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

Racial differences in stroke are known to exist with persons in the black race having a higher morbidity, mortality and incidence of stroke compared to whites. We evaluated coagulation factors in black and white stroke patients and compared the results between races. D-dimer was elevated more frequently in blacks than whites to a statistically significant degree. There were non-significant trends for blacks to have a positive lupus anticoagulant, low protein C and protein S, higher platelet factor 4, and hyporesponsive platelets to 10 microM epinephrine. The significance of these findings in understanding racial differences in stroke is discussed.
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PMID:Racial differences in coagulation studies in stroke. 135 61

We studied whether hemostatic abnormalities contribute to the increased risk of stroke in patients with nonvalvular atrial fibrillation. Hemostatic function was studied in four age-matched groups: 20 patients with nonvalvular atrial fibrillation and a previous ischemic stroke, 20 patients with nonvalvular atrial fibrillation without a previous stroke, 20 stroke patients with sinus rhythm, and 40 healthy controls. Both groups with nonvalvular atrial fibrillation had significantly higher concentrations of von Willebrand factor, factor VIII:C, fibrinogen, D-dimer (a fibrinolytic product), beta-thromboglobulin, and platelet factor 4; a significantly higher fibrinogen/antithrombin ratio; and significantly higher spontaneous amidolytic activity than the healthy controls. Prekallikrein levels were significantly lower in both groups with nonvalvular atrial fibrillation. Stroke patients with sinus rhythm had normal hemostatic function, normal concentrations of platelet-related factors, and a slightly increased concentration of fibrinopeptide A compared with the healthy controls. Both groups with nonvalvular atrial fibrillation differed from the stroke patients with sinus rhythm as they did from the healthy controls. No difference in hemostatic function was seen between the nonvalvular atrial fibrillation patients with and without a previous ischemic stroke. Thus, alterations in hemostatic function may contribute to the increased risk of stroke in patients with nonvalvular atrial fibrillation.
Stroke 1990 Jan
PMID:Coagulation factors and the increased risk of stroke in nonvalvular atrial fibrillation. 210 43

We compared combination therapy with low-dose aspirin plus ticlopidine to therapy with aspirin alone or ticlopidine alone in patients suffering transient ischemic attack or cerebral infarction. In 17, 24, and 23 patients, respectively, 300 mg/day aspirin, 200 mg/day ticlopidine, and 81 mg/day aspirin plus 100 mg/day ticlopidine were administered orally. Aspirin alone markedly inhibited platelet aggregation induced by arachidonic acid, partially inhibited platelet aggregation induced by adenosine diphosphate, and did not inhibit platelet aggregation induced by platelet activating factor. Ticlopidine alone inhibited platelet aggregation induced by adenosine diphosphate and platelet activating factor, but did not inhibit platelet aggregation induced by arachidonic acid. Combination therapy with aspirin plus ticlopidine markedly inhibited platelet aggregation induced by all three agonists. Plasma concentrations of beta-thromboglobulin and platelet factor 4 remained unchanged by aspirin alone, were slightly reduced by ticlopidine alone, and were markedly reduced by aspirin plus ticlopidine. Plasma concentration of thromboxane B2 was reduced by aspirin alone or with ticlopidine, but not by ticlopidine alone. The level of 6-ketoprostaglandin F1 alpha was reduced only by aspirin alone. Bleeding time was significantly prolonged by aspirin alone and by ticlopidine alone, although the greatest prolongation was produced by aspirin plus ticlopidine. Our results indicate that the combination of aspirin plus ticlopidine is a potent antiplatelet strategy, although the clinical importance of the changes observed need to be determined by a properly designed and controlled prospective study.
Stroke 1989 Dec
PMID:Combination therapy with low-dose aspirin and ticlopidine in cerebral ischemia. 253 43

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

We studied the effect of acetylsalicylic acid (ASA) versus placebo on B-thromboglobulin (B-TG) and platelet factor 4 (PF4) plasma levels and ADP-induced platelet aggregation in 25 male patients with transient ischaemic attacks (TIA). The patients were allocated randomly to two groups: 14 patients received oral treatment with ASA 500 mg b.i.d. for 14 days, 11 patients placebo b.i.d. for the same period. B-TG and PF4 plasma levels and ADP-induced platelet aggregation were determined in basal conditions, and two hours, and seven and fourteen days after starting with ASA or placebo. In addition, the same parameters were studied in a group of 20 healthy males of matched age. Basal levels of plasma B-TG and PF4 and the maximal amplitude of ADP-induced platelet aggregation were abnormally high in TIA patients. ASA caused a significant reduction of B-TG plasma levels in TIA patients 2 hours after the first administration, but no effect was observed at the 7th and 14th day of treatment. PF4 plasma levels were unaffected by ASA treatment. It is concluded that ASA, at the dose conventionally used in clinical trials, does not affect the release of two alpha-granule proteins.
Stroke
PMID:No effect of acetylsalicylic acid on B-thromboglobulin and platelet factor 4 plasma levels in patients with transient ischaemic attacks. 294 96

