Cases reported "Ventricular Fibrillation"

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1/81. ventricular fibrillation related to reversal of the neuromuscular blockade in a patient with long qt syndrome.

    The long qt syndrome (LQTS) is associated with syncopal attacks or even sudden death at a young age due to ventricular fibrillation. We report a patient with an undiagnosed LQTS who had an episode of cardiac arrest during the final part of general anesthesia, immediately after the drugs for reversal of the neuromuscular blockade were given. We suggest that the administration of glycopyrronium might have been the provoking factor in this patient.
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2/81. nicorandil, a potassium channel opener, abolished torsades de pointes in a patient with complete atrioventricular block.

    TdP is a serious complication of AV block. We report a case of complete AV block with QT prolongation who had bouts of TdP resistant to lidocaine and isoproterenol. Temporary pacing could not be performed, because insertion of a pacing lead triggered TdP that deteriorated into ventricular fibrillation. nicorandil, a potassium channel opener, shortened the QT interval and abolished TdP. This may suggest that potassium channel opening drugs are clinically effective against TdP associated with bradycardia-dependent QT prolongation.
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3/81. Sudden death of a young hockey player: case report of commotio cordis.

    Despite the use of protective gear, a 15-year-old hockey player died when he was struck in the chest by a puck. This is the fifth recorded hockey death related to so-called commotio cordis, that is, blunt chest injury without myocardial structural damage. In light of inadequacies of commercial chest protectors currently in use for hockey, the authors hope to educate players and coaches about the danger of blocking shots with the chest. physicians should be aware that commotio cordis represents a distinctive pathological condition, in the event of which immediate recognition, precordial thump, CPR, and defibrillation are potentially lifesaving. Appropriate medical supervision at amateur hockey games, 911 telephone access, and on-site automated external defibrillators are issues that deserve careful consideration.
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4/81. Idiopathic verapamil-sensitive left ventricular tachycardia complicated by right ventricular outflow tract ventricular tachycardia and ventricular fibrillation.

    Idiopathic ventricular tachycardias (VTs) are generally divided into those arising from the right ventricle and those arising from the left ventricle. There has been few reports of two morphologically distinct VT occurring in patients with no apparent structural heart disease. We report a patient with verapamil-sensitive left VT with a right bundle branch block pattern that spontaneously changed to VT with a left bundle branch block pattern. Ventricular fibrillation was induced by the application of programmed stimulation. Although it is unclear if our patient with pleomorphic VT has ventricular vulnerability, it is necessary to investigate further and follow him carefully.
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5/81. 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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6/81. Dangerous impact--commotio cordis.

    Sudden death following blunt chest trauma is a frightening occurrence known as 'commotio cordis' or 'concussion of the heart'. It is speculated that commotio cordis could be caused by ventricular fibrillation secondary to an impact-induced energy that was transmitted via the chest wall to the myocardium during its vulnerable repolarization period. We describe a survivor of commotio cordis caused by a baseball. In this patient, an initial ventricular fibrillation was documented and converted by direct current defibrillation. Serial electrocardiographic changes (bifascicular conduction block and T wave inversion in precordial leads) were noticed in this patient. Our case suggested that coronary vasospasm might also play a role in commotio cordis.
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7/81. A novel SCN5A mutation associated with idiopathic ventricular fibrillation without typical ECG findings of brugada syndrome.

    Mutations in the human cardiac Na channel alpha subunit gene (SCN5A) are responsible for brugada syndrome, an idiopathic ventricular fibrillation (IVF) subgroup characterized by right bundle branch block and ST elevation on an electrocardiogram (ECG). However, the molecular basis of IVF in subgroups lacking these ECG findings has not been elucidated. We performed genetic screenings of Japanese IVF patients and found a novel SCN5A missense mutation (S1710L) in one symptomatic IVF patient that did not exhibit the typical Brugada ECG. Heterologously expressed S1710L channels showed marked acceleration in the current decay together with a large hyperpolarizing shift of steady-state inactivation and depolarizing shift of activation. These findings suggest that SCN5A is one of the responsible genes for IVF patients who do not show typical ECG manifestations of the brugada syndrome.
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8/81. Successful management of intractable coronary spasm with a coronary stent.

    Although the long-term survival of patients suffering from coronary spasm is usually excellent, serious complications can develop, such as disabling pain, myocardial infarction, ventricular tachyarrhythmias, atrioventricular block and sudden cardiac death. A 40-year-old man who had intractable chest pain from coronary artery spasm suffered ventricular fibrillation and an acute anterior myocardial infarction upon first admission. The patient underwent a coronary angiogram, which revealed a spontaneous focal spasm at the proximal left anterior descending coronary artery (LAD). He was treated by the combination of nitrate and calcium channel blocker, but continued to complain of severe chest pain despite intensive medical therapy and he had to be treated in the emergency room 5 times during an 8-month follow-up period. An ergonovine coronary angiogram was performed and an intracoronary ultrasound examination, which revealed a focal spasm at the same site of the proximal LAD with a small amount of localized eccentric atheromatous plaque. A coronary artery stent was placed in the proximal LAD and his symptoms resolved. A follow-up coronary angiogram was performed 3 years after stenting and the stent remained patent without any in-stent restenosis or spasm.
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9/81. Vasospastic angina accompanied by Brugada-type electrocardiographic abnormalities.

    brugada syndrome and Vasospastic Angina. We present two patients with vasospastic angina and Brugada-type ECG abnormalities. The first patient complained of chest pain, and transient ST segment elevation was confirmed on ECG. Coronary angiogram showed no organic stenosis. The second patient had syncopal episodes following anginal chest pain, and the same symptoms were reproduced by intracoronary acetylcholine injection that induced vasospasm. In both patients, ECG at rest showed ST segment elevation in leads V1 and V2 and a right bundle branch block pattern that were accentuated by a Class I antiarrhythmic drug. ventricular fibrillation also was induced by programmed electrical stimulation. Susceptibility to ventricular fibrillation can be modulated by the interaction of coronary vasospasm with brugada syndrome or vice versa; therefore, it is important to study the clinical implications of the coexistence of the two diseases in such patients.
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10/81. Inappropriate shock therapy in a heart failure defibrillator.

    A 63-year-old male with dilated cardiomyopathy underwent implantation of a "heart failure" defibrillator capable of biventricular pacing. He received an inappropriate shock 5 hours after the procedure. Stored electrograms revealed that during each sinus beat the ventricular channel recorded up to three separate events. These resulted from far-field atrial sensing by the coronary venous lead, appropriate right ventricular sensing, then delayed left ventricular sensing (the result of left bundle branch block). As a consequence of far-field left atrial sensing the two subsequent ventricular electrograms fell within the VF zone. Following an atrial premature beat, VF detection criteria were satisfied and shock therapy delivered. Although coronary venous lead repositioning eliminated far-field atrial sensing, double counting of the widely split right and left ventricular electrograms still occurred during sinus rhythm. Shortening the programmed AV delay resulted in constant biventricular pacing with a single electrogram.
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