Ischemic Stroke Mechanism and Likelihood of Having a Positive Family History of Stroke

Abstract

P122 Introduction: It is not known whether the magnitude of the inherited component to ischemic stroke risk varies according to presumed mechanism. Differences in familial aggregation of stroke might imply differences in the magnitude of inherited stroke risk. Methods: Probands were eligible for entry into a two-center prospective consecutive patient registry if they presented with an ischemic stroke within 180 days of onset of symptoms. Stroke was defined using WHO criteria. A stroke was considered ischemic if CT or MR imaging done within 7 days of onset of symptoms failed to reveal an alternative diagnosis. Probands were excluded if they had onset of symptoms within 48 hours of a cerebrovascular or cardiovascular proceedure or within 60 days of a nontraumatic subarachnoid hemorhage. Probands were also excluded if they were known to have: CADASIL, Fabry’s disease, homocysteinuria, MELAS, sickle cell disease, mechanical aortic or mitral valve, or biopsy-proven CNS vasculitis. Proband family history was obtained by systematic interview of the proband or next-of-kin. Proband past medical history was obtained by proband interview, record review, or both. A neurologist confirmed the diagnosis of and assigned a TOAST subtype to all index ischemic strokes. A positive family history was defined as a history of stroke in at least one parent or full sibling. Results: We enrolled 283 probands (median age, 75 yrs; male, 52%). Frequencies of TOAST subtypes were: cardioembolic, 17.0% (n=48); large-vessel, 24.7% (n=70); small-vessel, 23.0% (n=65); other, 2.5% (n=7); and unknown, 32.9% (n=93). Frequencies of positive family history by proband ischemic stroke subtype were: cardioembolic, 43.8% (95%CI, 29.5–58.8); large-vessel, 40.0% (95%CI, 28.5–52.4); small-vessel, 47.7% (95%CI, 35.1–60.5); other, 42.9% (95%CI, 9.9–81.6%); and unknown 48.8% (95%CI, 37.9–59.0). Frequencies were not significantly different among subtypes (P=0.718, chi square). Conclusions: The magnitude of inherited risk may not differ dramatically for various clinical subtypes of ischemic stroke. Qualitative differences in inherited stroke risk may exist at the molecular level.