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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hematologic disorders in patients with acute cardioembolic stroke are not fully understood, and no reliable measures are available to identify patients at high risk for recurrent embolism. We analyzed coagulation and fibrinolytic functions in 22 patients with cardiogenic cerebral embolism less than or equal to 24 hours after onset and in 25 age-matched controls. The levels of antithrombin III, protein C, and alpha 2-plasmin inhibitor were significantly lower in the patients than in the controls (p less than 0.001, 0.02, and 0.05, respectively). In contrast, the plasma concentrations of thrombin-antithrombin III complex and crosslinked D-dimer were markedly higher in the patients than in the controls (p less than 0.01 and 0.001, respectively). At the time of admission, the plasma concentrations of thrombin-antithrombin III complex and crosslinked D-dimer in the eight patients at high risk for recurrent embolization (one with prodromal embolism, three with intracardiac thrombi, and four with recurrent embolization) were 2.8 and 3.5 times, respectively, higher than those in the 14 patients without recurrence or thrombus formation. The lowest concentration of crosslinked D-dimer in the eight patients at high risk for recurrent embolization was 600 ng/ml on admission. Our results suggest that patients with acute cardioembolic stroke have various degrees of consumption coagulopathy and that the plasma concentrations of thrombin-antithrombin III complex and crosslinked D-dimer can be useful indicators of those who are prone to recurrent embolization during this stage.
Stroke 1991 Jan
PMID:Activation of coagulation in acute cardioembolic stroke. 198 67

Defibrotide, a deoxypolyribonuclide, has been found to modulate endothelial cell function causing increase in t-PA and decrease in PAI levels and also increase in PGI2 production. In addition, it increases platelet c-AMP levels and decreases MDA and TXB2 formation in human. Defibrotide inhibits platelet aggregate formation in vitro experiments as well as end-to-end anostomosis in rats. So, defibrotide inhibits the activation of platelets. Besides an increase of protein C and S levels a synergic action of heparin was observed in animal experiments. A strong antithrombotic effect has been observed in animal models. The drug has a beneficial effect in the cases of DVT, POVD, stroke and thromboembolism. Through its action we may say that the drug acts in a novel fashion in contrast to the other drugs used in this area. Defibrotide is a single-stranded polydeoxyribonucleotide obtained from deoxyribonucleic acid of mammalian lungs by controlled depolimerization. Since 1981 in our laboratory and in the clinical department we have been investigating a newly developed agent defibrotide in vitro experiments, animal experiments, and also its clinical pharmacology and clinical application. Some of our findings are already published and compared with literature (40, 43, 46). Because of the limited space we are not going to review the literature in detail but we are going to summarize our observations on this compound in the following order. I--in vitro experiments, II--Animal experiments, III--clinical pharmacology in human.
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PMID:The pharmacology and clinical pharmacology of defibrotide: a new profibrinolytic, antithrombotic and anti-platelet substance. 210 24

Lipodermatosclerosis of the lower extremity, with or without ulceration, is a common manifestation of severe venous disease and the result of sustained venous hypertension. The latter is generally a sequela of deep vein thrombosis. Factors that enhance clot formation or impair fibrinolysis contribute to the pathogenesis of venous disease. It is already established that faulty fibrinolysis may play a pathogenic role in patients with venous disease. We examined the possibility that patients with venous disease have abnormally low plasma levels of proteins C and S, two proteins whose deficiencies have been reported to cause an increased frequency of thromboembolic disease. Using immunologic and functional assays for plasma proteins C and S, we found that 4 (21%) of 19 patients with lipodermatosclerosis and leg ulcers had abnormally low levels of protein C or protein S. One of 7 patients with lipodermatosclerosis without ulceration had a profoundly depressed level of protein C and a history of cerebral stroke at a young age. Plasma levels of protein C were normal in five patients with arterial insufficiency severe enough to cause leg ulceration. We conclude that abnormally low plasma levels of proteins C and S may be found in patients with lipodermatosclerosis and venous ulceration. As with the abnormally low fibrinolytic activity in these patients, our findings indicate a possible propensity for increased thrombotic disease.
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PMID:Protein C and protein S plasma levels in patients with lipodermatosclerosis and venous ulceration. 203 43

