Cases reported "Ventricular Fibrillation"

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1/17. Transient local changes in right ventricular monophasic action potentials due to ajmaline in a patient with brugada syndrome.

    A 48-year-old patient with recurrent episodes of palpitations and syncope presented with transient ST segment elevation in the right precordial ECG leads. Structural heart disease was excluded. No arrhythmias were inducible by programmed ventricular stimulation. Parallel to ST elevation after intravenous ajmaline, a gradual and reversible delay in the upstroke of right ventricular (RV) monophasic action potentials (maps) occurred that was most marked in the RV outflow tract and nearly absent at right free-wall recordings. ajmaline led to a cycle length-dependent increase in RV dispersion of repolarization. Thus, right endocardial maps may demonstrate regionally different action potential changes that may contribute to the ECG changes in brugada syndrome.
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2/17. syncope in pharmacologically unmasked brugada syndrome: indication for an implantable defibrillator or an unresolved dilemma?

    A 30-year-old Caucasian male was referred for evaluation of a 2-year history of recurrent post-exertion lightheadedness and near syncopal spells in the setting of a family history of unexplained sudden cardiac death. Cardiac evaluation demonstrated normal heart structure, but the 12-lead surface ECG was suggestive of but not diagnostic of brugada syndrome. An exercise stress test reproduced the patient's usual symptoms during the recovery period, and was consistent with a typical vasovagal faint. The same symptoms were observed during a head-up tilt table test. However, given the family history and ECG, pharmacological testing with procainamide, isoprenaline and metoprolol, as well as programmed ventricular stimulation, were undertaken. Pharmacological provocation further supported a diagnosis of brugada syndrome, whereas programmed ventricular stimulation was considered non-diagnostic regarding ventricular tachyarrhythmia susceptibility. Consequently, despite ECG and pharmacological findings suggestive of brugada syndrome, there appeared to be sufficient evidence to believe that this patient's symptoms were the result of neurally mediated syncope and not due to ventricular tachyarrhythmias. The patient was treated with midodrine, and has remained symptom-free for 16 months. Thus, given the frequency with which vasovagal syncope occurs in young patients, its occurrence is not unexpected in individuals with concomitant diagnoses such as brugada syndrome. In as much as current recommendations favour implantable defibrillators in symptomatic brugada syndrome, the identification of other causes of syncope in such patients poses an uncomfortable, and currently unsettled dilemma.
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3/17. Successful prevention of recurrent ventricular fibrillation by intravenous isoproterenol in a patient with brugada syndrome.

    Intravenous administration of isoproterenol restored the ST-segment configuration to nearly normal in the right precordial leads and completely prevented spontaneous VF attacks in a patient with brugada syndrome. The formation of a Brugada-type ECG has been attributed to the transmural dispersion of repolarization of the right ventricular epicardium and related to modulation of the autonomic nervous system. Our case may provide clues to the pathophysiological mechanism of this syndrome.
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4/17. amiodarone used in successful resuscitation after near-fatal flecainide overdose.

    We report the case of a 45-year-old woman who had ingested 2000 mg of flecainide with suicidal intent. She developed therapy-resistant ventricular fibrillation (VF) with cardiopulmonary arrest. cardiopulmonary resuscitation and advanced life support were sustained for 64 min. Following intravenous amiodarone, the patient developed an effective spontaneous rhythm and resumed breathing. An amiodarone infusion was started and continued over a period of 72 h. She recovered completely after 5 days, leaving the hospital without neurological sequelae. serum flecainide levels approximately 5 h post-ingestion were 850 mg/l. This case report confirms the value of amiodarone in drug-resistant VF, even when the cause may be another antiarrhythmic drug such as flecainide.
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5/17. Successful resuscitation of two near simultaneous cases of cardiac arrest with a review of fifteen cases occurring during supervised exercise.

