Cases reported "Tachycardia, Ventricular"

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1/108. Histopathologic effects of radiofrequency catheter ablation in previously infarcted human myocardium.

    INTRODUCTION: The use of catheter-based radiofrequency (RF) ablation for the treatment of ventricular tachyarrhythmias due to previous myocardial infarction has been steadily increasing. The histopathologic changes caused by this technique are not well described in humans. methods AND RESULTS: Three patients with hemodynamically tolerated ventricular tachycardias (VTs) due to previous myocardial infarction underwent endocardial mapping and catheter based RF ablation. All patients received between 5 and 11 RF lesions each of 60-second duration. One patient underwent myocardial resection of a left ventricular aneurysm 1 day following RF ablation, one expired 7 days after RF ablation, and one expired 9 months after RF ablation. None of the deaths occurred as a result of RF ablation. Pathologic specimens obtained early after RF ablation revealed areas of focal acute inflammation and fibrin deposition. Later specimens revealed several focal areas of fibrosis and granulation tissue. Specimens obtained late after RF ablation revealed a dense band of fibrosis, measuring 17 x 17 x 5 mm (1,250 mm3). CONCLUSION: Catheter-based RF ablation of ischemic VT in humans causes lesions that initially resemble coagulation necrosis. This is followed by the development of an inflammatory infiltrate and, finally, the development of fibrosis. Repeated application of RF ablation may result in much larger lesions than have been previously reported.
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2/108. commotio cordis: sudden cardiac death in athletes.

    commotio cordis due to blunt trauma to the precordium is a rare cause of death in young athletes, occurring less frequently than all of the other athletics-related deaths. Several measures, such as the use of safety baseballs and the use of chest protectors, can help protect young athletes from commotio cordis. In general, sudden cardiac death in athletes is receiving increasing attention from the public as a result of recent deaths of high-profile athletes. Sudden cardiac death, however, is rare, with an estimated 1 out of 200,000 high school athletes at risk each year. However, the personal, physiological, and cardiovascular benefits of athletics far outweigh the risks. Therefore, the message to parents is to allow their children to participate in athletics because the benefits far outweigh the risks.
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keywords = death
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3/108. A variant of long qt syndrome manifested as fetal tachycardia and associated with ventricular septal defect.

    Two patients with a novel variant of long qt syndrome are described. The clinical course was characterised by an in utero onset of ventricular tachycardia and atrioventricular block (at 26 and 30 weeks' gestational age, respectively), and an association with a ventricular septal defect. Studies of both patients' families identified relatives with prolonged QT interval, syncope, or sudden death. One patient died of intractable ventricular tachycardia at 4 days old. The other received beta blocker treatment and a pacemaker. She died suddenly at the age of 10 months. The unique association with ventricular septal defect and the malignant clinical course warrants further molecular diagnosis of this novel variant of long qt syndrome.
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4/108. Spontaneous sustained monomorphic ventricular tachycardia after administration of ajmaline in a patient with brugada syndrome.

    We present the case of a 13-year-old boy with an episode of aborted sudden death, absence of structural heart disease, and a characteristic ECG pattern of right bundle branch block with persistent ST-segment elevation in the right precordial leads, in whom a monomorphic sustained ventricular tachycardia developed spontaneously after the administration of ajmaline. This effect may be related to an increased inhomogeneity of repolarization mediated by the drug and demonstrates the arrhythmogenic potential of Class I antiarrhythmic drugs in patients with brugada syndrome.
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5/108. Early prenatal management of a fetal ventricular tachycardia treated in utero by amiodarone with long term follow-up.

    Fetal cardiac arrhythmias are one of the causes of intra-uterine congestive heart failure and non-immune hydrops fetalis leading to fetal death. As ventricular tachycardia (VT) is rarely diagnosed in utero, it leads to emergency deliveries. We report a prenatal diagnosis of fetal tachycardia at 20 weeks of gestation associated with non-immune hydrops fetalis. The tachycardia seemed to be supraventricular and was initially treated by digoxin and sotalol. The hydrops increased and sotalol was stopped in order to give the mother a high dose of amiodarone by mouth over a long period. Although the tachycardia, which the ECG recorded at birth revealed to be of ventricular origin, persisted but at a lower rate, the new treatment proved successful. The child is three years old now and health, though with persistent VT. In conclusion, fetal tachycardia with similar ventricular and atrial rates can be a VT and the drug of choice in this case seems to be amiodarone.
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6/108. Implantable defibrillator therapy in Naxos disease.

