Clinical significance of new coagulation and fibrinolytic markers in ischemic stroke patients.

Several measures of haemostasis and fibrinolysis were tested in 34 patients with cerebral haemorrhage and 47 patients with cerebral infarction within 11 days of the event. No significant differences were found between the two groups, but in comparison with a control group the following values were significantly elevated as the result of coagulation and fibrinolysis: fibrin monomers, thrombin-antithrombin-III, D-dimers and tissue plasminogen activator activity. In approximately 11 % of the patients the fibrin monomer levels were elevated to such an extent (> 30 mmol/1) that they were compatible with activation of the coagulation system. It is not possible to differentiate between cerebral infarction and cerebral haemorrhage by means of coagulation or fibrinolysis parameters. In the fibrin-monomer-negative group 22 % of the patients died, compared with 56% in the fibrin-monomer-positive group. Thus a state of hypercoagulability may have a negative effect on prognosis. Follow-up of 4 patients with cerebral haemorrhage showed that the abnormalities of coagulation and fibrinolysis parameters could last as long as 4 weeks.

Section: Discussionsupporting

confidence: 92%

Haemostasis and Fibrinolysis after Recent Stroke

Franke¹,

Buscher²,

Wersch

1992

“…3, 4), since atherosclero sis is strongly dependent on age. This age-related increase in TAT and other hemostatic marker levels was also found by Ono et al [22], The normal distribution for TAT, Fl+2, and probably for other recently developed markers of hemostatic activity should therefore be cor rected for age.…”

Section: Discussionsupporting

confidence: 81%

“…Ono et al [22] found that the differences of TAT and D-dimer levels between patients and healthy controls increased with age. In our study, even with a limited number of patients, a relationship of TAT and Fl+2 levels and older age ( > 70 years) was also suggested.…”

Section: Discussionmentioning

confidence: 99%

“…In an earlier study [3 1 ] significant dynamic fluctua tions o f TAT levels were not seen during daytime in healthy subjects, but these fluctuations may occur with longer intervals, especially in patients with atherosclerotic disease, in whom periodic exacerbation of athcrolhrombotic activity is known to occur. Several studies recently discussed the existence of a prcthrombotic state [7]; this condition has been evoked in patients with recent stroke, but on the basis of only a single measurement, which also was a 'postthrombotic' analysis [22,32].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Hemostatic Activity in Patients with a Transient Ischemic Attack or Minor Ischemic Stroke with or without Chronic Non-Valvular Atrial Fibrillation

Pop

Meeder²,

Oudenaarden

et al. 1993

In this study we determined the prevalence of hemostatic hyperactivity in patients with recent cerebral ischemia and its relation to the presence of chronic nonvalvular atrial fibrillation. Plasma levels of thrombin-antithrombin III complexes (TAT) and prothrombin fragments 1+2 (F1+2) were used as hemostatic parameters and were studied in four groups of 14 patients each: patients with or without recent cerebral ischemia, and with or without chronic nonvalvular atrial fibrillation. Irrespective of their cardiac rhythm, patients with recent cerebral ischemia showed significantly higher F1+2 levels than patients without signs of previous cerebral ischemic events (median 1.16 vs. 0.96 nmol/1; p < 0.001). No significant differences were found between the TAT levels in the different groups. A higher level of hemostatic activity was found in the patients over 70 years of age compared to those younger than 70 years.

“…Coagulation and fibrinolysis are activated to different degrees in various subtypes of acute ischemic stroke [19, 20, 21, 22, 23, 24]. These differences are ascribed to the different pathogenesis of cardioembolic (CE) and non-cardioembolic (non-CE) ischemic stroke, with more pronounced activation of the coagulation system in CE stroke as compared with atherothrombotic or lacunar strokes [24, 25, 26].…”

Section: Introductionmentioning

confidence: 99%

Lipoprotein(a), Other Lipoproteins and Hemostatic Profiles in Patients with Ischemic Stroke: The Relation to Cardiogenic Embolism

Dahl

Kontny²,

Slagsvold³

et al. 2000

Lipoprotein and hemostatic profiles including coagulation inhibitors were determined in 136 patients with acute ischemic stroke. Based on clinical examination, cerebral computed tomography, Doppler ultrasonography of precerebral arteries and transthoracic echocardiography, the strokes were classified as cardioembolic (n = 38), non-cardioembolic (n = 92), and mixed cardioembolic/hypertensive (n = 6). Patients with cardioembolic stroke were older than patients with non-cardioembolic stroke. Lipoprotein(a) was higher in the cardioembolic than in the non-cardioembolic group. Lipoprotein(a) was not significantly correlated to the other lipid levels and may represent an independent lipid risk factor. The non-cardioembolic group had higher levels of total cholesterol, triglycerides, total cholesterol/high-density lipoprotein cholesterol ratio, low-density lipoprotein cholesterol, apolipoprotein A1, and apolipoprotein B. The cardioembolic group had higher concentrations of fibrinogen and D-dimer, and lower levels of antithrombin, protein C, protein S and heparin cofactor 2 than the non-cardioembolic group. The differences in the hemostatic profile are consistent with thrombosis due to activated coagulation being more involved in the pathogenesis of cardioembolic than of non-cardioembolic stroke. Lipoprotein(a) seems to be more associated with coagulation markers of thrombosis than with atherosclerosis, whereas the other lipids mainly seem to be risk factors for atherosclerosis.