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.
