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We present a patient with pericardial tamponade due to amyloid heart disease. A 64-yr-old man was admitted to the hospital because of fatigue and the abrupt development of chest pain and dyspnea. Echocardiography showed severe pericardial effusion and total pericardiectomy was necessary. Ten months later laboratory studies revealed proteinuria and high serum creatinine. A rectal biopsy showed amyloid deposition that was also found in the pericardial tissue. Pericardial tamponade is an extremely rare complication of cardiac amyloidosis. To our knowledge, only one previous case of cardiac tamponade due to amyloid heart disease has been reported.
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PMID:Cardiac tamponade as presentation of systemic amyloidosis. 142 40

Autopsy or surgical specimens from six patients with primary cardiac angiosarcoma seen at the Mayo Clinic (all in men) between 1939 and 1988 were studied (patients' ages, 31 to 80 years; mean 50 years). The symptoms were nonspecific and included dyspnea and thoracoabdominal pain in six; anorexia in five; fatigue, hemoptysis, or orthopnea in four; nausea and vomiting, fever, or weight loss in three; and night sweats in two. Cardiomegaly was present in five, and a pericardial effusion or density, a mass adjacent to the heart, or nonspecific ST-T wave changes were present in three. All six neoplasms arose from the right atrium and exhibited epicardial or endocardial extension; three produced obstructive intracavitary right atrial masses. Pulmonary metastatic lesions were noted in five patients. The cardiac neoplasm was diagnosed by computed tomography or magnetic resonance imaging in the three most recent patients, and surgical resection was performed in two of them. Mean survival was 6 months after presentation. Causes of death were pulmonary hemorrhage in three, thoracic metastasis in two, and hemopericardium in one. The diagnosis of primary cardiac angiosarcoma was established at operation in two patients and at autopsy in four. Despite diagnosis by noninvasive imaging procedures and aggressive early surgical intervention, survival was less than 6 months. Thus optimal therapy is unclear.
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PMID:Primary cardiac angiosarcoma: a clinicopathologic study of six cases. 154 8

Since it is very rare that cardiac tamponade due to myocardial rupture caused by infective endocarditis, occurs we are reporting this case. A 62 year old man, who had underlying diseases of pneumoconiosis and hypertensive heart disease, visited Chikuho Rosai Hospital complaining of chest oppression and general fatigue on Feb. 7, 1987. He was diagnosed as having ischemic heart disease by electrocardiogram. Two days later, he suddenly had chills and a fever, and the laboratory data showed leukocytosis and a positive C-reactive protein (CRP). The echo cardiogram showed mitral regurgitation (MR) and aortic regurgitation (AR), but neither vegetation nor pericardial effusion was observed. On Feb. 16, he was admitted with shock, and he died the next day. The blood cultures grew gram-positive cocci, respectively. From the clinical symptoms, chest roentgenogram and electrocardiogram, we suspected a cardiac tamponade. On autopsy findings, though coronary arteries were intact, the aortic valves had severe valvular adhesions, calcifications and hypertrophies. The rupture hole was observed in the left ventricles, which was just under the aortic valve through the pericardiac space. It seemed that he died of a cardiac tamponade due to the outflow of blood from this hole. On histopathologic findings of the cardiac wall, gram-positive cocci and many of neutrophils were observed.
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PMID:[An autopsied case of infective endocarditis with cardiac tamponade due to myocardial rupture]. 207 73

A 61-year-old woman with low grade obesity index complained of general fatigue. Cardiomegaly had been present since the age of 45. According to a roentgenogram on admission, her cardia-thoracic ratio was 61%. Pericardial effusion was strongly suspected because of extra echo spaces on both posterior and anterior walls, and unsynchronized echocardiograph waves of epicardium and pericardium. However, values of dynamic CT measured at areas equivalent to the extra echo spaces were -120. On admission, T1-emphasized MRI image showed a high signal density in those areas. After significant weight reduction, the abnormal values and signs of the clinical examinations, as well as the patient's complaints were attenuated or disappeared. Together with these results, cardiomegaly of the patient was diagnosed to be due to excessive fat deposit between the epicardium and cardiac muscle. Dissociation between mildness of obesity index and excessive deposition of fat in the pericardium was discussed from the point of view of body mass index and time course of fat deposition.
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PMID:[A case of mild obesity accompanied by epicardial fat deposition]. 214 82

