Atrial fibrosis weighed as key stroke trigger

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Atrial fibrosis weighed as key stroke trigger

An essential part of the arrhythmic substrate in AF is atrial fibrosis. According to the available data, atrial fibrosis contributes to the arrhythmia patients’ increased risk of stroke. When examined by late-gadolinium enhancement MRI, atrial fibrosis manifests as atrial remodelling including morphological, functional, and electrical features in patients with embolic stroke of uncertain source (ESUS), who are believed to have AF but are infrequently shown to have it.

The authors of this study highlight the evidence that atrial illness, including fibrosis, increases the risk of an ischemic stroke in people with AF as well as in the ESUS population, where it has been associated to both recurrent stroke and new-onset AF. They also talk about how this link may affect future studies that could clarify the causes of stroke and how to prevent them in the AF and ESUS groups.

Blood stasis, hypercoagulability, and tissue injury are thought to play a role in the mechanisms underlying cardio-embolic stroke in AF, which are similar to other thrombotic events in vascular beds as previously described by Virchow.

An important part of laying the groundwork for AF is played by atrial fibrosis. Myocyte loss and collagen replacement in the extracellular space lead to fibrosis. This causes an increase in the heterogeneity of the atrial tissue, which when combined with electrical remodelling of the atrial myocytes, alters the anisotropy and conduction velocity of electrical wave propagation within the atrial myocardium and increases the likelihood of arrhythmia initiation and sustenance.

Atrial fibrosis as key stroke trigger

In light of supporting data from the AF patient group, the link between atrial fibrosis and stroke is receiving increased attention. Atrial fibrosis and stroke may be related independently of AF, according to new research in individuals with embolic stroke of unknown cause (ESUS).

According to Dr. Deependra pandey, AF causes hypercoagulability and stasis in the presence of cardiovascular risk factors, which then results in thrombus development and systemic embolization. Patients who have paroxysmal AF have a lower risk of stroke than those who have persistent and chronic patterns of AF, which are often linked to a larger burden of arrhythmia. Patients with paroxysmal AF have an increased risk of stroke when their AF burden is larger.

These results raise concerns about AF’s potential contribution to thrombo-embolic stroke in this cohort. The researchers of the LOOP study came to the conclusion that not all cases of AF are worth screening for and anticoagulating for. This is because anticoagulation based on detected arrhythmias using implantable loop recorders in patients with stroke risk factors did not show a beneficial decrease in stroke rates.


A complex disease, atrial fibrosis exhibits quantifiable abnormalities in cardiac imaging and biomarkers. Atrial fibrosis has been linked to both atrial arrhythmia and thromboembolic illness, according to current research. However, the exact mechanism by which fibrosis causes thrombus formation and predisposition to embolization, including stroke, is yet unknown. Fibrosis may potentially be a sign of total cardiovascular risk, including stroke, given that it is linked to several cardiovascular risk factors.

Fibrosis may have a significant role in the development of an electromechanical dysfunctional state that results in stasis and localised contractile dysfunction that may create a nidus for thrombus formation in the context of AF. The mechanics of fibrosis might potentially be at work. The pathophysiology of a hypercoagulable state is also connected to research into these processes. utilising computational modelling of AF absence, electromechanical dysfunction, and changed blood flow dynamics in tissue fibrosis discovered through cardiac imaging, is currently underway.



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