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1.
BMJ Case Rep ; 20092009.
Artigo em Inglês | MEDLINE | ID: mdl-21686342

RESUMO

Brugada syndrome is one of the important causes of sudden cardiac death in young adults. The condition is associated with typical electrocardiogram (ECG) changes in anteroseptal leads V1 and V2 that can be unmasked by various medications, electrolyte disturbances, and even by the febrile state in susceptible individuals. The case history is reported of a patient with atrial flutter and atrial fibrillation who developed Brugada-like ECG changes when treated with propafenone. He was mistakenly diagnosed as having acute myocardial infarction when he presented to the emergency room with acute precordial chest pain. Cardiac catheterisation revealed normal coronary arteries and normal left ventricular systolic function. A review of previous ECGs showed the temporal relationship of ECG changes to initiation of propafenone a few years earlier. The ECG changes resolved with discontinuation of propafenone and re-emerged when he was rechallenged with oral propafenone. This case highlights the importance of recognising the characteristic ECG changes of Brugada syndrome and being able to differentiate them from those of acute myocardial infarction and other conditions manifesting with similar changes.

2.
Emerg Med J ; 25(2): 117-8, 2008 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-18212157

RESUMO

Brugada syndrome is one of the important causes of sudden cardiac death in young adults. The condition is associated with typical ECG changes in anteroseptal leads V1 and V2 that can be unmasked by various medications, electrolyte disturbances, and even by the febrile state in susceptible individuals. The case history is reported of a patient with atrial flutter and atrial fibrillation who developed Brugada-like ECG changes when treated with propafenone. He was mistakenly diagnosed as having acute myocardial infarction when he presented to the emergency room with acute precordial chest pain. Cardiac catheterisation revealed normal coronary arteries and normal left ventricular systolic function. A review of previous ECGs showed the temporal relationship of ECG changes to initiation of propafenone a few years earlier. The ECG changes resolved with discontinuation of propafenone and re-emerged when he was rechallenged with oral propafenone. This case highlights the importance of recognising the characteristic ECG changes of Brugada syndrome and being able to differentiate them from those of acute myocardial infarction and other conditions manifesting with similar changes.


Assuntos
Antiarrítmicos/efeitos adversos , Síndrome de Brugada/induzido quimicamente , Síndrome de Brugada/diagnóstico , Erros de Diagnóstico , Infarto do Miocárdio/diagnóstico , Propafenona/efeitos adversos , Idoso , Fibrilação Atrial/complicações , Fibrilação Atrial/diagnóstico , Fibrilação Atrial/tratamento farmacológico , Fibrilação Atrial/cirurgia , Flutter Atrial/complicações , Flutter Atrial/diagnóstico , Flutter Atrial/tratamento farmacológico , Flutter Atrial/cirurgia , Ablação por Cateter , Eletrocardiografia , Humanos , Masculino , Resultado do Tratamento
3.
Metabolism ; 48(11): 1470-3, 1999 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-10582559

RESUMO

The increase in leg and forearm blood flow induced by insulin could be secondary to its metabolic effect on glucose uptake. We therefore investigated whether insulin causes vasodilation of the internal carotid artery, since the brain is not dependent on insulin for glucose uptake, to demonstrate that the vasodilatory effect of insulin is primary and independent of its metabolic effect. Internal carotid artery diameter was continuously monitored using a 7.5-MHz transducer linked to an Acuson XP10 ultrasonograph (Mountainview, CA) during infusion of 125 mL 10% dextrose mixed with 3 U regular insulin and 5 mmol potassium chloride over 1 hour. The internal carotid artery diameter increased progressively with time from a mean of 5.4+/-1 mm to 5.7+/-1 mm at 15 minutes, 5.9+/-1.1 mm at 30 minutes, 6+/-1.1 mm at 45 minutes, and 6.1+/-1.1 mm at 60 minutes (P < .05), an increase of 13% over baseline. Glucose was maintained between 93 and 106 mg/dL, and insulin increased from 15+/-14 microU/mL and was maintained between 34 and 47 microU/mL. There was no change in mean arterial blood pressure (MABP) or heart rate during the infusion. We conclude that insulin dilates the internal carotid artery consistently at physiological concentrations, probably independently of glucose uptake by the brain. Alterations in this effect of insulin may be of relevance in the pathogenesis of abnormalities of cerebral blood flow in type 1 and type 2 diabetics as described by our group previously.


Assuntos
Artéria Carótida Interna/efeitos dos fármacos , Insulina/farmacologia , Vasodilatação/efeitos dos fármacos , Vasodilatadores/farmacologia , Adulto , Glicemia/efeitos dos fármacos , Glicemia/metabolismo , Pressão Sanguínea/efeitos dos fármacos , Artéria Carótida Interna/diagnóstico por imagem , Circulação Cerebrovascular/efeitos dos fármacos , Feminino , Humanos , Insulina/sangue , Masculino , Pessoa de Meia-Idade , Valores de Referência , Fatores de Tempo , Ultrassonografia , Vasodilatadores/sangue
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