diuretics, statins (p < 0.001, respectively), and ASA (p = 0.004). Diabetic patients displayed higher glycaemia and HbA1c (p < 0.001), higher creatinine and triglycerides (p < 0.001) but lower total and HDL cholesterol (p < 0.001) and haemoglobin (p < 0.001). Diabetic patients had higher fibrinogen levels (p = 0.003), however neither diabetes nor glucose homeostasis parameters resulted as independent predictors of hyperfibrinogenemia. Furthermore, among diabetic patients, higher fibrinogen levels did not affect platelet reactivity and were not associated with the prevalence of CAD (adjusted OR[95% CI] = 0.99 [0.82-1.19], p = 0.9). Similar results were found for severe CAD (adjusted OR[95% CI] = 0.94 [0.82-1.08], p = 0.40). Conclusions: Our study showed that diabetes and glycaemic control are not independent predictors of hyperfibrinogenemia. Among diabetic patients, elevated fibrinogen is not associated with platelet reactivity and the prevalence and extent of CAD. (C)

Impact of diabetes on fibrinogen levels and its relationship with platelet reactivity and coronary artery disease: A single-centre study

DE LUCA, GIUSEPPE
Ultimo
2015-01-01

Abstract

Background: Previous reports have suggested an association between elevated fibrinogen and CAD. Few studies have so far investigated the impact of diabetes on fibrinogen levels and its association with coronary artery disease (CAD) and platelet reactivity in diabetic patients that are therefore the aims of the current study. Methods: We measured fibrinogen in 3280 consecutive patients undergoing coronary angiography. Samples were collected at admission for fibrinogen levels assessment. Coronary disease was defined for at least 1 vessel stenosis > 50% as evaluated by QCA. Results: Diabetes was observed in 1201 out of 3280 patients. Diabetic patients were older with more hypercholesterolemia, hypertension, higher BMI, more renal failure, previous MI or coronary revascularization (p < 0.001, respectively) and smoking (p = 0.001). Diabetic patients were more often on ACE-inhibitors, ARBs, b-blockers, calcium-antagonists, diuretics, statins (p < 0.001, respectively), and ASA (p = 0.004). Diabetic patients displayed higher glycaemia and HbA1c (p < 0.001), higher creatinine and triglycerides (p < 0.001) but lower total and HDL cholesterol (p < 0.001) and haemoglobin (p < 0.001). Diabetic patients had higher fibrinogen levels (p = 0.003), however neither diabetes nor glucose homeostasis parameters resulted as independent predictors of hyperfibrinogenemia. Furthermore, among diabetic patients, higher fibrinogen levels did not affect platelet reactivity and were not associated with the prevalence of CAD (adjusted OR[95% CI] = 0.99 [0.82-1.19], p = 0.9). Similar results were found for severe CAD (adjusted OR[95% CI] = 0.94 [0.82-1.08], p = 0.40). Conclusions: Our study showed that diabetes and glycaemic control are not independent predictors of hyperfibrinogenemia. Among diabetic patients, elevated fibrinogen is not associated with platelet reactivity and the prevalence and extent of CAD. (C)
2015
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3256458
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