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

We studied the effect of antiplatelet therapy not only on the secondary prevention of stroke but also on the suppression of vascular damages in patients with cerebral thrombosis at the chronic phase. We measured von Willebrand factor (vWF) as a marker for the endothelial system, and coagulation and fibrinolytic parameters in addition to platelet functions. The platelet aggregation and markers for platelet activation were monitored for the adequate inhibition of platelets. Twenty-one patients were treated with 200 mg ticlopidine. 9 patients with 100 mg ticlopidine and 60-150 mg acetylsalicylic acid, and 18 patients with 200 mg cilostazol daily. The mean duration of follow up was 8.4 +/- 3.0 months. A patient was attacked by a recurrent stroke, but no fatal vascular events occurred during the period. A significant decrease was observed in the collagen- and ADP-induced platelet aggregation and markers for platelet activation such as platelet factor 4 (PF4) and beta-thromboglobulin (beta TG) by the antiplatelet therapy. In addition, the activities of coagulation factor VIII (FVIII) and vWF, markers for vascular damages, showed a significant decrease. The results suggest that the antiplatelet therapy could ameliorate the vascular damage through the inhibition of platelet function. Moreover, thrombin-antithrombin III complex (TAT) and alpha 2-plasmin inhibitor-plasmin complex (PIC), markers for the activation of coagulation and fibrinolytic systems, decreased significantly, suggesting that the treatment inhibits the activation of coagulation and fibrinolytic systems induced by the platelet activation. The activities of FVIII and vWF decreased significantly when the level of beta TG or that of PF4 lowered sufficiently by the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Antiplatelet therapy in patients with cerebral thrombosis at the chronic phase--assessment of its effect on coagulation and fibrinolytic parameters]. 799 82

The share of platelets in the process of atherosclerosis and its thrombotic complications depends on the rate of their activation, which can be assessed by investigating the plasmatic levels of platelet factor 4 (PF4). Authors made use of this method in 68 patients with ischemic stroke and searched for the correlation between the found results, clinical picture and supposed etiopathogenesis of the disease. On the grounds of given findings they reached the conclusion that the increased PF4 levels represent no sign of a cerebral complication but only characterize the group of risky patients threatened by their platelets function status.
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PMID:The platelet functions in stroke. 859 71

We report a patient who developed severe thrombocytopenia and ischemic stroke following pentosan polysulfate treatment. An ELISA test employed in type-II heparin-induced thrombocytopenia was highly positive. To our knowledge, this is the first case in which this test has been performed in a pentosan polysulfate-induced thrombocytopenia (PIT). Our data suggest that the antibody against pentosan polysulfate-platelet complex also cross-reacts with heparin-platelet factor 4 complex. Due to its greater sensitivity and wider availability, this ELISA test should be used in cases where PIT is suspected.
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PMID:Pentosan polysulfate-induced thrombocytopenia: a case diagnosed with an ELISA test used for heparin-induced thrombocytopenia. 869 27