    Naxos disease is a unique form of right ventricular cardiomyopathy with a high prevalence of malignant ventricular arrhythmias, including sudden cardiac death. As a hereditary systemic disease confined to a small island, it has been closely studied over the last 15 years. The implantation of an automatic defibrillator provides an alternative form of antiarrhythmic management to improve life expectancy in these high risk cardiac patients. We present the first two Naxos disease patients with malignant ventricular arrhythmias who had defibrillator implantation.
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7/108. brugada syndrome as the cause of syncope in a 49-year-old man.

    We report the case of a 49-year-old man in whom a diagnosis of brugada syndrome was made after he presented to the emergency department for evaluation of a syncopal episode. The diagnosis was made by ECG changes, after the characteristic findings of peculiar downsloping ST-segment elevation in leads V(1) and V(2) and QRS morphology resembling a right bundle branch block were identified. Emergency physician recognition of this syndrome and its ECG findings is essential, because without treatment the incidence of sudden cardiac death in these patients is high.
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8/108. The brugada syndrome: a recently recognised genetic disease causing sudden cardiac death.

    Australian doctors need to be aware of this little-known syndrome, which is a cause of sudden cardiac death. It is more common among Southeast Asian people, who make up a considerable proportion of our population. We report two cases which represent very different clinical presentations of this condition.
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9/108. Catecholaminergic polymorphic ventricular tachycardia. An important diagnosis in children with syncope and normal heart.

    syncope in children is primarily related to vagal hyperreactivity, but ventricular tachycardia (VT) way rarely be seen. Catecholaminergic polymorphic VT is a rare entity that can occur in children without heart disease and with a normal QT interval, which may cause syncope and sudden cardiac death. In this report, we describe the clinical features, treatment, and clinical follow-up of three children with syncope associated with physical effort or emotion and catecholaminergic polymorphic VT. Symptoms were controlled with beta-blockers, but one patient died suddenly in the fourth year of follow-up. Despite the rare occurrence, catecholaminergic polymorphic VT is an important cause of syncope and sudden death in children with no identified heart disease and normal QT interval.
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ranking = 2
keywords = death
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10/108. Mutations in the cardiac ryanodine receptor gene (hRyR2) underlie catecholaminergic polymorphic ventricular tachycardia.

    BACKGROUND: Catecholaminergic polymorphic ventricular tachycardia is a genetic arrhythmogenic disorder characterized by stress-induced, bidirectional ventricular tachycardia that may degenerate into cardiac arrest and cause sudden death. The electrocardiographic pattern of this ventricular tachycardia closely resembles the arrhythmias associated with calcium overload and the delayed afterdepolarizations observed during digitalis toxicity. We speculated that a genetically determined abnormality of intracellular calcium handling might be the substrate of the disease; therefore, we considered the human cardiac ryanodine receptor gene (hRyR2) a likely candidate for this genetically transmitted arrhythmic disorder. methods AND RESULTS: Twelve patients presenting with typical catecholaminergic polymorphic ventricular tachycardia in the absence of structural heart abnormalities were identified. dna was extracted from peripheral blood lymphocytes, and single-strand conformation polymorphism analysis was performed on polymerase chain reaction-amplified exons of the hRyR2 gene. Four single nucleotide substitutions leading to missense mutations were identified in 4 probands affected by the disease. Genetic analysis of the asymptomatic parents revealed that 3 probands carried de novo mutations. In 1 case, the identical twin of the proband died suddenly after having suffered syncopal episodes. The fourth mutation was identified in the proband, in 4 clinically affected family members, and in none of 3 nonaffected family members in a kindred with 2 sudden deaths that occurred at 16 and 14 years, respectively, in the sisters of the proband. CONCLUSIONS: We demonstrated that, in agreement with our hypothesis, hRyR2 is a gene responsible for catecholaminergic polymorphic ventricular tachycardia.
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ranking = 2
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