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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 14-year-old girl was admitted with chief complaints of edema and chest pain. She had hepatomegaly, but did not have heart murmur and accentuation of the pulmonary component of the second heart sound. The electrocardiogram showed right axis deviation, negative T wave in V3,4 and ST depression in III, aVF. But right ventricular hypertrophy was not dominant. Chest radiography showed a cardiothoracic ratio of 54% and a slight prominence of proximal pulmonary arteries. The edema was soon diminished only by the diuretics, but it appeared again without the diuretics. At the cardiac catheterization 3 months after the onset of symptoms, the pulmonary arterial pressure was 150/85 mmHg and the pulmonary resistance was 3,232 dyn/sec/cm5. The right atrial pressure was 9.5 mmHg and oxygen saturation at the pulmonary artery was 31.0%. Prostaglandin E1 reduced the pulmonary artery pressure only a little, but raised the systemic pressure. The patient was treated with several vasodilators, but her condition deteriorated rapidly and she developed severe right ventricular failure. She died only 8 months after the onset of symptoms and 5 months after the catheterization. At autopsy, histological examination demonstrated intimal fibrotic thickening of the small-sized pulmonary arteries and organizing thrombus. But there was not plexiform lesion. Heart failure was easily improved when she was first admitted. But after 3 months the cardiac catheterization revealed that her condition was already severe. Several vasodilators was not effective to such a rapidly progressive primary pulmonary hypertension.
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PMID:[A case of rapidly progressive pulmonary pulmonary hypertension in a 14-year-old girl]. 259 31

Multicentric hepatic hemangioendotheliomas are vascular lesions of the liver that usually present in the infant with hepatomegaly, high output congestive heart failure and cutaneous hemangiomas. The diagnosis, pathologic and physiologic conditions and treatment were discussed. Two of the patients we studied and 117 from the literature were reviewed. A total of 38 patients survived and 57 died with or without medical treatment. Thirteen patients survived and five died after ligation of the hepatic artery. Five patients survived and three died after embolization of the hepatic artery. (formula; see text) Of 119 patients with MHH, 81 (68 per cent) had congestive heart failure; 40 survived and 41 died. Of 56 patients with localized hepatic angiomas, 19 had congestive heart failure. Only two of the patients died of heart failure. Fifty localized hepatic angiomas in infancy that were treated with local resection or lobectomy were reviewed. Forty-six patients survived and four died of hemorrhage. Four patients survived and two died with or without medical treatment. Plans for management of multiple hepatic hemangioendotheliomas and localized hepatic angiomas in infancy were proposed.
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PMID:Hepatic hemangioendotheliomas in infancy. 264 92

A 17-year-old boy with muscular dystrophy developed a cardiomyopathy. His brother died of a cardiomyopathy, and muscle enzyme levels were elevated in asymptomatic family members. Examination revealed cardiomegaly, hepatomegaly, proximal muscle atrophy and weakness, and calf hypertrophy. Skeletal muscle and endomyocardial biopsy specimens were consistent with Becker's muscular dystrophy. Because of intractable heart failure, orthotopic cardiac transplantation was performed. Two years after transplantation, the patient has returned to work and regained previous exercise tolerance. Heart transplantation can be an acceptable treatment of patients who have muscular dystrophy, with preserved ambulation and favorable life expectancy, and also life-threatening cardiomyopathy refractory to medical management.
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PMID:Cardiac transplantation in a patient with muscular dystrophy and cardiomyopathy. 265 28

A case of mitral stenosis with left atrial thrombus which rapidly arose and reduced within a month was reported. A 61-year-old female was admitted to our hospital on November 14, 1986 because of a syncopal attack due to ventricular tachycardia. On admission she had typical auscultatory signs of mitral stenosis, mild hepatomegaly and no neurological abnormality. Laboratory findings included coagulation studies were normal, and atrial fibrillation was noted on ECG. Heart catheterization revealed low cardiac output, the mitral orifice area to be 2.4 cm2 and left ventriculography showed mild mitral regurgitation. Ventricular tachycardia was controlled following improvement of heart failure. On two-dimensional echocardiography performed on December 24, left atrial thrombus was revealed which was not detected on December 3. Through the continuous administration of warfarin and aspirin to prevent the thrombus' growth, it markedly reduced in size, from 3 x 2 x 4.5 cm on December 24, 1986 to 1.5 x 1 x 2.5 cm on January 30, 1987 without systemic embolism. Then a mitral valve replacement and a left atrial thrombectomy were performed on February 3, with the removal of a red thrombus, partially organized, measuring 1 x 0.7 x 2.5 cm. This case is unique in its clinical outcome and further investigation is necessary for the management of patients as our case.
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PMID:[A case of mitral stenosis with left atrial thrombus arose and reduced in a short-term]. 266 32

A distinct syndrome in infantile hemangioendothelioma consist of high-output congestive heart failure, hepatomegaly and cutaneous hemangiomas. Early therapy aimed at reduction of the shunt is essential if life is to be saved once cardiac failure becomes manifest. We report a case of infantile hemangioendothelioma with massive A-V and P-V shunt successfully treated by transcatheter embolization.
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PMID:[Therapeutic embolization of infantile hemangioendothelioma of the liver]. 268 11

