Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients are presented in whom cerebral angiography was complicated by bioccipital infarcts resulting in cortical blindness with persisting severe restriction of the visual field (case 1) and persisting cortical blindness (case 2). One patient (case 1) demonstrated a compensated, protracted disseminated intravascular coagulation (Table 1), which disappeared after treatment with phenprocoumon (Marcoumar). The other patient (case 2) demonstrated increasee spontaneous platelet aggregability (Table 2), which was treated sucessfully with acetylsalicylic acid (Magnyl) and dipyridamole (Persantine). We presume that the coagulation disturbances demonstrated after the angiography may be pathogenetic to the complications. We propose that patients with transient cerebral ischemia and apoplexy who are undergoing cerebral angiography should be studied with regard to coagulation before and after the cerebral angiography so that coagulation disturbances demonstrated may be treated before, or corrected after the angiography.
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PMID:Possible increased tendency to thrombosis after cerebral angiography. 45 38

Transient ischemic attacks (TIA) are neurological deficits of sudden onset and equally sudden reversal. They are considered to be precursors of stroke that (still) have a good prognosis. Since the symptoms have usually disappeared by the time of the first examination the physician must rely on the information provided by the patient or relatives for the medical history. Symptoms to look for include disordered speech, aphasia, vertigo, unilateral arm paralysis, crooked mouth. When a TIA is suspected, the following examinations are mandatory: neurological ultrasound, blood pressure, ECG, laboratory examinations (blood sugar, blood count, hematocrit), CT or MRI, Doppler-ultrasonography of the carotids and, where indicated, transcranial Doppler. Long-term prophylaxis with platelet antiaggregation agents or Marcumar (phenprocoumon) and appropriate changes in lifestyle are indicated for all TIA patients. When the indication is established, thrombarterectomy must be carried out within six months after the event.
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PMID:[Transient cerebral ischemia--precursors of stroke. Can warning signs be recognized?]. 1265 23

That tremor simulates atrial fibrillation and causes oral anticoagulation has not been reported. In a 69-year-old patient with diabetes, arterial hypertension and recurrent strokes, hand tremor developed since 1998. In September 2000 atrial fibrillation was diagnosed upon a routine and 24-hour ambulatory ECG. Because of the additional risk factors for stroke/embolism, phenprocoumon was begun. The diagnosis was changed to paroxysmal AF upon the following ECGs, showing sinus rhythm. Not earlier than 1 year after establishing the diagnosis,"atrial fibrillation" was identified as being due to a tremor artefact. Phenprocoumon was discontinued. Neurological investigations revealed Parkinson's disease as the cause of the tremor. Three weeks after initiation of pramipexol, the tremor artefact was no longer visible on ECG. Misinterpreting an ECG-artefact due to Parkinsons's tremor as atrial fibrillation may be followed by unnecessary diagnostic and therapeutic procedures, including long-term oral anticoagulation. Upon adequate treatment of Parkinson's disease, the tremor artefact immediately disappears from the ECG.
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PMID:Oral anticoagulation for ECG tremor artefact simulating atrial fibrillation. 1460 9

Atrial fibrillation (AF) is associated with a 6 fold increased risk for ischemic stroke. Observational studies suggest that one in four to five strokes is due to AF. Depending on the risk profile of an individual patient, the yearly risk for ischemic stroke is between 2% and 14%. AF is accompanied by an increased propensity for atrial clot formation due to a combination of decreased atrial blood flow, increased activity of the platelet/plasmatic coagulation system and prothrombotic changes at the atrial endocardium. This review summarizes the current guidelines for thromboembolic prevention in patients with AF. In many cases, continuous oral anticoagulation therapy (OAT) with vitamin K antagonists (VitKAs) is indicated if AF is accompanied by more than one additional risk factor for thromboembolic complications. However, therapeutic range of VitKAs (Phenprocoumon, Warfarin, and others), the most commonly used oral anticoagulants, is narrow and their use requires regular anticoagulation monitoring. Possibly due to these limitations, about one third of eligible patients are not treated with VitKAs. Furthermore, in many treated patients OAT is not well controlled. Thus, in clinical practice anticoagulation therapy in AF is suboptimal. Therefore, new and more convenient pharmacologic approaches to prevent thromboembolism with i.e. direct thrombin inhibitors (DTI), synthetic polysaccharides (factor Xa Inhibitors), and others are discussed, and their possible future role in the treatment of AF is evaluated.
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PMID:New pharmacologic approaches to prevent thromboembolism in patients with atrial fibrillation. 1762 64