Cases reported "Cardiomegaly"

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1/10. Localized left ventricular myocardial defect leading to fatal cerebral embolism.

    The case of a previously health 17-year-old youth who presented a fatal cerebral infarct is described. A localized defect in the anterior left ventricular myocardium with overlying thrombus, and left ventricular hypertrophy were found at necropsy. An old infarct was found in the left kidney. There were no signs of ischaemic or inflammatory heart disease. The possible origins of the lesion are discussed.
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2/10. An autopsied case of Eisenmenger syndrome complicated by recurrent thromboembolic phenomena in postpartal period.

    dyspnea, back pain, edema, and cyanosis developed suddenly in a 23-year-old woman during the last trimester of her first pregnancy. Although she had been noticed to have the enlarged heart and exertional shortness of breath to a slight degree, she had been apparently in good condition without any significant heart murmurs. Clinically, recurrent episodes of disseminated intravascular coagulation, including pulmonary thrombosis, were thought to be superimposed to Eisenmenger syndrome associated with toxemia of pregnancy. Anticoagulant and fibrinolytic treatments were tried, but their effectiveness was limited by hemorrhagic diathesis. She died of respiratory and circulatory failure after delivery of a moribund baby. autopsy revealed eisenmenger complex (a defect in the membranous portion of the interventricular septum and pulmonary vascular disease) and many fresh hemmorrhages in both lungs with a lot of new and organized thrombi. Fresh thrombi were also seen in the heart, the pancreas and the kidneys. The high peripartal mortality in Eisenmenger syndrome could be attributed to pulmonary thrombosis, which may be related to DIC, as well as to peripartal changes in circulatory function.
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3/10. Cardiopulmonary complications in multicentric reticulohistiocytosis. Report of a case.

    Multicentric reticulohistiocytosis (MR) is a rare disease. Only recently was its systemic nature appreciated. It affects the skin, mucous membranes, joints, muscles, tendon sheaths, synovial membranes, bones, liver, kidney, lymph nodes, heart, and lungs. Our patient, a 50-year-old woman, had life-threatening cardiopulmonary complications of MR. The connection between the skin lesions, the arthritis, and the pathologic changes in the heart and lungs is still obscure.
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4/10. 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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5/10. An autopsy case of mitochondrial encephalomyopathy (MELAS) with special reference to extra-neuromuscular abnormalities.

    An autopsy case of a 37-year-old man with mitochondrial encephalomyopathy is reported. Ragged-red fibers and crystalline inclusions in mitochondria were revealed by biopsy of the striated muscle of the patient. Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) was diagnosed clinically. In addition to severe atrophy and degeneration of the generalized striated muscles and many foci of laminar necrosis of the cerebral cortex, the following abnormalities were observed: 1) hypertrophy of the myocardium, 2) fatty change of the liver, 3) focal sclerosis of the glomeruli and dilatation of the tubules of the kidneys, 4) hyalinous degeneration of the Langerhans' islands of the pancreas and 5) wavy change of the smooth muscle fibers of the muscularis propria of the gastrointestinal tract. We suggest that mitochondrial encephalomyopathy affects various organs and tissues, among which susceptibility of the muscular tissues--skeletal muscle, myocardium and smooth muscle--is high.
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6/10. Cardiocyte storage and hypertrophy as a sole manifestation of Fabry's disease. Report on a case simulating hypertrophic non-obstructive cardiomyopathy.

    Fabry's disease was diagnosed in an adult patient as a lipid storage-induced non-obstructive hypertrophic cardiomyopathy. Stable angina pectoris started 15 years before death, was followed by slowly progressive heart failure and repeated pulmonary thromboembolism with death at 63 years. autopsy disclosed enormous cardiomegaly (1100 g), cardiac storage of ceramide trihexoside (CTH) of the same intensity as in classical cases of generalized Fabry's disease (11 mg lipid/g wet weight) restricted to cardiocytes. Other tissues (liver, kidney, brain, pancreas, pulmonary artery, coronary arteries) were free of storage. Using proton magnetic resonance analysis on formaldehyde-fixed tissue the stored CTH was identified as globotriaosylceramide. It was enzymatically degradable by control cell cultures but left uncleaved by mutant reference Fabry cells. alpha-galactosidase activities in peripheral leucocytes of all four of the patient's daughters were in the heterozygous range. The diagnostic difficulties in this monosymptomatic novel variant of Fabry's disease are stressed.
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7/10. Treatment of malignant hypertension with an angiotensin converting enzyme inhibitor.

    Malignant hypertension developed in an 18-year-old man whose primary hypertension had been diagnosed by chance. Standing blood pressure was 290/170 mmHg. Tests of renal function revealed high blood urea nitrogen and creatinine levels and low levels of both effective renal plasma flow and the glomerular filtration rate. Plasma renin activity and levels of angiotensin ii and aldosterone were greatly elevated. Severe concentric left ventricular hypertrophy was noted. The patient received standard antihypertensive treatment with furosemide, propranolol, nifedipine, and prazosin, but his blood pressure did not decrease and there was no improvement in the clinical or biochemical measures. The patient was then given 20 mg of enalapril daily for one year. The inhibition of angiotensin converting enzyme immediately reduced blood pressure. angiotensin ii and aldosterone levels became normal, kidney function and hemodynamics improved, and echocardiograms revealed that the left ventricular hypertrophy had regressed. The results confirm the pathogenetic role of angiotensin ii in the development of the malignant phase of hypertension.
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8/10. Symptomatic renal artery stenosis superimposed on chronic glomerulonephritis.

    We present two patients with proved chronic glomerulonephritis who had severe refractory hypertension and chronic renal failure. In both patients normal-sized kidneys were demonstrated in addition to vascular bruits and Grade III hypertensive retinopathy. These findings raised the suspicion of an etiological condition other than chronic glomerulonephritis underlying the hypertension and renal failure. Renal angiography revealed bilateral severe renal artery stenosis. In both cases renal revascularization was followed by a drop in blood pressure to normal or near normal levels. In selected cases with severe hypertension and chronic renal failure, renal artery stenosis should be considered, despite the coexistence of chronic glomerulonephritis.
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9/10. Acquired arterio-venous fistulas. Report of 223 operated cases.

    More than 200 years ago William Hunter described the first arteriovenous fistula (a.v.). Fragments of low velocity are the most frequent cause for a combined vascular trauma. However, a.v. fistulas may also develop after a skull fracture, after surgical interventions (lumbar disc operation, suture ligation for the removal of an organ like the kidney, the spleen and others). Three circulatory disorders may follow an a.v. fistula. Local signs at the location of trauma (machinery murmur, varicose veins). Cardiac dilatation due to the increase of heart volume. Degenerative changes and aneurysm formation in the artery above the fistula. Late complications may arise in the dilated central segment of the artery (aneurysm or thrombosis). The etiology of 223 traumatic a.v. fistulas (1939-1973) were in the majority (82%) of patients caused by war time injuries. Fractures and stab wounds were also common causes of a.v. fistulas. The location of a.v. fistulas was in about 50% in the lower extremities and only in 3% in the trunk. As to therapy - in contrast to the older quadruple ligature - the separation method should be the method of choice. The repair in arterio-venous fistulas should be done as early as possible. The operative cure rate in our series was 96%.
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10/10. Renal arteriovenous fistula--angiographic and sonographic correlation.

    We report a case of a markedly enlarged inferior vena cava and a cystic structure simulating a hydronephrotic kidney in the clinical setting of hypertension with cardiomegaly, congestive heart failure and a flank bruit. Ultrasonographic findings with the aid of angiography were highly suggestive of a renal arteriovenous fistula or malformation.
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