Atrial thrombogenesis in atrial fibrillation

Abstract

Atrial fibrillation (AF) is the most common cause of thromboembolic complications. The risk of suffering a thromboembolic complication depends on the accompanying cardiac risk factors and the patient's age. For patients who have an increased risk, which is now classified using the CHA2DS2-VASc score, initiation of long-term oral anticoagulation is the first-line treatment. In AF, thrombi arise in the left atrial appendage. The present review will summarize the basic pathophysiology of thrombogenesis in AF and will provide the molecular basis of a process called prothrombotic endocardial remodeling. Despite oral anticoagulation being a central component of therapy, the present results can be used to support concomitant therapy with statins, angiotensin II blockers, etc. to inhibit atrial thromogenesis.

Atrial Cardiomyopathy: Pathophysiology and Clinical Consequences

“…Studies have demonstrated endocardial changes in atrial tissue specimens. Prothrombogenic factors (vWF, adhesion molecules VCAM-1, P-selectin, MCP-1) are expressed at the surface of endothelial cells causing platelets and leucocytes to adhere to the atrial endocardium in particular in the left atrial appendage [83,193,209], which causes the initiation of thrombus formation [209,210]. Diseases or conditions such as diabetes mellitus, heart failure, and ageing (CHA2DS2VASc Parameters) are known to increase alterations by oxidative stress pathways within endothelial cells, and thereby further increase the expression of prothrombogenic molecules.…”

“…Recently, post hoc studies from large randomized controlled trials suggested that the burden of AF (Figure 3) as well as the type of AF (paroxysmal versus persistent/permanent AF) might be a factor, which drives differences in patient outcome [213][214][215][216][217]. Such clinical differences might be explained at least to some extent by differences in atrial cardiomyopathies and ventricular oxidative stress levels during various types of AF [210]. The recent hypothesis is that the burden of AF contributes to differences in the occurrence of specific clinical events such as cognitive decline, stroke, or myocardial infarction.…”

1199Sex differences in stroke and major adverse clinical events in patients with atrial fibrillation: a systematic review and meta-analysis of 993,600 patients

“…Sex-gender differences were reported in arterial structure, alterations in blood flow, shear stress and endothelial function [62]. Furthermore, an influence of sex has been described in atrial structure and function, which could affect atrial thrombogenesis mechanisms [63][64][65]. Also, gender-related alterations in inflammatory and pro-coagulant markers, thrombogenic particles and platelet aggregation may play a role [62].…”

Advances in cardiac cellular electrophysiology – Relevance for clinical translation

“…The last review of this series addresses the problem of thrombogenesis in AF as a major contributor to the high risk of stroke in this disease [19]. The authors recapitulate our current understanding of the coagulation cascade and explain the modern concept of "prothrombotic endocardial remodelling".…”