Abstract
Altered fibrin clot structure has been reported both in patients with coronary artery disease (CAD) and those with type 2 diabetes mellitus (DM2). The aim of the present study was to evaluate plasma fibrin clot permeability and susceptibility to lysis in patients with DM2 and CAD. We studied 132 consecutive CAD patients, including 67 subjects with DM2, scheduled for elective coronary artery bypass grafting surgery. Ex vivo plasma fibrin clot permeability (Ks) and lysis time (t50%) induced by 1 μg/mL recombinant tissue plasminogen activator (tPA), along with plasma levels of plasminogen activator inhibitor-1 (PAI-1), thrombin activatable fibrinolysis inhibitor (TAFI), tPA, von Willebrand factor (vWF), P-selectin, soluble CD40 ligand (sCD40L), were measured. Diabetic and non-diabetic patients did not differ in regard to demographics and remaining cardiovascular risk factors. Concomitant DM2 was associated with higher glucose (+24.3 %, p < 0.001), fibrinogen (+9.0 %, p = 0.037), PAI-1 (+58.7 %, p < 0.001), tPA (+24.0 %, p < 0.001) and P-selectin (+12.2 %, p < 0.001). Compared with the non-diabetic group, the CAD patients with DM2 had lower Ks (-6.1 %, p = 0.02) and prolonged t50% (+5.1 %, p = 0.04). Multiple regression analysis of the whole study group showed that vWF, PAI-1, fibrinogen and DM2 were the independent predictors of t50% (R 2 = 0.58, p < 0.001), while only vWF was an independent predictor of Ks (R 2 = 0.22, p < 0.001). This study indicates that DM2 is potent enough to unfavorably affect plasma fibrin clot characteristics despite abnormal clot phenotype typically observed in CAD. Of note, platelet and endothelial markers appear to contribute to fibrin clot properties in CAD concomitant with DM2.
Highlights
Type 2 diabetes mellitus (DM2) is an independent risk factor of coronary artery disease (CAD) and increases the risk of CAD two to three times [1]
Altered fibrin clot structure has been reported both in patients with coronary artery disease (CAD) and those with type 2 diabetes mellitus (DM2)
Multiple regression analysis of the whole study group showed that von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1), fibrinogen and DM2 were the independent predictors of t50% (R2 = 0.58, p \ 0.001), while only vWF was an independent predictor of Ks (R2 = 0.22, p \ 0.001)
Summary
Type 2 diabetes mellitus (DM2) is an independent risk factor of coronary artery disease (CAD) and increases the risk of CAD two to three times [1]. The coexistence of DM2 and CAD impairs cardiovascular prognosis and increases the risk of ischemic events [3, 4] This observation can be explained by several mechanisms, including concomitant risk factors such as arterial hypertension, obesity, and metabolic abnormalities such as hyperglycemia, hyperinsulinemia, insulin resistance and dyslipidemia, which are responsible for endothelial dysfunction [5]. It has been demonstrated that atherosclerotic plaques in DM2 patients are more prone to rupture [6] Both DM2 as well as CAD have been reported to unfavorably affect structural and functional characteristics of a fibrin clot relatively resistant to mechanical and enzymatic degradation [7,8,9]. There is evidence that fibrin is a consistent component of atherosclerotic plaques, and that the presence of fibrin can promote their growth, being involved in the progression of atherosclerosis [17]
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