(Stroke. 2000;31:1856.)
© 2000 American Heart Association, Inc.
Original Contributions |
From the Divisions of Neurology (R.C., F.B.) and Hematology (S.S., J.R.L.), Montreal General Hospital, and Department of Epidemiology and Biostatistics (C.W., F.R.), McGill University, Montreal, and the Division of Neurology, Hôpital de lEnfant Jésus, Laval University, Quebec City (A.M., D.S., B.L.), Canada.
BackgroundIncreased levels of markers of hemostasis may assist in the determination of the extent of carotid occlusive disease and the identification of neurologically intact individuals at increased risk of ischemic events.
MethodsWe conducted a prospective study of 304 subjects,
including 82 with a recent (
7 days) transient ischemic attack
(TIA), 157 asymptomatic individuals with a cervical bruit,
and 65 control subjects. Baseline evaluation included a neurological
assessment, ECG, cervical ultrasonography, and cerebral CT and/or MRI.
Levels of markers of coagulation and fibrinolytic activity were also
determined. Results were analyzed in relation to the degree of
carotid disease and the subsequent occurrence of cerebral and cardiac
ischemic events.
ResultsOver a mean follow-up period of 2.8 years (SD, 1.3
years), 114 ischemic events occurred. Survival analyses
showed that prothrombin fragment 1.2 (F1.2) was a predictor
of time to cerebral and cardiac ischemic events in the combined
TIA and asymptomatic bruit group (relative risk [RR],
1.46; 95% CI, 1.18 to 1.81) as well as in the asymptomatic
bruit group separately (RR, 1.70; 95% CI, 1.14 to 2.53). In the TIA
group, both F1.2 (RR, 2.36; 95% CI, 1.19 to 4.68) and
severe (
80%) carotid stenosis (RR, 3.53; 95% CI, 1.19 to
10.51) were predictive of time to ischemic stroke, myocardial
infarction, or vascular death.
ConclusionsIn patients with TIAs and in asymptomatic individuals with cervical bruits, F1.2 levels were found to be independent predictors of subsequent cerebral and cardiac ischemic events. Our results are consistent with an active role of the coagulation system through upregulation of thrombin in carotid disease progression and in the pathogenesis of ischemic events in patients at risk.
Key Words: : cerebral ischemia diagnosis hemostasis prognosis stenosis
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