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

PARD is a prospective study sponsored by the German Research Council with the aim to establish whether spontaneously enhanced platelet aggregation or changes of other hemostatic parameters are risk factors for new vascular occlusions in diabetic patients. 363 diabetic patients (aged 45-65, 232 men, 131 women) were observed for 5 years. Of the 232 men, 53 were on diet, 104 on oral antidiabetic drugs and 75 on insulin. Of 131 women 16 were on diet, 46 on oral antidiabetic drugs and 69 on insulin. At entry clinical examination and laboratory tests were performed, covering the known risk factors for cardiovascular complications. Hemostatic tests and clinical examination were performed at 3 months' intervals. The life status was followed for all patients. Endpoints were carefully defined. Until December 31, 1984, 42 patients died, 23 from cardiovascular disease and 19 from other causes. 13 patients suffered a myocardial infarction, 10 a stroke and 53 peripheral arterial occlusions. The occurrence of new vascular occlusions was significantly higher in those men with enhanced spontaneous platelet aggregation measured by PAT III angle alpha above 40 degrees at entry as compared to those with lower values. This was not the case for women. Other hemostatic parameters, which had also some relation to cardiovascular complications, in men were fibrinogen and F. VIII R:Ag. Established risk factors for which a significant relation to cardiovascular complications was observed in this study, were smoking, duration of diabetes, diastolic blood pressure, cholesterol, triglycerides and also HbA1. The results of the PARD-study have verified the hypothesis that spontaneous aggregation is a major risk factor for future vascular occlusions in diabetic men. They also lead to the hypothesis that high levels of F. VIII R:Ag and fibrinogen are further indicators of progressive vascular disease and may be useful as predictors of new vascular occlusions in combination with such established risk factors as smoking, duration of diabetes, diastolic blood pressure, cholesterol, and triglycerides.
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PMID:Spontaneous platelet aggregation and coagulation parameters as risk factors for arterial occlusions in diabetics. Results of the PARD-study. 310 11

Symptoms, therapy, and outcome of 49 cases of anaphylactic reaction are presented. Epinephrine (0.5-2.0 mg) did not produce any circulatory improvement but induced severe dysrhythmias and even ventricular fibrillation. Neither epinephrine nor prednisolone (2 g) prevented shock development, neurologic sequelae, or fatal outcome. Rapid infusion of 2000 ml 50% colloid (dextran 70 or starch, m.w. 450,000) with 50% Ringer's lactate, however, reliably restored circulation within 30 min. If elevated, airway resistance dropped in conjunction with colloid administration rather than with any other drug. Impairment of the pulmonary circulation is found to be the initial feature of anaphylaxis, manifested by a rise in pulmonary vascular resistance; then stroke volume and systemic blood pressure fall as left heart filling is reduced. Many findings indicate a high blood viscosity with resulting capillary occlusion: rapid clotting; low levels of factors I, II, V, VIII, and X; low plasma protein, which may be only 50% of its normal value; thrombocytopenia; and aggregation of white blood cells with fibrin in small lung vessels. Blood and plasma vanish from the circulation and appear to be sequestered in the pulmonary capillaries as the initial response to the antigen; later, the whole body is affected. Congestion and pain in the lymph nodes indicate that the lymphatic system may also become involved. On the basis of hemoconcentration, a blood volume deficiency in the range of 30% has been calculated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anaphylactic shock]. 360 58

Coagulation parameters were initially monitored in 8 patients receiving whole body hyperthermia (WBH). Patients were heated by the warm water blanket technique to 41.8 degrees C (Tmax), maintained at this temperature for 2 hours, then allowed to cool. A fall in platelets was apparent by the time Tmax was achieved and continued during the 18 hours after WBH. Levels of beta-thromboglobulin (BTG) and platelet factor 4 rose by 56% and 191% by the end of treatment but returned to baseline 18 hours later. Fibrinogen, plasminogen and alpha 2-antiplasmin levels declined and FDP and fibrinopeptide A (FPA) levels increased during WBH. Factor XII and Factor VIII:C fell moderately during WBH while Factors VIII R:Ag, VIII:RC and V did not change or showed a late rise. Factor VII levels fell in 7 of 8 patients, reaching levels of 30% of normal in four. To better define the sequence of these coagulations perturbations, earlier and more frequent timepoints were studied in an additional 3 patients. This revealed that decreases in fibrinogen and plasminogen and increases in FPA and BTG occur very early (by the time the patient reaches 39 degrees C). On the other hand, a decrease in Factor VII activity was not apparent until patients had reached Tmax. WBH is therefore associated with a consumption coagulopathy. Possible mechanisms are discussed and extrapolations to the situation seen in heat stroke are suggested.
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PMID:Activation of coagulation during therapeutic whole body hyperthermia. 373 68

