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

A patent foramen ovale (PFO) is found with increased frequency in patients with stroke of undetermined origin but the significance and therapeutic implications of this observation remain unclear. Several lines of evidence suggest a role for the PFO in stroke pathophysiology for some cryptogenic stroke patients, such as those whose PFO is accompanied by a prothrombotic state, atrial septal aneurysm, or lower extremity/pelvic DVT. Diagnostic evaluation of the patient with cryptogenic stroke and PFO is directed at identifying these subgroups. Appropriate therapy for primary and secondary stroke prevention in a subject with a PFO remains unclear given current uncertainties as to the pathophysiological significance of PFO. Additional studies are needed, such as those focused on lower extremity veins or the cardiac interatrial septum, to guide therapy in specific stroke subpopulations.
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PMID:Patent foramen ovale and stroke: prognosis and treatment in young adults. 1620 57

Paradoxical embolism to the cerebral circulation is often difficult to diagnose clinically. We report a case that illustrates the usefulness of transesophageal echocardiography in the detection of paradoxical embolism. An 84-year-old woman presented with bilateral hemispheric strokes. Despite the presence of atrial fibrillation, clinical suspicion of paradoxical embolism led to further investigation. An underlying lower limb deep venous thrombosis was found, lung scintigraphy showed pulmonary embolism, and a right-to-left shunt was detected using contrast-transcranial Doppler ultrasound even without the Valsalva maneuver. Transesophageal echocardiography confirmed a mobile 4-cm serpiginous thrombus wedged into a patent foramen ovale, extending from the right into the left atria. Multiple imaging modalities were used, allowing rapid diagnosis of paradoxical embolism, with an underlying DVT as the mechanism of stroke. Of all the investigations, visualization with TEE proved crucial in confirming the diagnosis.
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PMID:Paradoxical brain embolism in an acute stroke. 1730

Recent data have implicated a haplotype of the purinergic receptor P2Y, G-protein coupled, 12 gene (P2RY12), as potential risk determinant for atherothrombosis. However, to date, no prospective, genetic-epidemiological data are available. Using DNA samples collected at baseline in a prospective cohort of 14,916 initially healthy American men, we examined the possible association of P2RY12 genetic variants, in particular a haplotype H2 (constituted by dbSNP rs10935838, rs2046934, rs5853517, and rs6809699) amongst 708 white males who subsequently developed a thromboembolic event (incident myocardial infarction (MI), ischemic stroke, or deep venous thromboembolism/pulmonary embolism (DVT/PE)) and amongst an equal number of age- and smoking-matched white males who remained free of reported vascular disease during follow-up (controls). The P2RY12 gene variants tested were in linkage disequilibrium. The haplotype H2 distribution was significantly different between the DVT/PE cases (12%) and their matched controls (21%), p-permuted=0.02. In an adjusted conditional logistic regression analysis, the haplotype H2 was significantly associated with a lower risk of incident DVT/PE as compared to the reference haplotype H1 (odds ratio=0.50, 95% CI=0.27-0.93, p=0.028). However, we found no evidence for an association of the P2RY12 variants or the haplotype H2 with incident MI or ischemic stroke. The present investigation provides evidence for an association of the P2RY12 haplotype H2 with lower risk of DVT/PE; however these findings require replication in other well-designed studies.
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PMID:Purinergic receptor P2Y, G-protein coupled, 12 gene variants and risk of incident ischemic stroke, myocardial infarction, and venous thromboembolism. 1770 82