Recent epidemiological studies have suggested that 15 to 30% of all ischemic stroke is comprised of cardioembolic stroke. The presence of intracardiac thrombi might prove to be the most reliable tool when making a diagnosis of cardioembolic stroke, although not always easy to determine even with recent advanced technique. In this study, sensitivities to detect intracardiac thrombi of transthoracic echocardiography (TTE), transesophageal echocardiography (TEE), cardiac-enhanced CT (CCT) and scintigraphy with indium-111-tropolone-labelled platelets (PSG) were compared, in order to provide a relevant guideline for the diagnosis of intracardiac thrombi in 83 patients suspected of cardioembolic stroke. Also studied was the correlation of intracardiac thrombi with activation of platelets and coagulation-fibrinolysis through performing various hemostatic tests in order to investigate their utility for the evaluation of in situ thrombosis or prothrombotic state in the heart chamber. Detection rates of intracardiac thrombi were 35% in TEE, 26% in CCT, 19% in PSG, and 11% in TTE. There was a significant difference in the sensitivity between TEE and TTE (p < 0.05). Left atrial thrombi were frequently detected in TEE (4 out of 5 patients) and CCT (7 out of 10), while they were found less in PSG (2 out of 4) an TTE (4 out of 10). Thrombi in the left appendage were visualized in 3 out of 3 by TEE, while only in 1 out of 3 by PSG, 1 out of 4 by TTE and 1 out of 4 by CCT. Left ventricular thrombi; CCT (3 out of 3), TTE (2 out of 3), PSG (1 out of 1); TEE was not performed since this technique could not be expected to provide high-quality images of left ventricular thrombi. Thus, left atrial thrombi were considered to be more sensitively detected by TEE and CCT, left appendage thrombi by TEE, and left ventricular thrombi by TTE and CCT. There was no patient in whom an intracardiac thrombus was visualized by PSG alone. On the basis of the results above, we propose the following guideline for the detection of intracardiac thrombi in patients presented with cardioembolic stroke. First, TTE and CCT appear to be relevant for screening tests because of simple and non-invasive techniques. These two tools might be sensitive enough to find left ventricular thrombi. Second, TEE should be recommended when a thrombus is suspected in the left atrium or appendage. Finally, PSG may be used to determine the activity of the thrombus, according to its necessity. Among the patients having intracardiac thrombi, frequently observed was the increase of beta-thromboglobulin, platelet factor 4, platelet lysis, thrombin-antithrombin III complex, D-dimer in 67%, 75%, 71%, 80% and 80%, respectively, as well as the shortening of platelet survival in 100%, while anrithrombin III was reduced in only 38%. In addition, when hemostatic abnormalities were compared between positive and negative groups of intracardiac thrombi, the shortening of platelet survival (p < 0.0001), the increase of platelet lysis, and the increase of D-dimer (p < 0.04) were more frequent in the positive group than in the negative group. These results indicate that the findings of activation of platelets and coagulation-fibrinolysis, except for the reduction of antithrombin III, especially the findings of platelet consumption and lysis as well as fibrinolysis activation are useful as sensitive parameters of in situ thrombosis or prothrombotic state, which may lead to the formation of intracardiac thrombi.
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PMID:[Diagnosis of intracardiac thrombi by various imaging techniques and activation of platelets and coagulation-fibrinolysis in patients with cardioembolic stroke]. 874 45

A number of polymorphisms of the platelet glycoprotein (GP) Ib-V-IX and IIb/IIIa complexes have been described, and the PlA polymorphism of GP IIIa has been associated with coronary thrombosis. We determined the levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) and the genotype distributions of PlA and a variable number tandem repeat (VNTR) polymorphism of GP 1b in subjects with acute stroke (n=609) and healthy control subjects (n=435). Levels of beta-TG were higher in patients both initially (47.4 [44.7 to 50.2] ng/mL, P<0.0001) and after 3 months (42.9 [40.3 to 45.7] ng/mL, P=0.03) compared with control subjects (39.4 [37.7 to 41.2] ng/mL). Initial levels of beta-TG were significantly higher in those who subsequently died (58.7 [52.3 to 65.8] ng/mL) compared with those still alive (42.7 [40.1 to 45.5] ng/mL, P<0.0001). In a logistic regression model, beta-TG remained an independent predictor of poststroke mortality, with an odds ratio for an increase in 10 ng/mL of 1.12 (1.03 to 1.21, P=0.006). In subjects who had never smoked, there was a significant difference in the genotype distributions of patients with atherothrombotic stroke (A1/A1=147, A1/A2=70, and A2/A2=2) compared with controls (A1/A1=165, A1/A2=47, and A2/A2=5, P=0.03). The PlA distribution of subjects with atherothrombotic stroke before the age of 50 years (A1/A1=19 and A1/A2+A2/A2=18) was also significantly different from age- and sex-matched controls (A1/A1=54 and A1/A2+A2/A2=20, P=0.02). We found no association of VNTR with stroke or poststroke mortality. These data indicate that there is a persistent state of enhanced platelet activation in subjects with acute stroke, which is associated with poststroke mortality. The increased frequency of the PlA2 allele in young subjects with atherothrombotic stroke lends further support for a role of the PlA polymorphism in acute thrombosis.
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PMID:Platelet GP IIIa PlA and GP Ib variable number tandem repeat polymorphisms and markers of platelet activation in acute stroke. 967 73

