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1/51. Localized pericarditis with calcifications mimicking a pericardial tumor.

    A 62-year-old man was admitted with increasing palpitations. radiography of the chest demonstrated a calcified mass. magnetic resonance imaging revealed compression of the right ventricle by a tumor. At the time of cardiac catheterization, the coronary arteries were found not to supply blood flow of the mass, and no dip-and-plateau pattern was seen in the right ventricular pressure measurements. At the time of surgery, the mass was found to be a focal calcified thickening of the pericardium containing only pus. The thickening resembled an oval pericardial tumor. Microbiologic examination of the pus revealed propionibacterium acnes.
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2/51. Constrictive pericarditis following hemopericardium due to ascending aortic dissection: A case report.

    A 79-year-old woman, who had had no history of trauma, tuberculosis, or collagen diseases, was referred for examination of general fatigue and shortness of breath on exertion. physical examination revealed engorged neck veins, hepatomegaly, and ascites with abdominal distention. On chest x-ray the cardiac shadow was slightly enlarged and bilateral pleural effusion was present. An electrocardiogram showed low voltage of the QRS complex. Computed tomographic scans revealed two lumens in the remarkably dilated ascending aorta and the severely thickened pericardium. cardiac catheterization showed elevated right atrial pressure and elevated right and left ventricular end-diastolic pressures, in addition to a pressure record of early diastolic dip and end-systolic plateau in the right ventricle. aortography demonstrated aortic dissection localized to the ascending aorta. On the basis of these findings, the diagnosis of chronic ascending aortic dissection complicated with constrictive pericarditis was made. After subtotal pericardiectomy, graft replacement of the ascending aorta and proximal aortic arch was performed with successful results. Her postoperative recovery was uneventful. Histological studies of the pericardium showed fibrosis and marked infiltration of the inflammatory cells. No findings of specific pericarditis such as tuberculosis or collagen diseases were detected.
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3/51. Purulent pericarditis presenting as an extracardiac mass in a patient with untreated diabetes.

    A 50-year-old man with symptoms of bi-ventricular heart failure was transferred to our hospital with a diagnosis of extracardiac tumor. He had a 10 year history of untreated diabetes. Chest computed tomography (CT) revealed an extracardiac mass in the right atrio-ventricular groove. cardiac catheterization revealed an elevated mean right atrial pressure of 18 mmHg, mean pulmonary wedge pressure of 16 mmHg, and the right ventricular pressure curve demonstrated typical dips and plateaus. At surgery, there was severe adhesion between the pericardium and epicardium, and the pericardium was severely thickened and contained turbid pus. In the left thoracic cavity, there was large amount of pleural effusion and pus. Therefore, the patient was diagnosed with purulent pericarditis caused by left empyema. The thickened pericardium at the anterior portion of the heart was resected, however resection of the remaining portion was abandoned because the adhesion was so tight. After surgery, the patient underwent irrigation of the heart and left thoracic cavity by 1% povidone iodine solution and 0.5 mg/ml of imipenem for 7 days. Bacteriologic culture of the pus from the pericardium revealed anaerobic gram negative bacteria. After 4 months of antibiotics infusion, his C reactive protein became negative and the patient was subsequently discharged from our hospital.
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4/51. A case of constrictive pericarditis with local thickening of the pericardium without manifest ventricular interdependence.

    This is the first case report of postsurgical constrictive pericarditis confined to the left ventricle in which the majority of diagnosis tests were not indicative of the disease. A 50-year-old woman with a past history of mitral valve replacement was admitted for right heart failure. cardiac catheterization showed impaired diastolic filling but lacked the characteristic ventricular interdependence recently reported to be specific for the disease, without manifest radiological appearance of pericardial thickening. However, a new technique using magnetic resonance tagging cine revealed pericardial adhesion, limited to the left ventricle, which was confirmed during pericardiectomy. After the surgery, right heart failure and diastolic filling abnormality disappeared with restoration of normal heart pressures.
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5/51. Degos' disease with constrictive pericarditis: a case report.

    A 47-year-old man with Degos' disease was examined by echocardiography, which showed hypokinesis of the apical left ventricular wall with pericardial effusion. To evaluate the myocardial perfusion and coronary flow reserve, 201Tl scintigraphy and intracoronary Doppler flowmetry were performed. The coronary flow reserve was not decreased nor was there angiographical coronary stenosis, although a pressure study revealed constrictive dysfunction of both ventricles. The constrictive pericarditis might have been induced by pericardial vasculitis, thereby causing the left ventricular wall motion abnormality.
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6/51. Constrictive chronic pericarditis in children.

