Cases reported "Death, Sudden, Cardiac"

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1/30. 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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ranking = 1
keywords = myocarditis
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2/30. 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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ranking = 1
keywords = myocarditis
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3/30. association of rickettsia helvetica with chronic perimyocarditis in sudden cardiac death.

    BACKGROUND: rickettsia helvetica is the only non-imported rickettsia found in scandinavia. It was first detected in ixodes ricinus ticks, but has never been linked to human disease. We studied two young Swedish men who died of sudden cardiac failure during exercise, and who showed signs of perimyocarditis similar to those described in rickettsial disease. methods: Samples from the heart and other organs were analysed by PCR and dna sequencing. May-Grunwald-Giemsa, Grocott, and acridine-orange stains were used for histopathological examinations. Staining of R. helvetica grown on shell-vials in vero cells, and the early descriptions of R. rickettsii by H T Ricketts and S B Wohlbach served as controls. immunohistochemistry was done with proteus OX-19 rabbit antisera as the primary antibody. The structure of rickettsia-like organisms was investigated by transmission electron microscopy. Serological analyses were carried out by indirect immunofluorescence with R. helvetica as the antigen. FINDINGS: By use of a semi-nested PCR, with primers specific for the 16S rRNA and 17-kDa outer-membrane-protein genes, and sequence analysis of the amplified products, genetic material from R. helvetica was detected in the pericardium and in a lymph node from the pulmonary hilum in case 1, and in a coronary artery and the heart muscle in case 2. A serological response in case 1 revealed an endpoint titre for R. helvetica of 1/320 (1/256 with R. rickettsii as the antigen). Examination of PCR-positive tissue showed chronic interstitial inflammation and the presence of rickettsia-like organisms predominantly located in the endothelium. These organisms reacted with proteus OX-19 antisera, and their size and form were consistent with rickettsia. Electron microscopy confirmed that the appearance of the organisms was similar to that described for spotted-fever rickettsia. INTERPRETATION: R. helvetica, transmitted by I. ricinus ticks, may be an important pathogen in the aetiology of perimyocarditis, which can result in sudden unexpected cardiac death in young people.
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ranking = 6
keywords = myocarditis
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4/30. Subacute bartonella infection in Swedish orienteers succumbing to sudden unexpected cardiac death or having malignant arrhythmias.

    During the period 1979-92, an increasing number of sudden unexpected cardiac deaths (SUCD) occurred in young, Swedish, male elite orienteers. myocarditis was the most common diagnosis in the 16 victims, and in 4 cases was also associated with fatty infiltration mimicking arrhythmogenic right ventricular cardiomyopathy (ARVC). tissues from autopsies of 5 orienteers were tested for bartonella by PCR targeting the gltA (citrate-synthase) gene. The products were then sequenced. antibodies to B. henselae, B. quintana and B. elizabethae were measured by indirect fluorescence antibody assay. bartonella spp. dna was detected in the hearts of 4 deceased orienteers, and in the lung of a fifth deceased case. The sequences were close to B. quintana in 2 cases and identical to B. henselae in 3. Four of these 5 cases, as well as 2 additional cases of elite orienteers with ARVC, indicated antibodies to bartonella. It is suggested that bartonella-induced silent subacute myocarditis, eventually leading to electric instability, caused the increased SUCD rate among the Swedish orienteers. It is further suggested that bartonella infection may be a major pathogenetic factor in the development of ARVC-like disease. Although the mode of transmission is unknown, both zoonotic/vector-borne and parenteral person-to-person transmission may be involved.
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ranking = 1
keywords = myocarditis
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5/30. 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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ranking = 1
keywords = myocarditis
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6/30. exercise-induced bidirectional ventricular tachycardia with alternating right and left bundle branch block-type patterns--a case report.

    exercise-induced ventricular tachycardia in young adults may occur with various structural heart diseases or with structurally normal heart. The structural heart diseases reported to cause exercise-induced ventricular tachycardia in this patient population include arrhythmogenic right ventricular dysplasia, hypertrophic cardiomyopathy, dilated cardiomyopathy, myocarditis, congenital heart disease, and myocardial ischemia. The conditions well identified to cause exercise-induced ventricular tachycardia with structurally normal heart are congenital long-QT syndrome and familial polymorphic ventricular tachycardia. exercise-induced ventricular tachycardia may display polymorphic, monomorphic, or bidirectional morphologies. A case of exercise-induced catecholamine-sensitive bidirectional ventricular tachycardia with alternating right and left bundle branch block patterns is reported in a young boy in the absence of structural heart disease, the conditions causing bidirectional ventricular tachycardia, and family history of such an event or sudden cardiac death. The bidirectional tachycardia typically displays right bundle branch block in right precordial leads with alternating polarity of the QRS-complex in frontal plane leads but in this case the bidirectional morphology of tachycardia was caused by alternating right and left bundle branch block-type patterns. The conditions causing bidirectional ventricular tachycardia are digoxin toxicity, ischemic heart disease, hypokalemia, myocarditis, and familial polymorphic ventricular tachycardia syndrome but the exact cause in this patient remained obscure, and the possibility of an underlying electrical or ion channel disease of the heart could not be ruled out.
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ranking = 2
keywords = myocarditis
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7/30. Sudden death in a 21-year-old man caused by thrombosed coronary aneurysm: late sequelae or a very late onset of Kawasaki disease?

