Target CVD risk in migraine without aura

MIGRAINEURS without aura  should join those who experience aura in being regularly checked for vascular risk factors, after more evidence shows a link between  migraine and an increased risk of cardiovascular disease (CVD).    

A US case-control study involving 6102 migraineurs and 5243 patients without migraine, found those with self-reported migraines with and without aura had double the risk of myocardial infarction and a 50% greater risk of stroke than controls.

They also had almost three times greater risk of claudication after five years, after adjusting for gender, age, disability, treatment and CVD risk factors.

Migraineurs were also more likely than non-migraineurs to have cardiovascular risk factors including diabetes, hypertension and high cholesterol.

The authors said the results confirmed that migraine with aura was not only a risk factor for stroke, but also for myocardial infarction and claudication, as well as for CVD risk factors.

Although the absolute risk was relatively low overall, it was real, they said, and research was needed to define migraineurs at highest risk of these events.

Paul Mitchell, professor of ophthalmology at the University of Sydney, has published previously on the link between migraine and cardiovascular disease.

He said the results confirmed previous evidence, with the current results importantly showing a higher risk of cardiovascular events in patients with migraine with, and also without, aura.

Based on these findings, “it does seem reasonable to target vascular risk factors (e.g. blood pressure, smoking, abnormal blood lipids , overweight, diabetes etc) in people with a history of migraine”, he said.

The authors said while the mechanism for the association between migraine and cardiovascular disease remained unclear, the risk of MI or claudication with migraine might be associated with overall atherosclerosis or co-morbid risk factors.

An editorial said the increased risk of vascular events “cannot be explained by higher prevalence of risk factors alone and supports the notion that endothelial function outside the brain might also be compromised.”

Neurology 2010;74:628-635