Blood coagulation and plasma fibrinolytic enzyme system pathophysiology in stroke.

Abstract

SUMMARY Plasma fibrinogen chromatography is a method for quantification of high molecular weight fibrinogen complexes (HMWFC), native fibrinogen and other fibrinogen derivatives in plasma. Enhanced formation of fibrin, intravascular coagulation, thrombus formation, etc., are reflected by elevation of plasma HMWFC, and the method distinguishes between subjects with normal and pathological rates of fibrin formation.Serial standard blood coagulation assays, including plasma fibrinogen chromatography, and neurological studies were performed on 220 patients admitted to a stroke unit.Findings from patients with cerebral infarction were compared against those of three control groups: (1) normals, (2) a stroke control group and (3) a stroke risk factor group. Plasma HMWFC findings were significantly (p < 0.001) higher in the stroke risk factor group than in the normals. Plasma HMWFC values were significantly higher (p < 0.001) in the cerebral infarction patients than in any of the control groups, and plasma fibrinogen, plasminogen, alpha,-antitrypsin and alpha^macroglobulin also were significantly higher (p < 0.001) in the patients. The greater the degree of initial neurological deficit, the greater were plasma HMWFC values (p < 0.001), and high HMWFC values were associated with poor clinical outcome.Plasma HMWFC values were significantly higher (p < 0.001) in patients with intracerebral hemorrhage, subarachnoid hemorrhage and cerebral embolism.These findings document the fact that a high proportion of stroke patients have coagulopathy, characterized by pathological enhancement of fibrin formation.

Fibrinogen catabolism in patients with type II and type IV hyperlipidemia. Effect of dietary and clofibrate treatment on laboratory findings.

“…16 These studies have included the detection of clinically silent, deep vein thrombosis in postoperative patients 21 and the demonstration of local fibrin deposition in renal disease 27 and myocardial 28 and cerebral infarction. 8 In these acute situations, plasma fibrinogen chromatographic findings have returned to normal after disease resolution. Plasma HMWFC has also been shown to be significantly higher in patients with stroke risk factors, patients with coronary artery disease but a negative history of myocardial infarction, and in those who had experienced myocardial infarction at least 6 months earlier 17 -all conditions in which atherosclerotic disease is considered of primary etiological importance.…”

“…21 Fibrinogen, antithrombin III, a 2 macroglobulin, a, antitrypsin, and plasminogen were assayed by radial immunodiffusion. 8 Radial immunoassays are expressed as corrected mm 2 ; antigen concentration was proportional to this area. Coagulation factor XIII concentration was assayed by the methods of Lorand et al 22 and Ittyerah et al; 23 and the dextran sulphate-precipitated euglobulin lysis activity was assayed by the fibrin plate method.…”

“…7 Yet studies to demonstrate enhanced fibrin formation in patients with atherosclerosis have seldom been attempted. 8 patients with hyperlipidemia Types II and IV (namely, patients at risk of developing age-accelerated atherosclerosis), is unknown. Although studies with isotopically labeled fibrinogen have failed to show a shortened half-life survival time in the atherosclerotic subject, 9 fibrin formation under physiological conditions accounts for only 2% to 3% of overall fibrinogen catabolism.…”

“…Plasma fibrinogen chromatographic studies show that plasma HMWFC is significantly increased in patients with stroke risk factors, documented coronary artery disease, 8 and those followed long after acute myocardial infarction 17 -all conditions in which atherosclerotic disease is considered of primary etiological importance.…”

Do leukocytes have a role in the cerebral no-reflow phenomenon?

“…'8"' The blood changes may be part of the stress response which also elevates fibrinogen and erythrocyte sedimentation rate. 20 Only interventional studies could determine whether the peripheral leukocytosis is pathologically significant in acute stroke victims. The present study lends little support to such a proposal.…”