AF is clasically considered a cause of embolic strokes due to blood stagnation in the atrium. But AF is also a marker for left atrial dysfunction and fibrosis, which can lead to emboli, and strokes in AF often occur at a distance from AF episodes. Which argues for AF as a marker for atrial dysfunction/fibrosis. But AF also contributes to atrial fibrosis and dysfunction itself; AF begets more AF so it does have a causal role as well.
To what extent is AF a direct cause of stroke vs. a marker for left atrial dysfunction that is the proximal cause?
Do the majority of emboli really come from the LA appendage? What proof do we have of this? If they do, why isn’t LAA closure more effective than it has been?
How can we prevent atrial fibrosis and AF? Major risk factors?
If atrial dysfunction is a primary cause of emboli, how can we best evaluate the status of the atrium (echo parameters of LA size and function, bnp, troponins, mri)? Could an assessment of atrial function be used to better risk stratify patients for anticoagulation, better than or in addition to CHADS-VASC? Are other tools superior to CHADS-VASC?
Is there any role for CHADS-VASC or tools evaluating atrial function in patients without a history of AF? To target patients for screening for AF or even to consider anticoagulation in the absence of AF?
What is the role of rhythm control in managing AF?
Does it make sense to intervene early in the progression of AF (with drugs or ablation)?