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Posted on Thursday April 2, 2026 in Heart Rhythm Problems
An article by Dr Edward Leatham, Consultant Cardiologist © 2026 E.Leatham
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This blog is for people who have a diagnosis of atrial fibrillation or atrial flutter – especially if it is paroxysmal or persistent.
Patients diagnosed with atrial fibrillation (AF) who have a low CHA₂DS₂-VASc score (0–1) are often reassured that their risk of stroke is minimal. In many cases, this is correct when considering long-term stroke prevention. For more information about this group and CHA₂DS₂-VASc calculator see separate blog
However, there is an important and often underappreciated exception:
👉 The period surrounding cardioversion
Even patients with otherwise low stroke risk may face a transient but clinically significant risk of thromboembolism when AF is terminated—whether spontaneously or with medical intervention.
When atrial fibrillation or atrial flutter terminates and normal sinus rhythm is restored, the electrical rhythm may normalise immediately—but the mechanical function of the atrium does not recover instantly.
This temporary impairment is known as atrial paresis (also referred to as atrial stunning).
During this phase:
Crucially, this occurs despite a normal ECG rhythm.
This disconnect between electrical recovery and mechanical recovery is the key reason why stroke risk persists after cardioversion.
The left atrial appendage is a small, pouch-like structure arising from the left atrium. Under normal conditions, it contracts effectively and prevents blood stagnation.
However, during AF—and especially during atrial paresis:
It is well established that the majority of AF-related embolic strokes originate from the left atrial appendage.
The duration of atrial fibrillation prior to cardioversion is one of the most important determinants of thromboembolic risk.
👉 This means that even a young, otherwise low-risk patient may be at significant stroke risk if AF persists beyond 24 hours.
A low CHA₂DS₂-VASc score reflects baseline stroke risk, but it does not account for transient high-risk periods, such as:
This occurs when the heart restores normal sinus rhythm without medical intervention.
Common triggers include:
Most episodes resolve within 24 hours, particularly in younger patients. However:
This involves the use of medications to restore sinus rhythm.
Common agents include:
These are typically administered under medical supervision and may act over hours to days.
This is the most direct and controlled method.
✅ Critical Point:
Atrial paresis occurs after all forms of cardioversion, including spontaneous conversion.
When AF or atrial flutter has been present for more than 24 hours, there is a risk that thrombus may already have formed within the left atrium.
This approach reduces the risk of dislodging pre-existing thrombus and prevents new clot formation during atrial paresis.
In certain cases, a TOE (transoesophageal echocardiogram) can be used to visualise the left atrial appendage directly.
View a different blog to see what a left atrial appendage thrombus looks like on TOE
The period immediately following restoration of sinus rhythm is particularly important.
This reflects:
👉 Importantly, this risk exists even if the patient feels well and ECG is normal.
For patients treated with warfarin:
For patients on direct oral anticoagulants (DOACs), adherence and correct dosing are essential.
Patients with a low CHA₂DS₂-VASc score are often not anticoagulated long-term. However:
👉 This does not apply during the peri-cardioversion period
Key points:
A practical way to understand this:
Stroke prevention in atrial fibrillation is not simply about long-term risk scoring.
👉 It is also about timing, physiology, and atrial recovery
Recognising the role of atrial paresis ensures that even low-risk patients receive appropriate short-term protection during vulnerable periods.
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