A Study of Blood Coagulation Following an Acute Stroke

Gaston, Lamont W.; Brooks, John E.; Blumenthal, Harvey J.; Miller, Carlin J.

doi:10.1161/01.str.2.1.81

Cited by 27 publications

(13 citation statements)

References 20 publications

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“…This instrument can record continuously and simultaneously fibrin formation of three blood or plasma specimens and provide a permanent record photokymographically." Other studies utilizing thromboelastography for the study of overall coagulation abnormalities are reported by Rosato et al, 8 Sicuteri and co-workers, 4 and Fisch and his colleagues. 5 Kimche and Eisenkraft" had sufficient confidence in the clinical relevance of the TEG data to administer a proteinase inhibitor and low-molecularweight dextran for the treatment of postoperative thromboemboli on the basis of abnormal TEG data, and to utilize daily TEG studies as an index of adequate treatment.…”

Section: Discussionmentioning

confidence: 93%

“…In marked contrast to patients with myocardial infarction where the same authors had previously described an elevated plasma fibrinolytic activity five to eight hours after myocardial infarction, which was depressed 16 to 48 hours following onset of illness, the acute studies of fibrinolytic activity in these stroke patients did not differ significantly from controls. 7 Gaston et al 8 described abnormalities in blood fibrinogen, factor VIII, prothrombin, platelet factor 3, and PTT tests. 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.…”

Section: Ettingermentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 93%

Section: Ettingermentioning

confidence: 99%

Thromboelastographic Studies in Cerebral Infarction

Ettinger

1974

Stroke

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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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“…The mechanism of anticoagulant treatment in cerebral ischemia is obscure, but perhaps it acts by reducing the "hypercoagulate state" seen in patients with thromboembolic cerebrovascular disease and in elderly persons, 32 and not by stopping the atherosclerotic process.…”

Section: Discussionmentioning

confidence: 99%

Long-term anticoagulant therapy for TIAs and minor strokes with minimum residuum.

Olsson¹,

Müller²,

Berneli³

1976

Stroke

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One hundred seventy-eight patients with transient ischemic attacks (TIAs) or small strokes with slight symptoms persisting for more than 24 hours (incomplete recovery = IR) (TIA-IR) from both the carotid and the vertebrobasilar systems were treated with anticoagulants. Ten patients stopped the treatment because of severe side effects. Only one patient had a lethal cerebral infarction when the thrombotest values were above the therapeutic level; no other infarction happened during the treatment period. Moreover, the frequency of TIA decreased during the treatment, compared with descriptions of the natural course of TIA. One hundred four patients were observed for a mean of 21 months after the anticoagulant treatment ended. During the observation period, six patients had cerebral infarctions. This was a sixfold increase compared with the stroke incidence during treatment, and was almost identical with the incidence of strokes seen during the natural course of TIA. All the cerebral infarctions were in patients who had their initial TIA/TIA-IR from the carotid territory (within the same carotid artery which earlier had given symptoms). The investigation shows that long-term anticoagulant treatment is useful, especially in patients with carotid TIA/TIA-IR, and that this treatment should continue as long as the patients can manage it. In patients with vertebrobasilar symptoms of malignant character, it seems feasible to terminate the treatment after about one year. The mechanism of the anticoagulant treatment is obscure, but it does not appear to influence the progress of the atherosclerotic process.

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A Study of Blood Coagulation Following an Acute Stroke

Cited by 27 publications

References 20 publications

Thromboelastographic Studies in Cerebral Infarction

Thromboelastographic Studies in Cerebral Infarction

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

Long-term anticoagulant therapy for TIAs and minor strokes with minimum residuum.

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