The sticky platelet syndrome (SPS) is an autosomal dominant platelet disorder associated with arterial and venous thromboembolic events. It is characterized by hyperaggregability of platelets in platelet-rich plasma with adenosine diphosphate (ADP) and epinephrine (type I), epinephrine alone (type II), or ADP alone (type III). Clinically, patients may present with angina pectoris, acute myocardial infarction (MI), transient cerebral ischemic attacks, stroke, retinal thrombosis, peripheral arterial thrombosis, and venous thrombosis, frequently recurrent under oral anticoagulant therapy. Clinical symptoms, especially arterial, often present following emotional stress. Combinations of SPS with other congenital thrombophilic defects have been described. Low-dose aspirin treatment (80 to 100 mg) ameliorates the clinical symptoms and normalizes hyperaggregability. The precise etiology of this defect is at present not known, but receptors on the platelet surface may be involved. Normal levels of platelet factor 4 (PF4) and beta-thromboglobulin in plasma suggest that the platelets are not activated at all times; they appear to become hyperactive upon ADP or adrenaline release. In vivo clumping could temporarily or permanently occlude a vessel, leading to the described clinical manifestations. The syndrome appears to be prominent especially in patients with unexplained arterial vascular occlusions.
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PMID:Sticky platelet syndrome. 1054 69

A 27-year-old woman was admitted to our hospital because of headache, fever and right neck pain. Neurological examination revealed mild meningeal signs, and hyper-reflexia in all extremities. In the laboratory tests, white-cell count was 13,000/mm3, rheumatoid factor(RF) and C-reactive protein(CRP) were positive. The cerebro-spinal fluid showed pleocytosis (56/mm3, neutorophils and lymphocytes were 26 and 28, respectively). Thus, she was diagnosed as aseptic meningitis. A few days later, she had weakness and dysesthesia of the right face and the left extremities. Pulse therapy with intravenous methylprednisolone was started. A magnetic resonance imaging (MRI) of the brain showed a hemorrhagic infarction in the right parietal lobe. In hemostatic markers, thrombin-antithrombin III complex(TAT; 106 ng/dl), D-dimer 1234 ng/dl, prothrombin fragment 1 + 2(F1 + 2; 2.36 nmol/L), beta-thromboglobulin (beta TG; 4,300 ng/dl) and platelet factor 4 (PF-4; 1,770 ng/dl) were extremely elevated. On duplex ultrasonography, a low echo lucent plaque was observed at the right internal carotid artery and the mean blood flow velocity in the right carotid artery was decreased. She was placed on oral prednisolone and warfarin for suspected stroke due to hypercoagulability associated with vasculitis. Afterwards, she discharged from our hospital. Two months later, she was readmitted to our hospital because of irregular menses and vaginal bleeding. Endometrial uterus biopsy was conducted, which revealed a grade I endometrioid adenocarcinoma. She was under total uterectomy without tumor recurrence. After the radical operation, white-cell count, RF, CRP, TAT, D-dimer, F1 + 2, and beta TG were normalized, and the mean flow velocity of the right common carotid artery was increased. Thereafter, she did not experience stroke recurrence. Therefore, we speculated that she had stroke due to hypercoagulability in association with malignancy, that is Trousseau's syndrome. We also assumed that aseptic meningitis, brainstem encephalitis associated with vasculitis in this patient are other clinical variants of paraneoplastic syndrome through immunological mechanisms associated with malignancy. We emphasize that patients with Trousseau's syndrome can be associated with other paraneoplastic manifestations such as vasculitis as seen in this patient.
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PMID:[A young patient with endometrioid adenocarcinoma who suffered Trousseau's syndrome associated with vasculitis]. 1247 93

A 75-year-old man was admitted to our hospital with dysesthesia of the right lip, dysphagia and gait disturbance. He presented with right Wallenberg syndrome and brain MR image showed a fresh infarction in the right lateral medulla. Therapy with heparin and ozagrel sodium was started. For a time his symptom improved a little, but after 8 days he developed re-infarction, thrombocytopenia and DIC, while being treated with heparin for cerebral infarction. Heparin was discontinued, and these symptoms improved quickly. The clinical course and the positive anti-platelet factor 4-heparin complex antibody suggested that these symptoms were caused by heparin-induced thrombocytopenia (HIT). HIT should be included as a differential diagnosis for progression of ischemic stroke under heparin therapy.
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PMID:[A case of heparin-induced thrombocytopenia that worsened preexisting cerebral infarction]. 1551 11

