Cardiac Clot Formation Unique in Atrial Fibrillation-Related Stroke

Approximately 1 in 4 individuals will develop atrial fibrillation (AF). Most disconcerting is their potential for hemorrhagic and ischemic stroke, as this risk increases up to 5-fold in AF patients.

AF’s startling prevalence and severity have not dispelled misconceptions and challenges associated with managing related stroke and transient ischemic attack (TIA).

Despite advances in imaging technology, the precise mechanism of cardiac clot formation in AF patients remains unknown. Thrombi are typically less than a few millimeters in size, which may help explain low transesophageal echocardiography detection rates in patients with a recent stroke or TIA.

Understandably, not all strokes in AF patients are directly attributable to AF itself; other causes include intracranial large artery stenosis, small vessel disease, and atherosclerotic disease of neck vessels. AF patients treated with low-dose aspirin do see a moderate stroke reduction, but this may be explained by reduction in non-cardioembolic stroke alone.

AF-related stroke consistently results in greater disability and higher mortality compared with other stroke subtypes. The cause of this may be increased comorbidities in the AF population (who are usually elderly), though an independent mechanism has also been proposed; infarcts observed in AF are typically larger and often affect motor areas or cortical regions linked to higher brain functions such as speech, attention, and cognition.

Despite the well-documented efficacy of primary and secondary prevention, prescribers are often excessively cautious about using oral anticoagulants. However, the risk of intracranial hemorrhage secondary to vitamin K antagonist use is about 0.3% to 1% per year, so caution verging on fear is unfounded.

AF patients who have suffered a stroke or TIA have a higher incidence of ischemic recurrence and benefit from long-term anticoagulation. While current best practice guidelines advise against urgent anticoagulation in patients with ischemic stroke, they provide no further information on appropriate timing.

A majority of physicians make anticoagulation timing decisions based on clinical severity and infarct size. Many physicians choose to postpone anticoagulation until 5 to 14 days post-stroke for larger infarct volumes. In patients with small infarct volumes, anticoagulation typically begins within 24 to 72 hours of stroke onset.

These best practice recommendations were published in a review article in The European Journal of Internal Medicine.