A 40-year old female was admitted with complaints of general fatigue and dyspnoea brought on by effort. There were edema on the face, a diffuse and slightly hard goiter on the neck and non-pitting edema in the lower legs. Laboratory findings showed low levels of serum T3 (0.37 ng/ml) and T4 (2.0 micrograms/dl), a very high level of serum TSH (549.8 microU/l), positive thyroid test (x 400) and positive microsome test (x 102,400). The chest roentgenogram showed an enlargement (CTR 62%) of the cardiac silhouette in the shape an ice bag, and the electrocardiogram revealed low QRS voltage with T-wave flattening in all leads. Remarkable pericardial effusion was shown on the two-dimensional echocardiogram. Judging from the indications of hypothyroidism, positive antithyroid antibody and pericardial effusion. This patient was diagnosed as having myxedema heart due to chronic thyroiditis. The levels of plasma alpha-hANP did not elevate so much as the levels in normal controls after right atrial (RA) pacing, although mean right atrial pressure was higher than in normal controls after RA pacing. The levels of plasma alpha-hANP after RA pacing in euthyroid state were higher than those in hypothyroid state. The levels of plasma alpha-hANP after RA pacing became higher after the administration of ATP or db-cAMP both in euthyroid and hypothyroid states. These results indicate that the impaired alpha-hANP secretion in myxedema heart is improved by the administration of thyroxine, ATP or db-cAMP.
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PMID:[A case of myxedema heart showing the improvement of impaired alpha-hANP secretion by administration of ATP and dibutyryl cAMP]. 217 40

This case was a 51-year-old woman, who had been diagnosed as having rheumatoid arthritis at some clinic and had been treated with both non-steroidal anti-inflammatory drugs and steroid 3 years before visiting our clinic. When she noticed a decrease in visual acuity and general fatigue in June 1985, she was referred to an ophthalmologist of our hospital, and found to have blood pressure of 240/150 mmHg and KW grade IV retinal findings. She was admitted in our department to examine and treat malignant hypertension. On admission, remarkable hypergammaglobulinemia (29.3%), arthralgia, arthral deformity and pericardial effusion were present thus, she was suspected to be suffering from malignant rheumatoid arthritis. Anti-nuclear antibody (64X), anti-nuclear ribonucleoprotein antibody (64X) and anti-RNase sensitive antibody of anti-extractable nuclear antigens (ENA) antibody (81920X) were positive, while anti-RNase resistant antibody of anti-ENA antibody was negative. Immunologically, her condition was consistent with mixed connective tissue disease (MCTD). Since urinary protein was positive and creatinine clearance was 46.0 ml/min, renal function was thought to be diminished. Her chest roentgenogram revealed cardiomegaly (CTR 67.5%) and an increase in pulmonary vascular shadow. An echocardiogram demonstrated the presence of pericardial effusion. Plasma renin activity was 3.3 ng/ml/h and it was suspected that an intrarenal ischemic change resulted in increased renin release from the juxta-glomerular apparatus, leading to the marked hypertension. Treatment was started with prednisolone 60 mg/day during 4 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of mixed connective tissue disease complicated with malignant hypertension]. 219 30

The Patient was a 72-year-old man who presented with dyspnea and general fatigue. Chest X-ray and CT-scan at the admission showed bilateral pleural effusion with collapse of the left lung and pericardial effusion. Cytology from the left pleural effusion suggested malignant mesothelioma. For this reason, malignant mesothelioma of the left pleura was diagnosed clinically and it was supposed to have spread subsequently to the pericardium. At autopsy, entire surface of the heart was found to be encroached in a diffuse fashion by a thick layer of mesothelioma tissues, which formed a small mass around the left pulmonary vein over the left atrium and invaded deep into the myocardium of all cardiac chambers. The endocardium and the intima of the left pulmonary vein were free of the invasion. The parietal pericardium adhered in places to the cardiac lesion, but no direct invasion to the adjacent pleurae through the pericardial wall was present. The left pleura over the lung and chest cavity disclosed only a superficial invasion by similar mesothelioma which was identifiable only on microscopic study. No distant metastasis was present in any thoracic and other organs as well as lymph nodes including the hilar ones of the lung. It seemed most likely from this anatomical finding that the primary site of the present mesothelioma was in the pericardium (visceral) and the tumor spread to the left pleura by a continuous extension along the outside of the left pulmonary vein. Primary malignant mesothelioma of the pericardium is of very rare occurrence and we found only 51 cases of it in the Japanese literature since 1915.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Primary malignant mesothelioma of the pericardium masquerading as malignant pleural mesothelioma: report of an autopsy case and review of the reported cases in Japan as to its invasion to neighboring organs]. 268 98