Passive liver congestion secondary to increased hepatic venous pressure may accompany congestive heart failure. Abnormal patterns of hepatic parenchymal contrast medium enhancement in 25 patients with advanced congestive heart failure who were studied with computed tomography (CT) include a lobulated, patchy, inhomogeneous pattern in all 25 patients, an irregular perivascular enhancement in 14, and a global delay in parenchymal enhancement in nine. CT examinations showed cardiomegaly in the 20 patients with cardiac failure and pericardial effusion or thickening in the five patients with pericardial disease. Also noted were distention of the inferior vena cava (IVC) in 24 patients, hepatomegaly in 23, early reflux of contrast medium into the IVC in 21 and hepatic veins in 16, and hepatic perivascular lymph-edema in six. The abnormal patterns are thought to be due to slowing of hepatic blood flow. Confusion with Budd-Chiari syndrome and other forms of multifocal hepatic disease is avoidable with clinical and radiologic correlation.
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PMID:Inhomogeneous enhancement of liver parenchyma secondary to passive congestion: contrast-enhanced CT. 291 31

The liver in an infant or child is as liable to the same pathologies afflicting the adult liver but with certain differences in prevalence and causes. Genetic disorders are more likely to present in the paediatric age group where many involve metabolic processes such as galactosemia, phenylketonuria, glycogen storage disease and others. Many of these present in the newborn period. However, neoplasms and hamartomas also present in the newborn period, such as congenital neuroblastoma with an enormously enlarged liver, hepatoblastoma and haemangioma. The latter may present with intractable cardiac failure as a result of considerable shunting of blood. Acquired liver lesions often present in the newborn period or early infancy and this includes hepatitis and biliary atresia. The difficulties in the differentiation of the two lesions will be discussed together with the management of biliary atresia. As the child grows older, Reyes encephalopathy with microvesicular fat in the liver is not uncommon. The pathophysiology of Reyes encephalopathy as seen locally will be described. The choledochal cyst with direct (Caroli's disease) or indirect effect on the liver will be described. Problems of childhood portal hypertension as well as congenital hepatic fibrosis will be described. Hemosiderosis of the liver is chiefly seen in homozygous beta-thalassaemia patients who have been kept alive with repeated blood transfusions. Amoebic and pyogenic hepatitis, fatty liver due to protein malnutrition, biliary ascariasis, etc, which are common in tropical and subtropical countries are rarely seen now in Singapore children.
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PMID:Paediatric liver disorders in Singapore. 346 38

A 65-year-old male patient underwent two bypass operations because of coronary artery disease. After the second operation he developed congestive heart failure with breathlessness, ankle swelling, hepatomegaly and poor exercise tolerance. Echocardiographic and haemodynamic findings were characteristic of constrictive pericarditis. Pericardiectomy was performed three months after the second operation. The retrosternal space was replaced with fibrotic, patchy hyalinic tissue, and the pericardium was thick and rigid. Histologically, the thickened pericardium showed dense fibrosis and foreign-body granulomas with large multinuclear giant cells and irregular crystals. This report indicates that foreign body reaction following coronary artery bypass operation may result in constrictive pericarditis with severe heart failure.
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PMID:Constrictive pericarditis following coronary bypass reoperation. Fibrotic pericardium and a foreign body reaction. 353 48

Patients with chronic heart failure (CHF) can often develop such diseases as hepatitis of viral etiology, alcoholic hepatitis, drug affection of the liver and other diseases masked as congestive liver. In most cases CHF concomitant liver diseases have an atypical course with a tendency to a chronic course. CHF is one of the important pathogenetic mechanisms lying in the basis of chronicity of concomitant liver diseases. Refractory CHF, inconsistency of the hemodynamic indices of persistent hepatomegaly must lead a physician to the detection of probable independent liver diseases complicating the syndrome of heart failure. CHF is a factor causing an enhanced fibrosing liver reaction. An important diagnostic test of fibrinogenesis lying in the basis of chronicity of liver diseases, is the determination of enzymatic markers reflecting synthesis and catabolism of the main substance of connective tissue. Change in the levels of haptoglobin, ceruloplasmin and glutamic acid dehydrogenase is an indirect sign of damage of the liver parenchymal endoplasmic reticulum. These indices can serve as differential criteria of the prevalence of cardiovascular disorders in the liver or concomitant independent liver diseases.
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PMID:[Pathogenetic mechanisms of chronicity in liver diseases in patients with circulatory failure]. 361 41

Pathologic studies of the liver were performed on 30 autopsied cases of Kawasaki disease. The cases were classified into four groups (stages I-IV), and stage IV was further divided into two subgroups according to the duration of the illness at the time of death. Liver weights were markedly increased in stage II (12-25 days) and in stage III (28-36 days) but returned to normal in stage IVb (7 months to 6 years). Likewise, spleen weights were also markedly increased in stages II and III. Stage I (0-9 days) and stage II were characterized by acute inflammation in portal area, and degree of inflammatory changes decreased gradually. There was significant correlation between hepatomegaly and the degree of inflammation in portal areas, but not with definite heart failure or the use of drugs. These data suggest that the pathogenesis of hepatomegaly in acute-stage Kawasaki disease involves the inflammation in portal areas and/or latent heart failure.
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PMID:Hepatomegaly and splenomegaly in Kawasaki disease. 383 50


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