Hemorheologic parameters were measured in cerebrovascular patients with a history of stroke or recurrent ischemic attacks in a quiescent phase of the disease. All patients were submitted to aortic arch angiography and then classified according to the presence or absence of detectable arterial lesions. In comparison with a group of control subjects, cerebrovascular patients had significantly elevated levels of blood and plasma viscosity, fibrinogen, factors VIII:C and VIIIR:Ag and lowered values of erythrocyte filtration. Blood viscosity was increased and erythrocyte filtration reduced only in male patients. Elderly patients had higher blood viscosity and fibrinogen levels, and those with a history of stroke also showed the highest hematocrit and plasma viscosity values. Patients with a stroke history compared with those affected by remittent ischemic attacks, and patients with positive in comparison with those with negative angiograms were characterized only by higher fibrinogen (and sometimes factor VIII) levels, but not by other differences in hemorheologic values. It is concluded that changes in hemorheologic values consistent with hyperviscosity are a feature of cerebrovascular patients also in the quiescent phase of the disease and not only as a result of acute ischemic attacks. These changes are however most frequent in males and in elderly subjects, while they seem to be almost evenly distributed in patients with or without evidence of arterial disease.
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PMID:Hemorheologic changes in patients with a history of stroke or cerebral remittent ischemic attacks. 392 40

A variety of mechanisms may cause intravascular coagulation. Fibrinolysis is nearly always secondary to the initial clotting. In the acute form, ICF is characterized by depletion of platelets and several coagulation factors together with active fibrinolysis. There is a decrease in Factors V and VIII because they are sensitive to coagulation. The stable coagulation factors may be decreased as well because after activation they are removed from the circulation by the liver and reticuloendothelial system. Severe bleeding is the usual accompaniment of the acute syndrome, which may also occur in cancer and infection of all types. The acute syndrome may also occur in prolonged, extensive operations, after transfusion of incompatible blood, heat stroke, acute injury, certain snake bites, and with the administration of certain drugs. The chronic syndrome of intravascular coagulation is much more common and is associated with many diseases, including collagen diseases or immune diseases and malignancy. Many patients with chronic intravascular coagulation have normal or even increased levels of coagulation factors, and these patients have no unusual bleeding. The diagnosis depends on the demonstration of circulating complex of "soluble" fibrin revealed by the ethanol gel and protamine sulfate gelation tests. The secondary fibrinolysis results in elevation of FSP. Many laboratories are investigating the use of other procedures in the diagnosis of intravascular coagulation, including fibrinopeptides A and B, the VIII:C VIIIR:AG ratio, antithrombin III, PF 4, beta-thromboglobulin, D dimer, urinary FSP, and fibrinogen chromatography.
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PMID:The clinical pathology of intravascular coagulation. 642 Dec 71

A variety of platelet function tests were performed in patients with four forms of obstructive cerebrovascular disease (CVD); transient ischemic attacks (TIA), reversible ischemic neurological deficit (RIND), cerebral infarct, and cerebral embolism of cardiac source in rheumatic valvular heart disease (RVHD). Platelet studies included platelet aggregation induced by ADP and ristocetin, spontaneous platelet aggregation, von Willebrand factor (VIII:vWF), platelet aggregation enhancing factor (PAEF), and percentage of large platelets (megathrombocytes). Serial testing was carried out in acute stroke patients. The effect of aspirin therapy was also evaluated. A clear difference in results was observed between patients with cardiogenic embolism and those with other forms of CVD. In patients with TIA, RIND, and cerebral infarct, platelet aggregation, both induced and spontaneous, was enhanced along with elevation of plasma VIII:vWF and PAEF, and increased percentage of megathrombocytes. In patients with cardiogenic embolism, however, these studies were negative except for percent megathrombocytes. This value was increased in the embolic patients with RVHD in comparison with non-embolic patients with RVHD. Increase in platelet aggregation to ADP and percent megathrombocytes developed slowly over a week following stroke. Induced and spontaneous platelet aggregation, and percent megathrombocytes could be normalized with 600 mg aspirin p.o. These studies suggest that a systemic increase of hyperaggregable platelets and of plasma activators of platelet function exists in thrombotic CVD and may be related to its pathogenesis, while local hemodynamic factors may be more important in the thrombogenesis of cardiogenic embolism.
Stroke
PMID:Platelet function tests in thrombotic cerebrovascular disorders. 665 25