Primary cardiac tumor is an extremely rare disease entity. Only three cases of primary malignant cardiac schwannoma, the subject of this report, have been recorded in Japan. Recently, we encountered a case of malignant schwannoma in which retention of pericardial effusion was the first clinical finding. This case was a 30-year-old female, who had dyspnea at work, general fatigue, and fever. Striking cardiac expansion was seen, with a cardiothoracic ratio (CTR) of 69% on chest x-ray. Two-dimensional echocardiograms showed a large volume of pericardial effusion between the side wall of the left ventricle and the epicardium, and the presence of a parenchymatous tumor. An increase in tumor size was detected on chest computer tomography (CT) scan. Using a pump oxygenator, median sternotomy was performed to reach the epicardium. A pale yellow, soft tumor was seen in the left atrium near the left ventricle. Histologically, the patient was diagnosed as having a malignant schwannoma. We have reported a case of primary malignant schwannoma which was surmised to have arisen from the boundary between the atrium and the ventricle.
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PMID:Malignant schwannoma of the heart. 334 6

The characteristic hemodynamic features of restrictive cardiomyopathy (normal or reduced cardiac index, normal ventricular systolic function, and "dip and plateau" early in diastole) are traditionally associated with pathologic evidence of inflammation, infiltration and fibrosis. Prognosis is usually poor. Nine patients with restrictive hemodynamic features were recently identified in our laboratory; six were males, three were females, and ages ranged from 23-57 years (mean 47 years). Only one was asymptomatic. Chest pain, dyspnea on exertion and fatigue were the most common symptoms. Echocardiography revealed various degrees of left ventricular wall thickening, but no significant pericardial effusion, pericardial thickening or calcification. Mean left ventricular end-diastolic pressure was 25 mm Hg, cardiac index 2.8 l/min/m2 and ejection fraction 0.63. Endomyocardial and pericardial biopsies, obtained in two patients, were normal. Follow-up (mean 22 months, range 16-42 months) revealed no cardiac deaths. These findings support the hypothesis that the restrictive hemodynamic profile does not necessarily indicate the presence of a specific pathologic process in the subendocardium or myocardium and that the prognosis is not necessarily ominous. The common pathophysiologic feature for this syndrome appears to be reduced ventricular diastolic compliance, but the etiology in many cases is unclear.
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PMID:Clinical profile of restrictive cardiomyopathy. 644 42

With advancing age of the population and with echocardiographic means of diagnosis, amyloid disease of the heart is of increasing clinical interest. Advanced age, restrictive myocardiopathy, arrhythmias, and conduction disorders are familiar features of this disease. A 92 year old man with past history of hemiblock followed by complete heart block and transvenous pacemaker was admitted to the hospital because of increasing fatigue and the abrupt development of dyspnea. Examination revealed paradoxic pulse, markedly elevated central venous pressure, and echocardiographically demonstrated large pericardial effusion. Shortly after admission signs of tamponade developed; 1,000 ml of pericardial fluid was removed with prompt relief of dyspnea dna disappearance of paradoxic pulse and return of central venous pressure to normal. However, dyspnea soon recurred and subsequent hemodynamic measurements indicated increased right ventricular and left ventricular filling pressures. Echocardiography revealed no recurrent effusion or ventricular hypokinesis. Left ventricular ejection fraction by radionuclide ventriculogram was 64 percent. Echocardiography revealed ventricular wall thickening, normal chamber size, and glittering, sparkling myocardial echoes. On postmortem examination, there was extensive myocardial amyloidosis. There was no evidence of constrictive pericarditis or recurrent effusion. The unique aspect of this case was the combined presence of restrictive myocardiopathy and pericardial tamponade. To our knowledge, no previous case of tamponade due to amyloid heart disease had been reported.
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PMID:Pericardial tamponade, a new complication of amyloid heart disease. 709 Nov 68


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