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15 hasil
[Drug-fever due to ajmaline (Tachmalin)].
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A report is given on a patient in whom during treatment and prophylactic measures of paroxysmal tachycardias after intravenous application of ajmalin large attacks of fever with chills developed. The oral application evoked subfebrile temperatures and weakness. The drug-fever which was to be
Prolonged cholestasis after ajmaline-induced acute hepatitis.
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We report the cases of 3 patients in whom ajmaline-induced acute hepatitis was followed by anicteric cholestasis persisting for more than 1 year after cessation of administration of the drug. Ajmaline was given for 8-16 days before the onset of acute hepatitis. Jaundice was preceded by fever, chills
[Anuria, cholestatic jaundice, thrombocytopenia, hemolysis. Immunoallergic complication due to ajmaline].
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A 75 year old man, treated with ajmaline, was admitted with malaise, fever, acute renal failure and cholestatic jaundice. Haemolytic anaemia and thrombocytopaenia were also found with a positive indirect Coomb's test in the presence of ajmaline. The immunological and haematological data are
[Prolonged hepatitis due to ajmaline--description of a case and review of the literature].
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A 60 years old woman was admitted for jaundice and fever which appeared after a treatment with ajmaline-butabarbital for two-weeks. Abdominal ultrasound examination and endoscopic retrograde cholangiography were normal. Mitochondrial antibodies were absent. Jaundice persisted for three years,
[Hepatitis due to ajmaline. Report of cases and review of the literature].
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The authors report the cases of 4 patients with jaundice following the administration of ajmaline. The disease had a pseudo- angiocholitic onset with fever, chills and pruritus in the 4 patients and abdominal pains in 2 patients. Serum transaminase activity and serum alkaline phosphatase activity
Hyperthermia Influences the Effects of Sodium Channel Blocking Drugs in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes.
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BACKGROUND
Fever can increase the susceptibility to supraventricular and ventricular arrhythmias, in which sodium channel dysfunction has been implicated. Whether fever influences the efficacy of sodium channel blocking drugs is unknown. The current study was designed to investigate the temperature
Brugada type 1 electrocardiogram unmasked by a febrile state following syncope.
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Brugada syndrome is a genetic disease characterized by persistent or transient ST elevation in the right precordial electrocardiogram (ECG) leads with or without right bundle branch block. It represents an increased risk for sudden cardiac death despite a structurally normal heart. Brugada-type ECG
Brugada syndrome masquerading as febrile seizures.
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Fever can precipitate ventricular tachycardia in adults with Brugada syndrome, but such a link has not been reported in children. A 21-month-old white girl presented repeatedly with decreased conscious level and seizures during fever. During a typical episode, rapid ventricular tachycardia was
Double Anomalies: Brugada Syndrome Presenting with a Persistent Left Superior Vena Cava
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BACKGROUND The presentation of Brugada syndrome (BrS) with a persistent left superior vena cava (PLSVC) is expected to be a rare entity. It is unknown if this venous anomaly is linked to the arrhythmogenesis seen in BrS, or it is coincidental. This case describes a clinical presentation of the 2, in
[Chagasic myocardiopathy: historical perspective].
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Considerable advances in the clinical pathological and pathogenic aspects of Chagas disease have been made since the Brazilian physician Carlos Chagas described the disease in 1909. The disease caused by the flagellate protozoon parasite Trypanosoma cruzi is transmitted to humans by a blood sucking
Update on the Diagnosis and Management of Brugada Syndrome.
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Brugada Syndrome (BrS) is an autosomal dominant channelopathy with variable penetrance affecting the sodium channel. It reduces the transport of sodium ions essential for proper generation of the cardiac action potential. The resulting inhomogeneous repolarisation in areas of the RV epicardium
Spontaneous alternans in Brugada ST-segment morphology within minutes.
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Brugada syndrome is an inherited, life-threatening, cardiac channelopathy where the electrocardiogram (ECG) characteristically depicts a classic pattern of complete or incomplete right bundle-branch block with ST-segment elevation in the right precordial leads V(1) to V(3). These, almost
Brugada Pattern Type 2 Diagnosis Unmasked by Aspiration Pneumonia
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Brugada syndrome (BrS) is a rare autosomal dominant mutation affecting sodium channels. Electrocardiography can show two Brugada patterns (BrP). Type 1 BrP usually causes sudden cardiac arrest (SCA). Type 2 BrP can appear during circumstances that result in delayed sodium channel opening, such as
Sudden Cardiac Arrest While Eating a Hot Dog: A Rare Presentation of Brugada Syndrome in a Child.
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Patients who are diagnosed with Brugada syndrome (BS) usually experience sudden cardiac arrest (SCA) and arrhythmia when they have a high fever, consume alcohol, and, more frequently, during their night sleep. In some rare cases, an SCA can be seen depending on a possible vagal stimulus, such as
A novel rare variant in SCN1Bb linked to Brugada syndrome and SIDS by combined modulation of Na(v)1.5 and K(v)4.3 channel currents.
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BACKGROUND
Cardiac sodium channel β-subunit mutations have been associated with several inherited cardiac arrhythmia syndromes.
OBJECTIVE
To identify and characterize variations in SCN1Bb associated with Brugada syndrome (BrS) and sudden infant death syndrome (SIDS).
METHODS
All known exons and
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