    Kawasaki disease (KD; mucocutaneous lymph node syndrome) is an infantile febrile illness of unknown origin that occurs in worldwide epidemics. The main clinical features of the disease, such as fever, mucositis, cervical lymphoadenopathy and skin rash, associated with coronary aneurysms or arteritis are diagnostic. Late sequelae of coronary arteritis are very rare in the second decade of life; we describe the case of a 21-year-old male who died suddenly. The autopsy revealed a large thrombotic coronary aneurysm, coronary arteritis and myocarditis, supporting the diagnosis of a late fatal sequela of KD. The hypothesis of a very late onset of the disease is also considered and discussed.
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ranking = 1
keywords = myocarditis
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8/30. Focal parvovirus B19 myocarditis in a patient with brugada syndrome.

    The brugada syndrome is characterized by a distinct ECG pattern consisting of ST segment elevation in the right precordial leads and right bundle branch block, a propensity for life-threatening arrhythmias, and an apparently structurally normal heart. The authors describe the case of a patient with an aborted sudden cardiac death and the typical ECG signs of brugada syndrome. Nevertheless, magnetic resonance imaging displayed signal enhancement in the left ventricular myocardium. Additionally, histologic examination, in-situ hybridization, and PCR revealed evidence of a locally restricted inflammation due to parvovirus B19. brugada syndrome is regarded as a primary electrical disease due to dysfunction of distinctive ion channels, but focal myocarditis may serve as a trigger for ventricular arrhythmias in this patient. Further morphologic studies will be helpful to establish the possible role of structural changes in the pathophysiology of this syndrome.
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ranking = 5
keywords = myocarditis
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9/30. Sudden death due to granulomatous myocarditis: a case of sarcoidosis?

    INTRODUCTION: We report a case of sudden death due to granulomatous myocarditis and propose that cardiac sarcoid could have been the underlying aetiology. This is the first case reported in singapore. The differential diagnoses for granulomatous myocarditis including sarcoidosis and its cardiac manifestations as well as idiopathic giant cell myocarditis are discussed. CLINICAL PICTURE: A 53-year-old Indian woman died suddenly and autopsy revealed bilateral hilar adenopathy and myocardial infiltrates which proved to be granulomatous in nature. CONCLUSION: sarcoidosis may not be a rarity here and it is important to recognise the different clinical manifestations.
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ranking = 7
keywords = myocarditis
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10/30. Sudden arrhythmia death syndrome: importance of the long qt syndrome.

    In approximately 5 percent of sudden cardiac deaths, no demonstrable anatomic abnormality is found. Some cases are caused by sudden arrhythmia death syndrome. A prolonged QT interval is a common thread among the various entities associated with sudden arrhythmia death syndrome. A number of drugs are known to cause QT prolongation (e.g., terfenadine), as are hypokalemia, hypomagnesemia, myocarditis, and endocrine and nutritional disorders. Recently, attention has focused on a group of inherited gene mutations in cardiac ion channels that cause long qt syndrome and carry an increased risk for sudden death. Some of the highest rates of inherited long qt syndrome occur in Southeast Asian and Pacific Rim countries. The median age of persons who die of long qt syndrome is 32 years; men are predominately affected. In addition to a prolonged QT interval, which occurs in some but not all persons with long qt syndrome, another characteristic electrocardiographic abnormality is the so-called Brugada sign (an upward deflection of the terminal portion of the QRS complex). Most cardiac events are precipitated by vigorous exercise or emotional stress, but they also can occur during sleep. torsades de pointes and ventricular fibrillation are the usual fatal arrhythmias. long qt syndrome should be suspected in patients with recurrent syncope during exertion and those with family histories of sudden, unexpected death. Unfortunately, not all persons with long qt syndrome have premonitory symptoms or identifiable electrocardiographic abnormalities, and they may first present with sudden death. Beta blockers, potassium supplements, and implantable defibrillators have been used for treatment of long qt syndrome. Identifying the specific gene mutation in a given patient with long qt syndrome can help guide prophylactic therapy.
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ranking = 1
keywords = myocarditis
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