Role of Platelets in Thromboembolism in Patients with Atrial Fibrillation

Abstract

of patients with AF is diversified. The rate of thromboembolic complications, predisposing factors and destination of embolism are different in valvular atrial fibrillation (VAF) and non-valvular atrial fibrillation (NVAF). Patients with VAF have a higher risk of thromboembolism and a higher prevalence of thrombus location within the body of the left atrium compared to NVAF. VAF is also associated with higher propensity for non-cerebral thromboemboli than in NVAF [5]. There are many as yet unanswered questions surrounding the increased thrombotic tendency in AF. One of the crucial questions is what determines the fact that a thrombus in the left atrium remains in situ in some patients, while in others it breaks off and leads to embolic complications.As in other disorders, the risk of thromboembolic complications in AF is related to the triad of factors proposed by Rudolf Virchow: abnormalities in blood flow, endocardial/vessels wall damage and alterations in blood composition.Symptomatic thromboembolic complications are diagnosed annually on average in 5% of patients with atrial fibrillation (AF); however, the incidence rate of these complications varies over a broad range, from 0.5 to over 20% per year depending on coexisting risk factors [1]. Thromboembolic complications secondary to AF are a major cause of mortality and disability. The most common complication of AF is stroke, accounting for between 80% and over 90% of all embolic events [2]. Embolization of peripheral arteries with thrombotic material originating in the left atrium occurs much less commonly; however, in the group of patients having surgery due to peripheral embolism, 60-95% are diagnosed with AF [3].Thrombus formation in the left atrium can be triggered by a range of factors, both inherited and acquired. It is necessary to take into account factors directly associated with the cardiac rhythm disorder and concomitant diseases [4] AbstractThromboembolic complications of atrial fibrillation (AF) are a major cause of morbidity and mortality but the mechanism of its process remain poorly understood. There are many as yet unanswered questions surrounding the increased thrombotic tendency in AF. One of the crucial questions is what determines the fact that a thrombus remains in the left atrium in situ in some patients, while in others it breaks off and leads to embolic complications. Recent studies indicated an important role of platelets in the left atrial's thrombus formation and suggest that the embolic potential of left atrial thromboses depends on the involvement of platelets in the process of fibrin stabilization rather than aggregation. New methods for investigating platelets function, such as the analysis of transcription activity of RNA coming from platelets contained in thrombi formed in AF, creates an opportunity for studying populations of platelets that are directly involved in homeostatic clot formation. In this paper we present current opinions on the participation of platelets in the pathogenesis of thromboembolism in patients with...

Impact of Thrombocytopenia in Patients With Atrial Fibrillation Undergoing Left Atrial Appendage Occlusion: A Propensity-Matched Comparison of 190 Consecutive Watchman Implantations

“…In the current study, cTCP patients had comparable rates of clinical thromboembolism to the control group, but the occurrence of stroke was independently less frequent in patients with a lower absolute platelet count. Our result was consistent with the conclusion in other studies (24,25) that patients who presented with ischemic strokes showed significantly higher platelet counts at baseline. It is also well-acknowledged that AFrelated hemodynamic abnormality can result in blood stasis in the left atrium, elevated intra-atrial pressure, and histological lesions in the endothelial lining of the atrial walls, followed by aggregated platelets releasing inflammatory mediators and substances to facilitate coagulation (26,27).…”

Reversible thrombocytopenia during hibernation originates from storage and release of platelets in liver sinusoids

“…Dislodging of such a thrombus upon restoration of blood flow may cause life-threatening pulmonary embolism (White 2003). In addition to venous thromboembolic complications, platelets are involved in arterial thrombus formation during relative stasis of blood, specifically in the cardiac atria in atrial fibrillation (Gosk-Bierska et al 2016;Watson et al 2009), which is associated with an increased risk of cerebrovascular accidents with a 30 day mortality as high as 55% (Bekwelem et al 2015). Furthermore, platelets can initiate thrombosis in vasculitides and in atherosclerotic blood vessels by adhering to the inflamed, activated endothelium (Emmi et al 2015;Nieswandt et al 2011).…”

Direct oral anticoagulation and severe obesity – One size fits all?

“…Even during phases of sinus rhythm, blood from patients with AF exhibits enhanced capacity for thrombin generation along with an increased clot density and resistance to thrombolysis [1] . Haemostatic deregulation progresses with AF severity in disease-matched patient cohorts, indicating that shifts in coagulation and fibrinolysis can be independently associated with the state of AF per se , and do not arise solely from the accompanying cardiometabolic co-morbidities [2] . Yet the causal relationship between AF and thromboembolism is complex and not fully understood.…”