This review highlights the emerging understanding that platelets contribute to thromboembolism in atrial fibrillation primarily through fibrin stabilization rather than aggregation.
Should not yet change AF antithrombotic practice; hypothesis-generating for fibrin stabilization as key embolic driver in left atrial thrombi.
Thromboembolic 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 AF.
No takes yet. Share an insight, caveat, or question.
Gosk−Bierska et al. (2015) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: