Cases reported "Death, Sudden, Cardiac"

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1/58. Potential proarrhythmic effects of implantable cardioverter-defibrillators.

    Implantable cardioverter-defibrillator (ICD) interventions have the potential to be proarrhythmogenic. New arrhythmias can occur in the setting of clinically appropriate therapies, as well as during a cardiac rhythm for which therapy is not intended. Cardioversion/defibrillation therapies, antitachycardia pacing, and antibradycardia pacing are potential triggers for the development of new arrhythmias. Newer ICDs allow better recognition and interpretation of the arrhythmias that are induced by delivered therapies. Two cases of ICD-induced proarrhythmias are described. Based on the course of these patients and review of previous reports, proarrhythmic effects of ICD interventions along with prevention and management strategies are discussed.
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2/58. Combining nonpharmacologic therapies for advanced heart failure: the Munster experience with the assist device-defibrillator combination.

    Implantable cardioverter defibrillators (ICDs) and ventricular assist devices (VADs) have been used as a bridge to cardiac transplantation. In selected patients, the combined implantation may be required. This study was motivated by a case of a 33-year-old female patient with giant cell myocarditis who died of ventricular tachyarrhythmias after having been placed on a VAD with which she had been treated on an out-of-hospital basis for a prolonged period of time. A subsequent retrospective analysis of our data showed that, of 73 patients who had to be bridged mechanically (54 Novacor, 12 TCI Heartmate, 4 Thoratec, 3 Medos) in our institution between 1993 and 1998, 10 patients had undergone defibrillator implantation either before (n = 8) or after (n = 2) implantation of a VAD. The cases are presented, and the feasibility of the combination therapy discussed.
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3/58. syncope in the pediatric patient. The cardiologist's perspective.

    The evaluation of syncopal children or adolescents relies heavily on a thorough, detailed history and physical examination. All syncope associated with exercise or exertion must be considered dangerous. The ECG is mandatory, but other laboratory tests are generally of limited value unless guided by pertinent positives or negatives in the history and physical examination. The ECG allows screening for dysrhythmias, such as wolff-parkinson-white syndrome, heart block, and long qt syndrome, as well as hypertrophic cardiomyopathies and myocarditis. Tilt table testing can be useful in selecting therapy by demonstrating the physiologic response leading to syncope in an individual patient. The most common type of syncope in otherwise healthy children and adolescents is neurocardiogenic or vasodepressor syncope, which is a benign and transient condition. Because syncope can be a predictor of sudden cardiac death, it must be taken seriously, and appropriate screening must be performed.
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4/58. torsades de pointes in a case of hypertrophic cardiomyopathy with special reference to the pathologic findings of the heart including the conduction system.

    A clinicopathologic study was performed in a 77-year-old female with hypertrophic cardiomyopathy who had experienced recurrent syncopal attacks due to Torsades de Pointes (TdP) following QT prolongation and atrioventricular block. She died suddenly two years later while eating dinner. Pathologic findings of the heart showed a dilated and hypertrophied left ventricle. The heart weighed 550 g. There were two foci of localized endocardial fibroelastosis (EFE) beneath the aortic valve, one with a size of 3.5 x 3.5 cm, and the other (2 x 1 cm) located on the upper ventricular septum. Histologic findings showed hypertrophy and disarray in the left ventricular myocardium. The conduction system using serial sectioning revealed remarkable bilateral bundle branch fibrosis and hypertrophied purkinje fibers in the left bundle branch adjacent to the EFE on the ventricular septum. These findings were thought to be related to the occurrence of TdP.
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5/58. Studies on the mechanism of a fatal clarithromycin-pimozide interaction in a patient with tourette syndrome.

    The authors report in detail the case of a 27-year-old man who experienced sudden cardiac death 2 days after coprescription of the neuroleptic pimozide and the macrolide antibiotic clarithromycin after the documentation of a prolonged QT interval. To determine the prevalence of this interaction, the authors referred to the Spontaneous Reporting System of the food and Drug Administration and identified one similar case in which clarithromycin was coprescribed with pimozide and sudden cardiac death occurred shortly thereafter. In addition, the search identified 39 cases of cardiac arrhythmia associated with pimozide, 11 with pimozide alone, and 6 with clarithromycin alone, 1 of which had a positive rechallenge. The mechanism of the interaction between clarithromycin and pimozide seems to involve the inhibition of the hepatic metabolism of pimozide by the macrolide. The authors demonstrated that clarithromycin is able to inhibit the metabolism of pimozide in human liver microsomal preparations (K(i) = 7.65 /- 1.18 microM) and that pimozide, but not clarithromycin or its primary metabolite, is able to prolong the electrocardiac QT interval in a dose-dependent manner in the isolated perfused rabbit heart. The increase was 9.6 /- 1.1% in male hearts (N = 5) and 13.4 /- 1.2% in female hearts (N = 4) (p < 0.05).
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6/58. Defibrillator challenges for the new millennium: the marriage of device and patient-making and maintaining a good match.

    Although it has become clear that implantable cardioverter defibrillators (ICDs) are effective, important challenges remain for the physician. Due to the limitations of available risk stratification tools, patient selection for primary sudden death prevention remains controversial in many populations. Additionally, the proliferation of device choices has led to challenges in matching the appropriate device to the individual patient: device size is balanced against longevity; the advantages of dual chamber systems is weighed against their increased complexity; physician and patient preferences in device implant site are constrained by site-dependent effects on defibrillation effectiveness and lead failure rates; and special consideration must be given to the patient with a preexisting pacemaker. After ICD placement, determination of appropriate follow-up frequency and methodology to assess device function must be considered. This article will review patient selection, device implant site selection, device-device interactions, single versus dual chamber ICD selection, and follow-up.
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7/58. arrhythmogenic right ventricular dysplasia. An illustrated review highlighting developments in the diagnosis and management of this potentially fatal condition.

    arrhythmogenic right ventricular dysplasia is an inherited, progressive condition. Characterised by fatty infiltration of the right ventricle, it frequently results in life threatening cardiac arrhythmias, and is one of the important causes of sudden cardiac death in the young. There are characteristic electrocardiographic and echocardiographic features that all physicians need to be aware of if we are to reduce these occurrences of premature death. diagnosis with magnetic resonance imaging is discussed along with current treatment options.
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8/58. Molecular autopsy of sudden unexplained death in the young.

    Sudden unexplained death (SUD) claims over 4,000 persons between the age of 1 and 22 each year in the united states. Nearly half of all pediatric SUD cases have a normal structural autopsy evaluation and are dismissed without a diagnosis. With the discovery of the genetic basis for potentially fatal arrhythmias associated with the inherited long qt syndrome (LQTS), postmortem molecular diagnosis of this disorder is possible. The authors describe the results of a molecular autopsy performed on a 17-year-old boy found dead in bed. A novel clinical test involving an epinephrine challenge in the decedent's mother implicated a potential defect in the phase 3 potassium current encoded by the gene KVLQT1. Exon-specific amplification by polymerase chain reaction and direct dna sequencing of KVLQT1 revealed a 5-base pair deletion in the genetic material recovered from the decedent's paraffin-embedded heart tissue. The ability to perform molecular autopsies on archived necropsy material undoubtedly will transform the forensic evaluation of SUD. The combination of catecholamine provocation testing in survivors and a postmortem LQTS gene analysis may unmask families with "concealed" LQTS and establish the cause and manner of death in SUDS.
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9/58. Sudden cardiac death with clozapine and sertraline combination.

    OBJECTIVE: To report a case of sudden cardiac death in a patient receiving combination therapy with clozapine and sertraline. CASE SUMMARY: A 26-year-old white man was discovered dead at his residence. His medical history included chronic paranoid schizophrenia, obsessive-compulsive disorder, major depressive disorder, obstructive sleep apnea, and akathisia. He had no prior history of cardiovascular disease. His medication regimen included clozapine 100 mg twice daily (started 4 y prior to his death), risperidone 3 mg twice daily, sertraline 200 mg once daily, atenolol 50 mg twice daily, and lorazepam 0.5 mg four times daily. autopsy and toxicology studies revealed cardiomegaly suggestive of idiopathic cardiomyopathy, single-vessel coronary artery disease, sertraline and clozapine blood concentrations in the expected range, undetectable lorazepam and risperidone blood concentrations, obesity, and moderate fatty changes to the liver. The most likely cause of death was sudden cardiac death due to acute cardiac arrhythmia. DISCUSSION: clozapine is structurally similar to the tricyclic antidepressants, which have type 1 A antiarrhythmic properties. case reports have described electrocardiographic abnomalities, cardiomyopathy, and fatal myocarditis associated with its use. Unexplained death in patients on clozapine therapy has also been reported. sertraline appears to have less cardiac effect; however, one report has observed clinically significant QT prolongation during sertraline therapy. CONCLUSIONS: clozapine-induced cardiomyopathy and cardiac arrhythmia from clozapine and/or sertraline use may have contributed to this man's death.
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10/58. Aborted sudden death, transient Brugada pattern, and wide QRS dysrrhythmias after massive cocaine ingestion.

    Although cocaine is one of the leading causes of drug-related deaths, there is little clinical information describing the precise sequence of events leading to death in the cocaine intoxication. Usually, cocaine-related sudden deaths are unwitnessed, its electrocardiographic features are not attainable, and the majority of these patients have a rapidly fatal course and die before arriving at the hospital. We report a patient with massive cocaine ingestion who developed psychomotor agitation and generalized seizures followed by asystolic cardiac arrest. ventilation with supplemental oxygen by endotracheal intubation immediately restored spontaneous heart beat. After resuscitation, a severe metabolic acidosis (pH 6.65) and cardiac dysrrhythmias consistent with sodium channel poisoning were detected. The electrocardiogram showed accelerated junctional rhythm at 85 beats/min with right bundle branch block and left anterior hemiblock configuration, prolongation of QRS (0.16 sec) and QTc (0.52 sec) intervals, and terminal J wave associated with coved ST-segment elevation in leads V(1) and V(2) resembling the brugada syndrome. sodium bicarbonate administration was quickly followed by normalization of the cardiac conduction disturbances. This article discusses the clinical and electrophysiologic implications of these findings.
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