Coagulation-fibrinolysis abnormalities in acute and chronic phases of cerebral thrombosis and embolism.

Abstract

We assayed plasma concentrations of fibrinogen, fibrinopeptide A, plasmin-os plasmin inhibitor complex, D dimer, and antithrombin III activity in 40 patients with cerebral thrombosis and nine patients with cerebral embolism during the acute (<7 days), subacute (7-27 days), and chronic (>28 days) periods and compared these with 69 controls. In cerebral thrombosis, fibrinogen and fibrinopeptide A levels were elevated significantly in all stages (/7<0.001), whereas plasmin-a, plasmin inhibitor complex and D dimer levels were elevated significantly in the subacute and chronic periods. The antithrombin III activity was significantly decreased in the acute stage. The elevation of fibrinogen and plasmin-tt 2 plasmin inhibitor complex levels in the acute stage was significantly greater in patients with an infarct size greater than 10 mm 2 compared to patients with an infarct size less than 10 mm 2 . We observed similar changes in patients with cerebral embolism. These results suggest that enhanced coagulation exists at all stages and endogenous fibrinolysis is activated in the subacute and chronic periods in a large proportion of patients with cerebral thrombosis and embolism.

A panel of biomarkers including caspase-3 and D-dimer may differentiate acute stroke from stroke-mimicking conditions in the emergency department

“…D-dimer, which is a product of the degradation of cross-linked fibrin by plasmin, is the most frequently used indicator of activation of blood coagulation [24]. In agreement with previous suggestions [25], we recently reported that a high level of D-dimer after stroke is an independent predictor of cardioembolic aetiology [10].…”

Etiologic Diagnosis of Ischemic Stroke Subtypes With Plasma Biomarkers

“…Various studies have shown that the coagulation and fibrinolytic systems are activated in cerebral ischemia, and DD is the most frequently used indicator of blood coagulation activation. 23 After stroke, enhancement of the coagulation system reflects the mechanism of thrombus formation and vessel occlusion. In fact, thrombus formation in the cardiac chambers is mainly due to blood stasis, leading to a fibrinrich clot very similar to venous thrombi.…”

Diagnostic Testing for Coagulopathies in Patients With Ischemic Stroke

“…Therefore, these tests should generally be performed when the patient is not in an active thrombotic state and the coagulation and fibrinolytic factors have stabilized, usually 6 to 8 weeks after the thrombotic event. 3,4,15,16 Genetic tests such as the PCR for FVL and prothrombin gene mutation are not influenced by acute thrombosis.…”