    Constrictive pericarditis is a uncommom disease in children. We have now encountered pericardial thickening as the cause of severe constrictive physiology in two patients, one also having haemodynamic features of restrictive cardiomyopathy. Both patients, who had refractory ascites and evidence of increased systemic venous pressure, underwent Doppler echocardiography, cardiac catheterisation, and magnetic resonance imaging. Resonance imaging failed to show any thickning of the pericardium, but cardiac catheterisation revealed diastolic equalisation of pressures in all four chambers, with only mild elevation of pulmonary pressure in the first patient, but nearly equalisation of diastolic pressure, and a very high pulmonary arterial pressure with a difference of 7 mm Hg between the end diastolic pressures in the two ventricles in the second patient. Doppler revealed a restrictive pattern of mitral inflow, with high E and small A velocities and a short deceleration time. The clinical background did not suggest pericardial disease in either of the patients. We conclude that a careful search is needed to uncover constrictive pericarditis when there is no previous disease which may suggest late pericardial constriction. The haemodynamic features of restrictive cardiomyopathy can co-exist with pericardial restriction, and differentiation between the two entities is critical in view of the diverse management and prognosis of the two conditions.
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7/51. A case of effusive-constrictive pericarditis after cardiac surgery.

    A 60-year-old woman who had undergone repair of an atrial septal defect was readmitted to the hospital with dyspnea, abdominal distention, and leg edema 31 months after surgery. An echocardiogram demonstrated massive pericardial effusion. cardiac catheterization revealed elevation and equilibrium of the 4-chamber diastolic pressure and a dip-and-plateau pattern in the right and the left ventricular pressures. Despite removal of pericardial fluid by pericardiocentesis, the findings and symptoms did not improve. The patient underwent both parietal and visceral pericardiectomy after which striking hemodynamic and symptomatic improvement occurred. Effusive-constrictive pericarditis is uncommon but should be considered in patients with refractory heart failure and massive pericardial effusion showing no improvement after removal of pericardial fluid.
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8/51. Rheumatic valvulitis and constrictive pericarditis. Report of case.

    A 13-year-old girl was admitted with congestive heart failure, edema, ascites, and jaundice. There was an apical pansystolic murmur of mitral insufficiency and marked cardiomegaly. Her venous pressure was elevated. Despite medical treatment her condition deteriorated, hepatic and renal failure as well as disseminated intravascular coagulation ensued, leading to her death. At post mortem she was found to have rheumatic mitral valvulitis and constrictive pericarditis. The pathologic picture of pericarditis was nonspecific, but in presence of a positive skin test for tuberculosis the latter is considered to be the most likely cause of the pericarditis, nevertheless, rheumatic etiology of pericarditis in this case cannot be excluded. The presence of rheumatic heart disease and cardiomegaly may have led to the exacerbation of symptoms and signs of constrictive pericarditis and severe right heart failure.
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9/51. Effusive constrictive pericarditis due to rheumatoid arthritis revealed by pericardiocentesis with simultaneous pressure recording--a case report.

    A 59-year-old man had a history of rheumatoid arthritis. He presented with incurable pericardial effusion. He was repeatedly treated with pericardiocentesis with only transient attenuation of his symptoms because the underlying pericardial constriction had been overlooked. This time the authors diagnosed effusive constrictive pericarditis due to rheumatoid arthritis using the hemodynamic findings observed before and after pericardiocentesis.
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10/51. The functional defect in amyloid heart disease. The "stiff heart" syndrome.

    Left ventricular performance was studied in three patients with heart failure due to amyloid deposits. The diagnosis of amyloidosis was proved by cardiac biopsy in two patients and by rectal biopsy in the third. One patient had myelomatosis, but the other two had no other identifiable disease. The investigative technique allowed simultaneous measurements of pressure and volume in the left ventricle. The functional defect with slow cardiac filling at high pressure and greatly reduced left ventricular contraction differed from that of constrictive pericarditis and other heart muscle disease. These features of a "stiff heart" are probably unique to amyloidosis and should make possible positive recognition of the condition on the basis of echocardiographic, angiographic and hemodynamic findings.
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