There is good evidence that patients with migraine with aura but not without aura have about a twofold increased risk of stroke. Why this is so, however, is not known. According to a new study, the cause may be cardiac embolism. Patients from the ARIC study of over 15,000 participants, aged 45 to 64 years who had migraine and stroke, were identified. The mean age of the patients was 59 years. Those with migraine with visual aura had increased risk of cardioembolic ischemic stroke of almost fourfold. Those with migraine without aura did not.
Cardioembolism was diagnosed if records showed evidence of heart valve disease, a recent intracardiac thrombus, bacterial endocarditis, cardiac arterial procedure, and especially paroxysmal atrial fibrillation or flutter. Patent foramen ovale was not considered a cardioembolic source. The role of PFO in causing ischemic stroke in patients older than 55 is controversial. It is seen on autopsy in 25% of the general population, though perhaps 50% of patients with “cryptogenic stroke” may have PFO seen on transesophageal echocardiogram.
The authors propose several mechanisms. Migraine with visual aura may promote vasospasm, activate platelet aggregation, and increase concentration of pro-coagulant factors. Secondly, calcitonin gene-related peptide (CGRP), consistently elevated during a migraine attack, also can cause coronary vasodilatation. Perhaps that effect could trigger coronary blood flow or velocity changes and thus increase risk of atrial fibrillation.
Keep in mind that these results may not apply to people younger than 45. The important take-home message is that migraineurs who have visual aura and who have ischemic stroke of unknown cause may have significant probability of paroxysmal atrial fibrillation as the cause. Thus, it seems prudent that they undergo long-term cardiac monitoring, as findings would lead to anticoagulation, which would serve to lower risk of recurrent stroke.
See Neurology, December 13, 2016, pages 2504-2505 and 2527-2532.