A lacunar infarct is defined as the occlusion of a single perforating artery. Certain researchers have proposed that patients with lacunar infarcts can be classified into two clinically distinct entities: patients with a single, symptomatic lacunar infarct, and patients with multiple lacunar infarcts together with hypertension and leukoaraiosis. The present study attempted to delineate the characteristics of lacunar infarcts and evaluate the validity of the aforementioned hypothesis. A total of 130 consecutive patients with first-time symptomatic lacunar infarct were studied. All patients were dichotomized into two groups according to two different kinds of models as follows. Model-1: patients with a single lacune and patients with multiple lacunes; and Model-2: patients with large lacune and patients with small lacune. Associated factors for the multiple lacune group compared with the single lacune group as well as the large lacune group compared with the small lacune group, were analyzed by multivariate logistic regression analysis. Associated factors included age, sex, hypertension, diabetes mellitus, dyslipidemia, smoking, extracranial and intra-cranial vascular lesions, extent of lacunes and white matter lesions, progression status and blood pressure in the acute stage, and coagulation markers such as fibrinogen, thrombin-antithrombin complex, D-dimer, beta-thromboglobulin, platelet factor 4. Results for Model-1: hypertension (age-and sex-adjusted OR: 2.58, p = 0.017) and elevated systolic blood pressure (>160mmHg for the mean value during the first post-ictal week; OR: 2.55, p = 0.016) were significantly associated with the multiple lacune group. Large lacunes (>10mm in diameter) were negatively associated with the multiple lacune group (OR: 0.38, p = 0.017). Association between confluent white matter lesions and the multiple lacune group approached significance (OR: 2.16, p = 0.056). Results for Model-2: female sex (OR: 0.39, p = 0.021), mild stenosis of intracranial and extracranial arteries (<25%) (intracranial; OR: 5.42, p = 0.0042, extracranial; OR: 3.30, p = 0.016), progressing stroke (OR: 6.77, p<0.0001), and high levels of TAT (>3ng/ml) (OR: 2.80, p = 0.039) were significantly associated with the large lacune group. Multiple lacunes (OR: 0.38, p = 0.016) and confluent white matter lesions (OR: 0.28, p = 0.007) exhibited a significant negative association with the large lacune group. In conclusion, underlying vasculopathy in the presence of multiple lacunes may correspond to lipohyalinosis resulting from hypertension. Moreover, large lacune may correspond to microatheroma at the orifice of penetrating arteries.
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PMID:[Clinical classification for lacunar infarct. An investigation of 130 consecutive cases of lacunar infarctions]. 1571 93

Argatroban, a synthetic peptidomimetic antithrombin agent, is the first clinical anticoagulant solely to target thrombin. For some time, this drug has been used in Japan for the management of thromboembolic disorders. Recently, it has been approved in Japan for use in thrombotic and ischaemic stroke. Despite a large number of preclinical studies on the pharmacology of this agent, clinical trials in Europe and North America were only initiated in 1996. Argatroban produces anticoagulant effects comparable to therapeutic heparinisation at concentrations of approximately 1 microg/ml. At concentrations of 5-10 microg/ml, this agent produces adequate anticoagulation for inteventional cardiovascular procedures and prolongs the activated clotting time (ACT) to 400-600 s. The predictable anticoagulant effect of this agent is relatively short lasting, and may not warrant pharmacologic neutralisation in the majority of patients. However, patients with hepatic dysfunction may need some means of neutralisation. Unlike heparin, this drug produces its anticoagulant effects by direct inhibition of thrombin and thrombin-mediated processes. This agent is not influenced by endogenous factors such as platelet factor 4 and other proteins which bind heparin. Argatroban's use does not lead to the formation of antiplatelet antibodies. Thus, this drug is useful in the management of heparin induced thrombocytopenic (HIT) patients. Although argatroban was initially developed for the management of deep vein thrombosis (DVT), based on its pharmacologic properties, it can be developed for safer anticoagulation in such indications as acute coronary syndromes, as an adjunct to thrombolytics, thrombotic and ischaemic stroke and inflammatory diseases resulting in thrombotic complications.
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PMID:Pharmacology of argatroban. 1599 20


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