Plasma protein C exerts anticoagulatory effects by inactivating factors V and VIII. Hereditary protein C deficiency is transmitted as an autosomal dominant disorder. Homozygous individuals usually develop purpura fulminans as newborns; heterozygous protein C-deficient individuals are at increased risk for venous thrombosis and pulmonary embolism. However, arterial thrombosis has been only rarely observed. We describe a young patient with heterozygous protein C deficiency who experienced a severe stroke due to thrombotic occlusion of the left middle cerebral artery.
Stroke 1990 Jul
PMID:Ischemic stroke due to protein C deficiency. 219 15

More than a dozen primary hematologic disorders have been associated with ischemic stroke. Inherited deficiencies of antithrombin III, protein C, and protein S have been linked with stroke in case reports; optimal screening requires functional as well as antigenic assays. Antiphospholipid antibodies and lupus anticoagulants are the most frequently identified acquired states associated with ischemic stroke. Polycythemia vera, sickle cell anemia, sickle-C disease, and essential thrombocythemia are the major disorders of formed blood elements causing stroke. Special, step-wise screening for occult prothrombotic entities in stroke patients is recommended for young persons with stroke of uncertain cause, for those with prior venous thrombosis, for those with a family history of unusual thrombosis, and for those with no other explanation for recurrent stroke. Acquired, perhaps transient, abnormalities of platelets, coagulation inhibition, and fibrinolysis may contribute importantly to brain ischemia in synergy with other mechanisms, but at present these remain ill-defined. The contribution of prothrombotic diatheses to stroke is probably underrecognized and warrants further investigation.
Stroke 1990 Aug
PMID:Hematologic disorders and ischemic stroke. A selective review. 186 63

A congenital deficiency of protein C (PC) is reported in a 42-year-old male, suffering from his first spontaneous episode of deep venous thrombosis in the left lower limb. The only defect found in laboratory assays for hemostasis and hepatic function was half normal level of PC, measured by both immunological and functional assays. To confirm congenital PC deficiency, the functional activity levels of PC were compared with those of other vitamin K-dependent factors during stabilized anticoagulant therapy under stable conditions. Although the patient's father had a history of a cerebral vascular accident, his PC level was found to be within normal levels. The patient's mother, free from thromboembolic events, also had a normal PC level. So the patient seemed to be a sporadic case. However, the patient's 14-year-old son, who has been asymptomatic to this time, has the same PC deficiency state.
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PMID:[A sporadic case of protein C deficiency]. 228 72

Anticardiolipin antibodies and, rarely, protein C deficiency have been described in patients with stroke. The familial coexistence of these two prothrombotic defects has not been previously reported. We describe a family with debilitating strokes occurring at an early age in whom both anticardiolipin antibodies and protein C deficiency were found. The propositus and her deceased mother both suffered a stroke at age 50 years. The propositus had both anticardiolipin antibodies and protein C deficiency. After a detailed study of the remainder of the family, the tendency to form anticardiolipin antibodies appeared to be inherited independently of the protein C deficiency. The simultaneous occurrence of these abnormalities in one family suggests that it may be useful to test for both anticardiolipin antibodies and inherited anticoagulant protein deficiencies in patients with unusual or unexplained stroke. The differential expression of both protein C deficiency and anticardiolipin antibody production in various members of the described family may allow insight into the relative contributions of these two prothrombotic abnormalities for the development of thrombotic complications, including stroke.
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PMID:Protein C deficiency and anticardiolipin antibodies in a family with premature stroke. 201 79

