Hemostatic Markers in Patients at Risk of Cerebral Ischemia

Autor: Robert Côté, Christina Wolfson, Susan Solymoss, Ariane Mackey, Jacques R Leclerc, Denis Simard, Fabrice Rouah, France Bourque, Barbara Léger
Rok vydání: 2000
Předmět:
Zdroj: Stroke. 31:1856-1862
ISSN: 1524-4628
0039-2499
DOI: 10.1161/01.str.31.8.1856
Popis: Background —Increased 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. Methods —We 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. Results —Over 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 (F 1.2 ) 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 F 1.2 (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. Conclusions —In patients with TIAs and in asymptomatic individuals with cervical bruits, F 1.2 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.
Databáze: OpenAIRE