Abstract
Background and Purpose—
Hypercoagulable
states in migraine patients may play a role in the pathophysiology
underlying the association between migraine and ischemic stroke. This
study aims to provide more insight into the potential association of
headache, ischemic stroke, and the intrinsic coagulation pathway.
Methods—
We
included patients from the RATIO study (Risk of Arterial Thrombosis in
Relation to Oral Contraceptives), a Dutch population-based case-control
study including young women (age <50) with ischemic stroke and
healthy controls. We defined a headache group based on a questionnaire
on headache history. Intrinsic coagulation proteins were measured
through both antigen levels (FXII, FXI, prekallikrein, HK [high
molecular weight kininogen]) and protein activation, determined by
measuring activated protein complex with C1esterase-inhibitor
(FXIIa-C1-INH, FXIa-C1-INH, Kallikrein-C1-INH) or antitrypsin-inhibitor
(FXIa-AT-INH). We calculated adjusted odds ratios and performed an
interaction analysis assessing the increase in stroke risk associated
with high levels of intrinsic coagulation and history of headache.
Results—
We
included 113 ischemic stroke cases and 598 healthy controls. In total,
134 (19%) patients had a history of headache, of whom 38 were cases and
96 controls. The combination of headache and high intrinsic coagulation
protein levels (all but FXII antigen level and both FXIa-inhibitors) was
associated with an increase in ischemic stroke risk higher than was
expected based on their individual effects (adjusted odds ratio FXI
antigen level alone: 1.7, 95% CI, 1.0–2.9; adjusted odds ratio headache
alone: 2.0, 95% CI, 1.1−3.7; combination: 5.2, 95% CI, 2.3−11.6)
Conclusions—
Headache and high intrinsic coagulation protein levels may biologically interact, increasing risk for ischemic stroke.
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