Hemostatic markers in patients at risk of cerebral ischemia

Citation
R. Cote et al., Hemostatic markers in patients at risk of cerebral ischemia, STROKE, 31(8), 2000, pp. 1856-1862
Citations number
40
Categorie Soggetti
Neurology,"Cardiovascular & Hematology Research
Journal title
STROKE
ISSN journal
00392499 → ACNP
Volume
31
Issue
8
Year of publication
2000
Pages
1856 - 1862
Database
ISI
SICI code
0039-2499(200008)31:8<1856:HMIPAR>2.0.ZU;2-M
Abstract
Background-Increased levels of markers of hemostasis may assist in the dete rmination 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 (less than or equal to 7 days) transient ischemic attack (TIA), 1 57 asymptomatic individuals with a cervical bruit, and 65 control subjects. Baseline evaluation included a neurological assessment, EGG, cervical ultr asonography, and cerebral CT and/or MRI. Levels of maskers of coagulation a nd fibrinolytic activity were also determined. Results were analyzed in rel ation to the degree of carotid disease and the subsequent occurrence of cer ebral and cardiac ischemic events. Results-Over a mean follow-up period of 2.8 years (SD, 1.3 years), 114 isch emic events occurred. Survival analyses showed that prothrombin fragment 1. 2 (F-1.2) was a predictor of time to cerebral and cardiac ischemic events i n the combined TIA and asymptomatic bruit group (relative risk [RR], 1.46; 95% CT, 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, 3.36; 95% CI, 1.19 to 4.68) and severe (greater than or equal to 80%) carotid ste nosis (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 cerv ical bruits, F-1.2 levels were found to be independent predictors of subseq uent cerebral and cardiac ischemic events, Our results are consistent with an active role of the coagulation system through upregulation of thrombin i n carotid disease progression and in the pathogenesis of ischemic events in patients at risk.