Cases reported "Cardiomegaly"

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1/43. Sudden death due to ventricular septal defect.

    Ventricular septal defects (VSD) are usually considered non-life-threatening, usually closing spontaneously or causing symptoms of congestive heart failure, which can be surgically treated in time to save the patient's life. Despite the usually benign clinical course of VSD, serious arrhythmias occur in 16-31% of patients. Sudden death accounted for one-third of all deaths in a series of medically managed patients and occurred in 4.2% of patients in a study of VSD and arrhythmias. Cardiac hypertrophy is the common denominator in all cases reported in detail of VSD-associated sudden death. We have encountered four cases of sudden unexpected death from VSD in infants ranging in age from 1 week to 3 and (1/2) months. In each case there was cardiomegaly and in one case there was pulmonary arteriolar medial thickening, with extension of smooth muscle into small intralobular vessels. In half of our cases the attending physician was sued for malpractice. We believe that VSD in infants and young children are potentially life-threatening malformations which warrant careful clinical follow-up.
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2/43. Sudden death in a traveler following halofantrine administration--togo, 2000.

    On July 17, 2000, a previously healthy 22-year-old U.S. student collapsed and died suddenly while leading a teenage exchange group in West africa. This report summarizes the results of the investigations of this incident, which implicate use of halofantrine for treatment of malaria as the cause of death. Travelers should be warned that halofantrine treatment may be dangerous in persons with cardiac abnormalities or in those taking mefloquine for malaria prophylaxis.
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3/43. Small aortic root as a cause of sudden death in a young adult: a controversial topic revisited.

    BACKGROUND: Sudden cardiac death over the age of 35 years is mostly due to coronary atherosclerosis, whereas under the age of 35 years, a variety of mainly congenital malformations prevail. However, hypoplasia of the aortic root in adults, first introduced by Laurie in 1968 as a cause of sudden cardiac death in adults, is never included. CASE REPORT: We present a case of a 29-year-old female who suddenly and unexpectedly collapsed during recreational bicycling. ventricular fibrillation was recorded, but resuscitation attempts failed, and the patient was declared dead about 1 h after the event. autopsy revealed cardiac hypertrophy with extensive scarring and a small aortic root (calculated inlet/outlet diameters=14.9/14.3 mm), without obstructive coronary artery disease or any other plausible cause for sudden cardiac death. CONCLUSIONS: The observations strongly suggest that small aortic root (less than 2 cm in diameter) provided the background for cardiac hypertrophy and, eventually, myocardial ischemia and ventricular fibrillation. Pathologists should be aware of this possibility while evaluating cases of sudden cardiac death without an obvious pathologic substrate.
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4/43. Surgical "correction" of solitus-concordant, double-outlet left ventricle with L-malposition and tricuspid stenosis with hypoplastic right ventricle.

    This report concerns a 2-year-old boy who had situs solitus and atrioventricular concordance with double-outlet left ventricle, L-malposition of the aorta, pulmonary stenosis, tricuspid stenosis, hypoplastic right ventricle, ventricular septal defect, and secundum atrial septal defect. These lesions were correctly diagnosed preoperatively, and "correction" was achieved by closing the atrial septal defect and tricuspid valve and performing a fontan procedure using an antibiotic-sterilized aortic homograft for the conduit. The patient initially did well postoperatively but, despite vigorous diuretic therapy, developed large bilateral pleural effusions necessitating frequent aspiration. He died unexpectedly one month after the operation. Postmortem examination showed the repair to be intact. Despite his death, we are encouraged to consider this operation in such cases in the future.
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5/43. Atrial myxoma in a family.

    A family is described in which the mother and three of seven children had atrial myxoma. The mother had biatrial myxoma; surgical treatment resulted in massive intraoperative embolization and death. Surgery was sucessful in two sons with left atrial myxoma and systemic arterial embolization. A third son had calcified right atrial myxoma with destruction of the tricuspid valve and episodes of syncope and pulmonary embolism; surgery including valve replacement, was successful. The mother's father and a brother had died suddenly without a definite diagnosis. The family data are consistent with dominant transmission. The possibility of finding affected relatives should be borne in mind when studying patients with atrial myxoma.
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6/43. Cardiac haemangio-endotheliosarcoma. review of the literature and report of a case.

    A case of primary haemangio-endotheliosarcoma of the right atrium is reported. A review of the literature is given and in all but four of the 56 cases, the tumour originates in the right atrium projecting into the cavity. This explains why these tumours present a rather uniform clinical picture characterized by superior vena caval syndrome combined with pericardial effusion, cardiomegaly, dyspnoea and chest pain. A male dominent sex distribution of 3 to 1 is found. The tumour is highly malignant and has caused death within an average of six months. We emphasize the possibility of early diagnosis particularly since eht clinical symptoms are rather typical and cases are reported where therapy apparently was successful.
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7/43. Infantile periarteritis nodosa or mucocutaneous lymph node syndrome. A report on four cases and diagnostic considerations.

    Coronary artery aneurysm in childhood is a rare disease and has in most cases been ascribed to infantile periarteritis nodosa (IPN). In recent years a mucocutaneous lymph node syndrom (MLNS) has been found almost exclusively in japan first described by Kawasaki 1967; this disease frequently involves the coronary arteries and myocardium. Four cases with coronary aneurysms are presented from sweden and seem to be first described from scandinavia. Three of these patients died a sudden death with cardiac arrest. Since MLNS and IPN have identical clinical and pathological features, we suggest that MLNS and IPN constitute a pathologic entity and that to separate them on a clinical or histological basis is nonsensical. The risk of coronary aneurysm and possible sudden death must be considered in patients with uncharacteristic symptoms including prolonged fever, conjunctivitis, exanthema, lesions in the oral mucosa, elevated sedimintation rate, and leukocytosis.
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8/43. Cardiomyopathy in an adult with Bartter's syndrome and hypokalemia. Hemodynamic, angiographic and metabolic studies.

    A case of an adult with Bartter's syndrome (hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis) is described; the patient had the unusual manifestation of cardiomyopathy, probably secondary to severe hypokalemia. Results of metabolic studies and kidney biopsy were consistent with Bartter's syndrome; angiographic and hemodynamic findings were abnormal. The cardiomyopathy was confirmed at autopsy after the patient's sudden death. Conclusions from this case are that severe hypokalemia can pose a serious threat both immediately in the form of dangerous arrhythmias and in the long term in the form of cardiomyopathy.
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9/43. Sudden and unexpected death of a 6-month-old baby with silent heart failure due to anomalous origin of the left coronary artery from the pulmonary artery.

    A 6-month-old girl died suddenly without any previous symptoms of heart failure. autopsy examination showed cardiomegaly (97 g) with a severely fibrotized myocardium. The left coronary artery was originating from the pulmonary artery. Histologically, the myocardium showed myocardial infarcts of different ages, as well as grossly thickened arterial branches due to increased flow in left-right shunt. We suggest that rare anomalies of the coronary arteries should be considered in the autopsies of suspected sudden infant death syndrome cases.
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10/43. Familial nonobstructive cardiomyopathy with endocardial fibroelastosis beyond infancy.

    A 10-year-old boy with congestive heart failure died in five months in spite of comprehensive medical treatment. autopsy showed patchy areas of endocardial fibroelastosis of the left ventricle. The sister of this patient had followed a similar course at 13 years of age with death within six months of the onset of congestive failure. Her postmortem examination also showed endocardial fibroelastosis. The clinical presentation of familial endocardial fibroelastosis in the preteen and teenage years is a rare event. Probably the endocardial fibroelastosis was secondary to a familial nonobstructive cardiomyopathy.
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