Ultrastructural analysis of platelets and fibrin networks in stroke patients

Abstract

Ischaemic stroke represent more than 80% of the total stroke instances. The location of the occlusion and the amount of brain tissue involved determines the effect of the stroke. Stroke can result in paralysis, memory loss, speech impairment and even a “lock-in” state. The amount of neuronal damage will determine whether these symptoms will be temporary or permanent. Stroke is deemed the second leading cause of death for individuals over the age of 60. According to the World Stroke Organization (WSO) every six seconds stroke claims a life, regardless of age or gender. Stroke is a global burden and the medical costs and disability related to stroke in America for 2010 was projected at almost $73.7 billion. The morphology of platelets, fibrin networks and erythrocytes as well as the differential white blood cell counts of 20 thrombo-embolic ischaemic stroke patients were investigated. Internal and external alterations were revealed in the platelets of stroke patients when compared to healthy controls. The decreased numbers of alpha granules in the platelets of the stroke patients indicated these platelets to be activated. Substances released by activated platelets promote fibrin network structure, specifically the formation of fibrin strands and accumulation of additional platelets. The fibrin network of healthy individuals consists of major, thick fibers with minor, thin fibers distributed between them. The fibrin network of stroke patients exhibited an abnormally layered and matted ultrastructure comprising of mainly thin, minor fibrin fibers packed closely together. An uncharacteristic circular morphology was also observed. These alterations in the fibrin network indicate the activated platelets to be actively involved in the thrombotic event. Neuronal damage related to stroke is also advanced by the vasoactive substances released by activated platelets. It can therefore be deduced that the morphology of the fibrin network is altered long before the concrete thrombotic event transpire. Large numbers of abnormal erythrocytes were distinguished in the blood of stroke patients. Among these abnormal forms of erythrocytes specifically codocytes, knizocytes, stomatocytes and echinocytes were identified. Abnormal erythrocyte forms were significantly increased in hypertensive patients and females independently. Alterations in the ultrastructure of erythrocytes disturb blood flow in the microcirculation and could possibly augment the ischaemic event. Inflammation is closely related to ischaemic stroke. An increased monocyte count and a reduced number of neutrophils were a significant feature among all the stroke patients of this study. Patients with hypertension as well as patients consuming aspirin on a daily basis showed the greatest influence on the observed differential white blood cell counts. These morphological alterations observed in the platelets, fibrin network and erythrocytes as well as the differential white blood cell count could be incorporated in an analysis regime that could probably indicate an impending thrombotic event. Therefore treatment could be initiated before the ischaemic event to possibly prevent the stroke. For future studies a larger study population, a more refined patient enrolment as well as the analysis of follow-up blood samples from patients could substantiate the above-mentioned findings and provide additional information concerning the thrombotic event and the effectiveness of treatment procedures.