A great variety of clinical and immunological features have been described in patients with the antiphospholipid syndrome (APS), but information on their prevalence and characteristics in Latin American mestizo patients with the primary APS is scarce. To analyze the prevalence and characteristics of the main clinical and immunological manifestations in a cohort of patients with primary APS of mestizo origin from Latin America and to compare them with the European white patients, clinical and serological characteristics of 100 patients with primary APS from Colombia, Mexico, and Ecuador were collected in a protocol form that was identical to that used to study the "Euro-Phospholipid" cohort. The cohort consisted of 92 female patients (92.0%) and eight (8.0%) male patients. They were all mestizos. The most common manifestations were deep vein thrombosis (DVT; 23.0%), livedo reticularis (18.0%), migraine (18.0%), and stroke (18.0%). The most common pregnancy morbidity was early pregnancy losses (54.1% of pregnancies). Several clinical manifestations were more prevalent in the Latin American mestizo than in the European patients (transient global amnesia, pulmonary microthrombosis, arthralgias, and early pregnancy losses) and vice-versa (DVT, stroke, pulmonary embolism, and thrombocytopenia). Latin American mestizo patients with primary APS have a wide variety of clinical and immunological manifestations with several differences in their prevalence in comparison with European white patients.
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PMID:Primary antiphospholipid syndrome in Latin American mestizo patients: clinical and immunologic characteristics and comparison with European patients. 1815 95

A soluble form of the complement receptor CD21 (sCD21) is shed from the lymphocyte surface. The sCD21 is able to bind all known ligands such as CD23, sCD23, Epstein-Barr virus and C3d in immune complexes. Here, we show the serum levels of sCD21 in sera the of antiphospholipid syndrome (APS) patients. Antiphospholipid syndrome is an autoimmune disorder in which autoantibodies cause heart attack, stroke and miscarriage. Antiphospholipid syndrome may appear as primary or in association with systemic lupus erythromatosus (SLE) and other autoimmune diseases. Here, we ask whether APS patients have different sCD21 titers compared to healthy persons and whether sCD21 levels correlate with the presence of anti-beta2-GPI autoantibodies. We show that autoimmune APS patients have significantly reduced amounts of sCD21 in their sera, irrespective of the presence of anti-beta2-GPI autoantibodies. In our APS patients cohort additional SLE, vasculities, DVT (deep vein thrombosis), fetal loss or thrombosis did not correlate to the reduced level of sCD21.
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PMID:Antiphospholipid syndrome patients display reduced titers of soluble CD21 in their sera irrespective of circulating anti-beta2-glycoprotein-I autoantibodies. 1817 55

In a 12-member, 3-generation kindred with conjoint inheritance of G1691A factor V Leiden (FVL) and G20210A prothrombin gene (PTG) mutations, identified through a proband with amaurosis fugax and his father with nonarteritic ischemic optic neuropathy (NAION), the authors' hypothesis was that ocular thrombosis was a diagnostic window to familial thrombophilia-thrombosis. The authors used polymerase chain reaction (PCR) measures for thrombophilia (FVL, PTG, C677T-A1298C methylenetetrahydrofolate reductase [MTHFR], platelet glycoprotein PLA1A2) and hypofibrinolysis (plasminogen activator inhibitor-1 4G4G). The 39-year-old white male proband, with amaurosis fugax and transient ischemic attacks (TIA), was found to be a compound heterozygote for FVL and PTG mutations. His symptoms resolved only after coumadin. His 44-year-old brother (deep venous thrombosis [DVT]) and 46-year-old sister (DVT, pulmonary embolus [PE]) were compound FVL-PTG gene heterozygotes. Of 4 asymptomatic children born to these 3 siblings, 2 were FVL heterozygotes and 2 PTG heterozygotes. The proband's 69-year-old father, with NAION and ischemic stroke, had PTG heterozygosity, familial high factor VIII, and compound MTHFR C677T-A1298C mutation with homocysteinemia. The proband's 61-year-old aunt had PTG heterozygosity, recurrent DVT, and mesenteric artery thrombosis. The proband's 67-year-old mother, free of thrombotic events, was a FVL heterozygote, had high factor VIII, and PAI-1 4G4G homozygosity. In this extended kindred, ocular thrombotic events (amaurosis fugax, NAION) were associated with variegated thrombotic events, including TIA, ischemic stroke, DVT, PE, and mesenteric artery thrombosis, and opened a diagnostic window to family screening and treatment for complex thrombophilias, which had previously been undiagnosed.
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PMID:Ocular vascular thrombotic events: a diagnostic window to familial thrombophilia (compound factor V Leiden and prothrombin gene heterozygosity) and thrombosis. 1879 59