It remains uncertain whether platelet activation in ischemic stroke is contributory or secondary to brain ischemia. The efficacy of aspirin (ASA) in stroke prevention suggests that platelet activation contributes to the occurrence of stroke. On the other hand, platelet activation may be simply a generalized consequence of cerebral ischemic damage. To examine this issue, plasma levels of the platelet specific proteins beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured in fifty-eight patients with various defined types of acute ischemic strokes. beta-TG was a broader indicator of platelet activation than PF4. Compared with an age-matched control group, thromboembolic and cardioembolic stroke patients had significantly elevated beta-TG levels (p less than 0.001). Also, beta-TG levels in these stroke categories were significantly higher in samples drawn within the first week after the event than in those drawn later (p less than 0.001). In contrast, beta-TG levels in lacunar stroke patients and in most TIA patients were normal. beta-TG levels did not correlate with the volume of cerebral infarction as measured by planimetry from CT scans. Moreover, beta-TG levels in patients on chronic ASA therapy at the time of stroke did not differ from those in patients of the same diagnostic categories not taking aspirin. These data indicate that platelet activation may be important in some, but not all, subtypes of ischemic stroke and that platelet activation can occur in stroke even though the platelet cyclooxygenase pathway is suppressed.
Stroke
PMID:Enhanced in vivo platelet activation in subtypes of ischemic stroke. 316 Dec 20

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

Although platelet activation is known to occur during migraine attacks, the cause-effect relationship remains to be determined. This problem was approached by studying the possible occurrence of platelet activation in vivo in headache-free periods of subjects affected by common or classic migraine and, subsequently, by verifying the possibility of its pharmacological control through administration of a classic anti-aggregation drug such as aspirin (ASA). The plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), indices of the occurrence of platelet activation in vivo, were therefore first assayed in both groups of migraine sufferers in the absence of therapy and then during the administration of aspirin (50 mg/daily). In the group of 15 patients affected by classic migraine, basal plasma levels of beta-TG and PF4 were significantly higher than control subjects. On the other hand, only beta-TG plasma levels were significantly higher in the group of 18 patients affected by common migraine. Patients suffering from classic migraine showed a high incidence of platelet activation (greater than 90%) in comparison with common migraine patients (approximately 33%). This suggests that platelet activation occurs in vivo in migrainous patients also during headache-free periods. Administration of aspirin to the patients affected by common and classic migraine caused a decrease in plasma beta-TG and PF4 concentration. Consequently, pharmacological treatment with aspirin in adequate dose may prove to be helpful in diminishing the vascular side-effects known to occur in migraine sufferers.
Stroke
PMID:Study of platelet activation in migraine: control by low doses of aspirin. 623 Jul 78

Some patients with clinical evidence of atherosclerosis and others with diabetes were compared with appropriate controls. The intraplatelet level of platelet factor 4 (PF4) was significantly decreased in the arteriopaths and was lower in the diabetics when compared with controls. Patients with transient ischaemic attacks and stroke have even lower values. Intravenous heparin liberates large amounts of PF4 from an unknown reservoir, perhaps the endothelium, into the plasma. Arteriopaths liberated significantly more PF4 than the controls and the diabetics most. If a second heparin injection is given 24 hr after the first, the resultant plasma PF4 level was on average half that achieved after the first injection and again the patients had higher levels than the controls. Thus the reservoir originally "emptied" of PF4 by the heparin had been partially refilled in 24 hr and the reservoir in the atherosclerotic patients then contained more than the controls. Patients with atherosclerosis and especially diabetics differ from controls in the PF4 content of their platelets and in their response to heparin and in the rate of refill of the "heparin-mobilisable pool of PF4".
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PMID:Intra-platelet platelet factor 4 (IP.PF4) and the heparin-mobilisable pool of PF4 in health and atherosclerosis. 649 55

Mitral valve prolapse (MVP) is a predisposing factor for cerebral ischemia, especially in young adults. Cerebral embolization of intracardiac thrombi is the probable mechanism in many cases. Platelets play a key role in the development of thrombi. We found that platelet factor 4, a marker protein of platelet activation, was elevated in 12 of 33 MVP patients (36%) without a history of stroke. This finding indicates that platelets are frequently activated in asymptomatic MVP patients and may allow identification of a subgroup of MVP patients with activated platelets who are at increased risk for emboli.
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PMID:Platelet activation and mitral valve prolapse. 668 86


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