Stroke and Blood Coagulation

Todd, Margaret; McDevitt, Ellen; McDowell, Fletcher

doi:10.1161/01.str.4.3.400

Cited by 39 publications

(10 citation statements)

References 7 publications

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“…However, changes in blood coagulation in patients suffering from acute stroke have been described for at least 40 years. Parameters that are well-known, and that confirms this changed coagulation include an activated intrinsic pathway, prothrombin consumption, increased thrombin activity, elevated fibrinogen levels and augmented platelet counts [16,17]. Also, increased thrombin activity on platelet surfaces has directly been attributed to fibrin mesh architecture [18].…”

Section: Discussionmentioning

confidence: 96%

A descriptive investigation of the ultrastructure of fibrin networks in thrombo-embolic ischemic stroke

Pretorius

Swanepoel

Oberholzer

et al. 2011

J Thromb Thrombolysis

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Stroke is one of the leading causes of death worldwide. Formation of a fibrin clot is controlled by a group of tightly regulated plasma proteases and cofactors and a change in the fibrin fiber formation causes an alteration in clot morphology. This plays an important role during thrombotic events. In the current study we investigated the ultrastructure of fibrin networks from fifteen ischemic stroke patients by using scanning electron microscopy. Clot morphology was investigated with and without the addition of human thrombin to the platelet rich plasma. Previously it was shown that, when studying the ultrastructure of fibrin networks, the addition of thrombin is necessary to form an expansive, fully coagulated layer of fibers. Results from the addition of thrombin to the plasma showed thick, matted fibrin fibers and a net covering some of the major fibers in stroke patients. Typical control morphology with major thick fibers and minor thin fibers could be seen in some areas in the stroke patients. In stroke patients, without the addition of thrombin, a matted fibrin network still formed, indicating that the factors responsible for the abnormal fibrin morphology are present in the circulating plasma and is the cause of the observed matted, layered morphology. This is not present in healthy individuals. From the results obtained we suggest that this changed morphology might be useful in a screening regime to identify the possibility of a stroke or even to follow the progress of stroke patients after treatment.

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Section: Discussionmentioning

confidence: 96%

A descriptive investigation of the ultrastructure of fibrin networks in thrombo-embolic ischemic stroke

Pretorius

Swanepoel

Oberholzer

et al. 2011

J Thromb Thrombolysis

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“…The clinical significance of these differences is not of practical value in the diagnosis or as a guide to therapy of stroke, in the opinion of the authors. 9 In contrast, both Hume 10 and Mathur and colleagues 11 noted elevations in fibrinogen and low fibrinolytic activity in patients with cerebral infarction, which they consider of clinical significance. Bang and McDowell 12 have reported 22 patients who had been studied by in vitro coagulation tests.…”

Section: Thromboelastographic Studies I N Cerebral Infarctionmentioning

confidence: 97%

“…He felt that these abnormalities were of no clinical significance because similar changes could be noted in the blood of healthy subjects of essentially the same age range. The most recent negative study was presented by Todd and colleagues, 9 who reported on coagulation studies in 87 normal controls, 33 patients with thrombotic stroke, and 55 patients …”

Section: Ettingermentioning

confidence: 99%

Thromboelastographic Studies in Cerebral Infarction

Ettinger

1974

Stroke

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Thromboelastographic Studies in Cerebral Infarction• Blood coagulability in patients following cerebral infarction was studied utilizing the thromboelastograph (TEG). Cerebral infarction patients from two separate institutions were studied within 24 to 48 hours after onset of stroke. Ninety-four stroke patients from one institution and 109 from another yielded a total stroke population of 203 patients for this study. Fifty-nine agematched normals were used as a control group. Frequency distribution curves were determined for a TEG ratio of ma/(r + k). The 59 controls exhibited a normal frequency distribution between the values of 1.6 and 4.0. Both groups of stroke patients revealed an increased number of patients with a ratio exceeding 4.0, suggesting a hypercoagulable state exists following cerebral infarction in approximately 29% to 38% of the patients studied.Additional Key Words clot lysis hypercoagulability platelet function fibrinolysis cerebrovascular disease• Our laboratory has been investigating abnormalities of blood clotting, clot lysis and platelet function in various categories of cerebrovascular disease. One of our objectives has been to identify a simple, reliable and clinically relevant test of blood or plasma which accurately identifies the overall consequences of the separate, yet simultaneously occurring reactions, which collectively result in the balance between clot formation and clot dissolution. A number of "global" tests of coagulation have been described, including the plasma recalcification test, partial thromboplastin time (PTT), the activated partial thromboplastin time, and the whole blood clotting time. All have their limitations with respect to reliability, sensitivity, and lack of correlation with clinically significant clotting or bleeding events. A somewhat different approach to a laboratory measurement of overall coagulation and fibrinolysis, which also is sensitive to platelet dysfunction, has been the development of the thromboelastograph. The thromboelastograph (TEG) provides a continuous recording of the process of blood coagulation and subsequent clot retraction. The instrument is capable of analyzing three blood samples simultaneously ( fig. 1). Stainless steel sample containers maintained at 37°C are set in motion around a vertical axis. A cylindrical dragbar is lowered into the . slowly oscillating metal containers and remains im- This investigation was supported by Research Grant NS03364 from the National Institute of Neurological Diseases and Stroke.Presented at the 46th Scientific Session of the American Heart Association, November 9, 1973, in Atlantic City, New Jersey. mobile as long as the blood or plasma sample is fluid. As the clot forms, the dragbar, suspended by the torsion wire, becomes dynamically coupled to the cup resulting in transmission of the oscillatory rotation of the cup to the cylinder. The cylinder then oscillates with an amplitude governed by the specific mechanical properties of the clot ( fig. 2). A mirror, coupled to the cylinder tors...

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“…1 - 4 and fibrinolysis (plasminogen activator, 1 plasminogen, a r antitrypsin, and a 2 -macroglobulin 5 ), similar findings have been thought to have no clinical importance in studies in which the influence of age or sex was considered. 3 - 4 Factor VHI-related activities and antithrombin HI have been reported to be normal in the acute period 6 or to be elevated in the chronic period.…”

mentioning

confidence: 91%

“…3 - 4 Factor VHI-related activities and antithrombin HI have been reported to be normal in the acute period 6 or to be elevated in the chronic period. 7 -9 Such conflicting results may be due to lack of sensitivity of the tests used, timing of blood sampling after stroke, the age of patients, medications administered, the presence of associated diseases, the type of stroke (thrombosis or embolism), or differences among the involved cerebral arteries.…”

mentioning

confidence: 99%

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

Tohgi

Kawashima

Tamura

et al. 1990

Stroke

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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.

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Stroke and Blood Coagulation

Cited by 39 publications

References 7 publications

A descriptive investigation of the ultrastructure of fibrin networks in thrombo-embolic ischemic stroke

A descriptive investigation of the ultrastructure of fibrin networks in thrombo-embolic ischemic stroke

Thromboelastographic Studies in Cerebral Infarction

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

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