To test the hypothesis that plasma contains native constituents capable of impairing microcirculatory flow in zones of acute ischemic tissue damage, we performed 14C-antipyrine autoradiographic blood flow studies in splenectomized dogs subjected to 35 min of cerebrospinal fluid compression ischemia followed by 30 min of recirculation to the neuraxis. The animals were anticoagulated with heparin and were divided into 4 groups by exposure to various measures before induction of ischemia. Groups 1 and 2 served for comparison with the other groups and underwent, respectively, no glass-wool filtration and glass-wool filtration via an arteriovenous shunt. Post-ischemic brain blood flows in Group 1 were low and focal zones of greatly impaired reperfusion were present. In Group 2, post-ischemic brain blood flows were high and focal perfusion impairment did not occur. Group 3 received homologous purified factor VIII/von Willebrand factor protein (F VIII/vWF) after glass-wool filtration but before induction of ischemia; Group 4 received F VIII/vWF-poor cryoprecipitate at the same time point. The purpose of administering the plasma preparations was to check for the presence of activity that nullified the enhancement of post-ischemic reperfusion expected after exposure to glass-wool. The results indicate that activity deleterious to post-ischemic reperfusion primarily resides in the F VIII/vWF fraction of cryoprecipitate. The F VIII/vWF-poor cryoprecipitate infusate, containing 250 to 800-fold more protein than the F VIII/vWF fraction, produced an intermediate reduction of blood flow.
Stroke
PMID:Influence of factor VIII/von Willebrand factor protein (F VIII/vWF) and F VIII/vWF-poor cryoprecipitate on post-ischemic microvascular reperfusion in the central nervous system. 678 87

Haemostatic measurements were undertaken in 132 patients diagnosed with heat stroke during the pilgrimage to Makkah, in two successive summers of 1989-90. The control group comprised 49 patients, all pilgrims, with a wide range of clinical conditions, but without hyperpyrexia or deranged haemostasis. Heat stroke patients showed (i) significant prolongation of the prothrombin (PT), activated partial thromboplastin (aPTT) and thrombin times (TT) but normal reptilase time (RT); (ii) significant reduction in plasma levels of antithrombin III (AT-III), factor V, proteins C and S, plasminogen activator inhibitor (PAI) and platelet count; (iii) increase in plasma factor VIII, tissue plasminogen activator (t-PA) and serum FDP; (iv) no significant changes in plasma fibrinogen, plasminogen, alpha 2-antiplasmin and factors VII and X. Heat stroke patients were then grouped into those with and those without bleeding symptoms. Bleeders showed greater prolongation of the PT, aPTT and TT and significant reductions in fibrinogen, AT-III, factors V, VIII and X, plasminogen, alpha 2-antiplasmin and platelet count. Logistic regression and discriminant analysis showed that AT-III was the parameter associated most with heat stroke and reliable enough to predict its occurrence, whether or not bleeding occurred. The results indicate that activation of the haemostatic mechanism, consumptive in nature, regularly accompanies heat stroke and highlights the physiological role of AT-III in checking this activation process.
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PMID:The coagulopathy of heat stroke: alterations in coagulation and fibrinolysis in heat stroke patients during the pilgrimage (Haj) to Makkah. 786 79

CDG syndrome (CDGS) type I is the most frequent form of a group of metabolic disorders characterised by a defect of the carbohydrate moiety of glycoproteins. A large number of plasma glycoproteins, including clotting factors and inhibitors, are decreased and stroke-like episodes have been described in about half of the reported patients. We studied blood coagulation factors, inhibitors and D-dimer plasma levels in four subjects, aged 12-23 years, with CDGS type I. Factors VIII, XI, antithrombin III activity, antigen plasma levels of antithrombin III, free protein S and protein C were decreased whereas protein C as activity was normal. In addition two patients had reduction of factors II, V, VII, IX, X reflecting the phenotypic heterogeneity associated with CDGS type I. D-dimer plasma concentrations were elevated in all subjects. The hypercoagulable state as consequence of the combined deficiencies of coagulation inhibitors could contribute to the stroke-like phenomena in CDGS type I.
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PMID:Haemostatic studies in carbohydrate-deficient glycoprotein syndrome type I. 890 85

We cross-sectionally measured plasminogen activator inhibitor-1 (PAI-1) activity, fibrinogen, factor VII (FVII:C) and VIII (FVIII:C) coagulant activity, and von Willebrand factor antigen (VWF:Ag) in 162 traditional horticulturalists older than 40 years from the tropical island of Kitava, Papua New Guinea, where the intake of western food is negligible and where stroke and ischaemic heart disease appear to be absent. Identical analyses were made in Swedish subjects of comparable ages. Kitavams had markedly lower PAI-1 activity, with 85% of males and 100% of females having PAI-1 activity < or = 5 U/ml, as compared with 22 and 14% in Swedish males and females (p < 0.0001). Surprisingly, Kitavans also had higher FVII:C. FVIII:C and VWF:Ag. Fibrinogen was 10% lower in Kitavan males while 25% higher in Kitavan females. The very low PAI-1 activity in Kitavans may explain some of their apparent freedom from cardiovascular disease and probably relates to their extreme leanness.
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PMID:Haemostatic variables in Pacific Islanders apparently free from stroke and ischaemic heart disease--the Kitava Study. 903 56


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