Abstract
Accelerated atherosclerosis is the main underlying factor contributing to the high risk of atherothrombotic events in patients with diabetes mellitus and atherothrombotic complications are the main cause of mortality. Like with many bodily systems, pathology is observed when the normal processes are exaggerated or uncontrolled. This applies to the processes of coagulation and thrombosis as well. In diabetes, in fact, the balance between prothrombotic and fibrinolytic factors is impaired and thus the scale is tipped towards a prothrombotic and hypofibrinolytic milieu, which in association with the vascular changes accompanying plaque formation and ruptures, increases the prevalence of ischaemic events such as angina and myocardial infarction. Apart from traditional, modifiable risk factors for cardiovascular disease like hypertension, smoking, elevated cholesterol; rheological properties, endogenous fibrinolysis and impaired platelet activity are rapidly gaining significance in the pathogenesis of atherosclerosis especially in diabetic subjects. Blood clot formation represents the last step in the athero-thrombotic process, and the structure of the fibrin network has a role in determining predisposition to cardiovascular disease. It is no surprise that just like platelets and fibrin networks, erythrocytes have been shown to play a role in coagulation as well. This is in striking contrast to their traditional physiological role of oxygen transport. In fact, emerging evidence suggests that erythrocytes enhance functional coagulation properties and platelet aggregation. Among the spectrum of haematological abnormalities in diabetes, erythrocyte aggregation and decreased deformability of erythrocytes predominate. More importantly, they are implicated in the pathogenesis of microvascular complications of diabetes. The morphology of platelets, fibrin networks and erythrocytes are thus essential role players in unravelling the pathogenesis of cardiovascular complications in diabetic subjects.
Highlights
The trend regarding the incidence of type 2 diabetes mellitus is that it is increasing in the general population because of increasing obesity and is likely to subsequently increase the incidence of coronary artery disease
It is known that risk factors such as obesity, hypertension and hypercholesterolemia are crucial to the development of atherosclerosis which results in inflammation [1]
An array of inflammatory diseases, including type 2 diabetes mellitus are associated with increased fibrinogen levels and hypercoagulability which results in markedly changed fibrin morphology, dense matted deposits (DMD) [53]
Summary
The trend regarding the incidence of type 2 diabetes mellitus is that it is increasing in the general population because of increasing obesity and is likely to subsequently increase the incidence of coronary artery disease. In the process of a thrombotic event many parameters (which are increased) play a role, increased levels of fibrinogen feature strongly This is of significance as it causes abnormal fibrin fibre formation visible as dense matted deposits (DMD) and the resulting coagulum causes blood cells to change shape and to be trapped in the abnormal mesh [52]. An array of inflammatory diseases, including type 2 diabetes mellitus are associated with increased fibrinogen levels and hypercoagulability which results in markedly changed fibrin morphology, DMDs [53]. Our research team has shown that when fibrin clots abnormally, erythrocytes are entrapped more tightly inside the clot as indicated in Fig. 2f [51, 56] The factors of both erythrocyte aggregation and fibrinogen interactions cause a changed viscosity which impacts on the optimal functioning of erythrocytes.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