Anti Phospholipid Syndrome (APS) is a relatively new conception of syndrome complex first noticed in 1983. It may be primary or secondary to other diseases like SLE, RA, Systemic sclerosis, behchet's syndrome, temporal arteritis, sjogren's syndrome psoriatic arthropathy etc. Clinical manifestations are consequences of vascular thrombosis and embolism like DVT, pulmonary embolism, stroke, TIA, complication of pregnancy with pregnancy loss. We report a 34 years married female housewife who presented with sudden onset of nausea, vomiting, vertigo, dysphagia, dysarthria and ataxia. She had a chronic leg ulcer. Neurological findings were consistent with lateral medullary syndrome due to stroke though she was normotensive, nondiabetic with normal lipid profile. She had history of two abortions in last three years. Investigations were done accordingly and she fulfilled the diagnostic criteria of APS. No secondary cause was detected after thorough clinical examination and laboratory investigations. She was treated symptomatically along with oral anticoagulation. She improved slowly but steadily.
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PMID:Anti phospholipid syndrome. 1918 54

A pro-thrombotic condition was described in 1983 which was characterised by the presence of circulating antiphospholipid antibodies, as well as peripheral thrombosis (e.g. DVT), a tendency to internal organ involvement, repeated miscarriage, and, occasionally, thrombocytopenia (aPL) (Hughes, Br Med J 287:1088-1089, 1983). Previously, there had been a number of observations, mainly in patients with lupus having "false positive" tests for syphilis, miscarriage and circulating lupus anticoagulants. The description in 1983 had three notable features (a) a detailed comprehensive clinical picture of the syndrome; (b) this description differed from other coagulopathies in showing a propensity for arterial thrombosis (e.g. stroke and heart attack); and (c) this was a syndrome quite independent from lupus. There are indications that the primary antiphospholipid syndrome will turn out to be more common than lupus, though this could still be a reflection of referral practice.
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PMID:Hughes syndrome (the antiphospholipid syndrome): a disease of our time. 2113 65

Protein S is a vitamin K-dependent anticoagulant protein. It functions as a cofactor of activated protein C to inactivate activated factor V (FVa) and activated factor VIII (FVIIIa). Its deficiency is a rare condition and can lead to deep vein thrombosis, pulmonary embolism or stroke. It is often treated with long-term anti-coagulant therapy. Protein S deficiency may be hereditary or acquired; the latter is usually due to hepatic diseases or a vitamin K deficiency. Protein S deficiency manifests as an autosomal dominant trait; manifestations of thrombosis are observed in both heterozygous and homozygous genetic deficiencies of protein S. This case report is of DVT due to Protein S deficiency in a 53 year old male. Venous Doppler was used to diagnose DVT and free Protein S level measured by ELISA. IVC filter was placed on the third day of admission.
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PMID:Deep vein thrombosis in protein S deficiency. 2118 Feb 23

Stroke is the third leading cause of death in the United States, with more than 140,000 deaths per year. Complications related to stroke resulting in morbidity and mortality are very common and may result from cerebral and extracerebral causes. Cerebral causes include cerebral edema, hemorrhagic conversion of an ischemic infarct, and progression of penumbra to infarction. Extracerebral complications include deep vein thrombosis and pulmonary embolism, urinary tract infection, and aspiration. Many of these complications are largely preventable and often tracked as "quality metrics" in institutions with a stroke center designation. The focus of the article is primarily on common poststroke complications, such as aspiration, DVT, decubitus ulcers, seizures, and urinary catheter infections. Knowledge about potential poststroke complications is critical to earlier diagnosis, proper preventive strategies, and management.
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PMID:The ABC's of stroke complications. 2120 42


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