    Two men with coronary heart disease experienced cardiac arrests during a recent exercise rehabilitation session. Fifteen cases of ventricular fibrillation have occurred in this program since 1968, making an average of one per six-thousand man hours of supervised exercise training. All were successfully resuscitated with no sequelae. Analysis of the patients who experience ventricular fibrillation suggests that treating patients with exercise-induced premature ventricular contractions with anti-arrhythmic drugs, proper attention to serum potassium levels, strict adherence to training pulse rates, and proper warm-up might help to prevent future similar events in an exercise program. Due to the unpredictability of ventricular fibrillation it seems preferable that individuals who have known coronary heart disease participate in exercise training under proper supervision with appropriate emergency equipment available.
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6/17. Thyrotoxic periodic paralysis complicated by near-fatal ventricular arrhythmias.

    A 35-year-old Chinese man presented with acute thyrotoxic periodic paralysis complicated by near-fatal cardiac arrhythmias due to persistent hypokalaemia, despite maximum potassium supplementation. He was eventually resuscitated with external cadioversion. In this unusual case of severe refractory hypokalaemia leading to ventricular fibrillation in a patient with underlying thyrotoxicosis, the potential dangers concerning the use of dextrose infusion and beta-adrenergic agent for resuscitation are highlighted.
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7/17. Idiopathic premature ventricular contractions arising from the pulmonary artery: importance of mapping in the pulmonary artery in left bundle branch block-shaped ventricular arrhythmias.

    A patient underwent radiofrequency (RF) catheter ablation of symptomatic idiopathic ventricular contractions (PVCs). RF energy applications at 2 sites in the right ventricular outflow tract (RVOT), where both the earliest ventricular activation and near-perfect pace mapping were obtained, did not abolish the PVC but resulted in changes in the QRS morphology of the PVC. Complete elimination of the PVC was achieved with RF energy application at a site within the pulmonary artery 13 mm above the pulmonary valve, which was greater than 20 mm away from the failed ablation sites within the RVOT.
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8/17. Myocardial dysfunction in polymyositis.

    Myocardial involvement in polymyositis is occasionally suspected, but symptomatic cardiac dysfunction is rarely reported. Described in the present report is a 48-year-old woman with a two-year history of polymyositis who suddenly developed near fatal ventricular arrhythmia, and a 56-year-old man with a relapsing polymyositis who developed severe systolic dysfunction. These two cases emphasize the importance of systematic cardiac evaluation when the diagnosis of polymyositis is initially made and the necessity of re-evaluating cardiac function, even in the presence of clinical remission and normalization of creatine phosphokinase with treatment.
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9/17. Reversible myocardial depression in survivors of cardiac arrest.

    Three patients under 40-years old who survived cardiac arrest due to ventricular fibrillation were originally diagnosed as having idiopathic dilated cardiomyopathy. Shortly after cardiac arrest, assessment of myocardial function revealed a globally dilated left ventricle in each patient with an estimated ejection fraction between 20% and 30%. Serial assessment of myocardial function, however, showed either normal or near-normal function by 2 weeks postevent. These findings suggest that myocardial stunning due to hypoperfusion during ventricular fibrillation or the effects of transthoracic shocks may result in profound, reversible myocardial depression in survivors of cardiac arrest. Serial evaluation of left ventricular function may be of value in selected survivors of cardiac arrest in order to evaluate time-dependent resolution of myocardial dysfunction and may prevent misdiagnosis of idiopathic dilated cardiomyopathy.
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10/17. Mineral spirits inhalation associated with hemolysis, pulmonary edema, and ventricular fibrillation.

    A previously healthy 42-year-old woman developed severe dyspnea, chest discomfort, and malaise several hours after prolonged exposure to concentrated vapors from mineral spirits. On the way to the hospital, she sustained a cardiopulmonary arrest; on arrival several minutes later, she was found to be in ventricular fibrillation and was resuscitated. Her hospital course included slowly resolving cardiac abnormalities, amnesia, noncardiogenic pulmonary edema, abrupt hemolytic anemia, sustained rhabdomyolysis, and other metabolic abnormalities. It is highly probable that this syndrome represented acute and near-lethal toxicity caused by the inhalational exposure to the petroleum distillate known as mineral spirits. It is important that physicians be aware of this syndrome in order to recognize it on presentation and to warn patients of the risk of such toxic exposure.
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