During the period January 1982 till June 1988, 536 patients underwent 577 carotid thrombendartectomies in the Department of Vascular Surgery RK in the University Hospital in Copenhagen. Preoperatively, 270 patients (47%) had experienced transient ischaemic attacks (TIA), 247 (43%) had experienced stroke (APC) and 19 (3%) had non-focal symptoms while 41 (7%) had asymptomatic stenoses. Postoperatively, 17 (2.9%) patients developed TIA, 22 (3.8%) developed slight neurological symptoms and 40 (7%) had more severe neurological complications and six of these (1%) died. None of the patients died from other causes during the first month. The frequency of complications had no relationship to the preoperative focal symptoms, but in patients with non-focal symptoms this was 37%. The degree of stenosis of the contralateral internal carotid artery (ICA) was correlated positively with the occurrence of severe neurological complications which were observed in 5% without contralateral ICA changes, in 7% with stenoses and in 20% with contralateral ICA occlusion. Patients with cerebral infarction developed complications significantly more frequently (20%) than patients with normal CT scans. The risk was also found to be increased in cases with a high pressure gradient across the stenosis and low pressure peripherally in the occluded artery (stump pressure). Follow-up examination of the 73 patients with complications on average 39 months after operation revealed that 37 patients (6.4%) had severe neurological symptoms resulting either from the operation or subsequent APC; seven patients required complete nursing care (1.2%) and 17 patients died during the period of observation. On follow-up examination, 15 patients had been occupationally active for at least 1.5 years.
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PMID:[Neurologic complications in connection with the surgical treatment of 577 cases of carotid artery stenosis]. 232 34

The well-known coagulation inhibitors antithrombin and protein C, and the more recently described inhibitors, heparin cofactor II and extrinsic pathway inhibitor, were measured in plasma during a 7-day observation period, from patients with pneumonia (n = 13), and in stroke patients with infarction (n = 9) and haemorrhage (n = 9). In patients with pneumonia, elevated fibrinopeptide A levels and subnormal antithrombin and protein C levels suggested some degree of consumption of the inhibitors. Later, an increase was observed for all the inhibitors, but was most conspicuous for heparin cofactor II which reached high normal values. C-reactive protein, initially markedly elevated, decreased rapidly. This finding suggests that heparin cofactor II might act as a delayed acute phase reactant. In stroke patients only small, not statistically significant, changes occurred during the observation period, except for heparin cofactor II which increased in patients with haemorrhagic stroke.
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PMID:Coagulation inhibitor levels in pneumonia and stroke: changes due to consumption and acute phase reaction. 247 68

Serial determinations of beta-thromboglobulin (BTG), platelet factor 4 (PF4), fibrinopeptide A (FPA), antithrombin III (ATIII), protein C (PC), fibrin (ogen) degradation product (FDP), FDP D-dimer, activated partial thromboplastin time (APTT), prothrombin time (PT), and euglobulin lysis time (ELT) were performed in 18 patients with non-progressing stroke and 14 patients with progressing stroke in order to predict the development of progressing stroke. Increasing levels of BTG, PF4 and FDP with frequent fluctuation were noted in both kinds of stroke. Fluctuation of FPA levels was also noted but was less pronounced. PC levels were found to be slightly decreased with fluctuation but the mean was still in the lower normal limit. BTG, PF4 and PC all elevated at the time of deterioration of physical condition in patients with progressing stroke, whereas FPA had no definite change at that time. From our study, we conclude that both platelet activation and coagulation process do occur in both kinds of stroke. But the latter plays a minor role in the formation of thrombosis. The hemostasis change, especially concerning the thrombosis formation, probably plays a role in the development of progressing stroke, but we cannot predict their development even by the detections of the newly known molecular substances appearing in various steps of the hemostatic mechanism. Development of new tests for understanding the whole dynamic change of the thrombosis process is necessary for accurate prediction of the progressing stroke in the future.
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PMID:The serial hemostasis-related changes in patients with cerebral infarction: comparison between progressing and non-progressing stroke. 253 1


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