Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Ann Thorac Cardiovasc Surg 1999 Aug
PMID:Constrictive pericarditis following hemopericardium due to ascending aortic dissection: A case report. 1050 55

A 12-year-old boy suffered a blunt chest trauma. Some hours later, a pulsatile bilateral jugular venous distension, a holosystolic murmur heard at the low parasternal border and hepatomegaly were observed. On echocardiography, ruptured chordae tendineae of the posterior leaflet of the tricuspid valve, as well as tricuspid regurgitation were detected. He remained asymptomatic during hospital stay and was discharged home in good condition. Thus, isolated ruptured chordae tendineae of the posterior leaflet of the tricuspid valve is another cause of tricuspid regurgitation following blunt chest trauma.
Cardiovasc Pathol
PMID:Ruptured chordae tendineae of the posterior leaflet of the tricuspid valve as a cause of tricuspid regurgitation following blunt chest trauma. 1142 4

Diabetes is associated with ventricular dysfunction. Ethanol consumption increases the risk of cardiovascular disease among diabetics. Acetaldehyde (ACA), the main ethanol metabolite, depresses cardiac contraction and contributes to ethanol-induced cardiac dysfunction. This study examined the influence of gender and diabetes on ACA-induced myocardial dysfunction. Adult male and female rats were made diabetic with streptozotocin (55 mg/kg). Left ventricular papillary muscles were isolated and stimulated to contract at 0.5 Hz. The mechanical parameters measured were peak tension development, time-to-peak tension (TPT), time-to-90% relaxation (RT90), and maximum velocities of tension development and decline (+/-VT). TPT and RT90 were comparably similar between genders. The +/-VT appeared to be slower in myocardium from female rats when compared to that of male counterparts, although the difference was not significant. Experimental diabetes elicited severe hyperglycemia, cardiac hypertrophy, hepatomegaly, and renal hypertrophy in both male and female animals. Myocardial mechanical properties exhibited prolonged TPT and RT90 in diabetic myocardium from both genders. The +/-VT was significantly reduced by diabetes in male but not in female myocardium. Acute ACA exposure decreased myocardial tension development and the +/-VT and shortened TPT and RT90 in myocardium from normal and diabetic rats of both genders. The ACA-induced depressant response on tension development was slightly enhanced by the diabetic state. In conclusion, these data suggest that the development of diabetes-induced myocardial dysfunction is similar between male and female animals and that the ACA-induced myocardial depressant action may be affected by diabetes but not by gender.
Cardiovasc Toxicol 2001
PMID:The influence of gender, diabetes, and acetaldehyde on the intrinsic contractile properties of isolated rat myocardium. 1221 95

Budd-Chiari syndrome (BCS) is an uncommon disorder caused by hepatic venous outflow obstruction. It is characterized by ascites, hepatomegaly and abdominal pain. Percutaneous interventions have recently been used for the treatment of BCS. We present a case of BCS with a closed mesocaval shunt which was reopened with a self-expandable metallic stent.
Cardiovasc Intervent Radiol
PMID:Stent angioplasty of closed mesocaval shunt in a patient with Budd-Chiari syndrome. 1232 21

We removed from 4 patients pacemaker leads that had migrated or become infected. Case 1: A 62-year-old man developed uncontrollable infection of the pacing leads. Case 2: A 78-year-old man, whose infected pacemaker was removed, had a second one implanted in the contralateral side; the pacing lead infection from the first procedure, however, was uncontrollable. Case 3: A 56-year-old woman presented with dyspnea and hepatomegaly subsequent to the second implantation of a pacemaker; the pacing leads from the first procedure caused severe stenosis in both the superior and inferior vena cavae. Case 4: A 60-year-old woman had a ruptured and migrated pacing lead in the right ventricle. We operated using a cardiopulmonary bypass and a specially designed plastic tube for removal of the leads. Although Case 2 required reconstruction of the vena cavae, all patients recovered. When removal of pacing leads is necessary, it should be done as soon as possible with cardiopulmonary bypass.
Jpn J Thorac Cardiovasc Surg 2004 Feb
PMID:A novel technique for removal of permanent pacemaker leads. 1499 76

Pericardial abscess is rare in healthy individuals, especially the amebic type. We report a case of pericardial abscess and cardiac tamponade due to intrapericardial rupture of an amebic liver abscess. A 31-year old Japanese male complained of fever to a local hospital. A liver mass was discovered in his left hepatic lobe by an abdominal echogram. He was referred to the internal department of our hospital and was treated with quinolone antibiotics. Two weeks after medication, he suddenly complained of epigastralgia and severe orthopnea and was admitted. Abdominal computed tomographic scan showed an enlarged liver mass, and massive pericardial effusion suggested cardiac tamponade. He underwent an emergency subxiphoid partial pericardiectomy under local anesthesia. 1,000 ml of light brownish fluid was removed and his condition improved. Although no ameba was cultivated from the pus, the amebic serological test was positive. Metronidazole was administered and the patient was discharged 31 days after surgery.
Jpn J Thorac Cardiovasc Surg 2005 Apr
PMID:Cardiac tamponade due to intrapericardial rupture of an amebic liver abscess. 1587 56

Tumors involving the heart are rare, and the majority of them are benign. Secondary lymphoma with localization to the heart is the third most common malignant heart tumor and is more common, by far, than primary cardiac lymphomas. In patients with human immunodeficiency virus, the risk of development of systemic lymphoma is 60 to 200 times higher than in the general population. Symptoms usually consist of chest pain and dyspnea. Patients can also present with obstructive symptoms, based on the location and size of the tumor, and signs such as elevated jugular venous pressure, peripheral edema, ascites, and hepatomegaly. Transthoracic echocardiography is the initial modality of choice for diagnosis of cardiac lymphomas because it is readily available and helps localize the tumor, but transesophageal echocardiography and magnetic resonance imaging remain the best tests for evaluation. Treatment consists primarily of chemotherapy, and anticoagulation can be used in certain cases where embolization of the tumor is likely. This case review describes a 37-year-old man with past medical history significant for herpes zoster and stage 1 syphilis who presented with complaints of weight loss, intermittent fevers, and vague chest pains of 1-month duration.
Rev Cardiovasc Med 2008
PMID:Symptomatic metastatic right atrial lymphoma in a patient with AIDS presenting with pulmonary embolization. 1912 86

Chronic constrictive pericarditis (CCP) is a clinical syndrome caused by compression of the heart due to a thickened or rigid pericardium. In the affluent West, the majority of cases of CCP are neither tuberculous nor calcific. In an American cohort undergoing pericardectomy for the condition, only 27% had calcification and under 10% had TB [1]. As a result, pericardial calcification (PC) as a marker of CCP has become neglected. We present a 48-year-old male admitted with atrial flutter, acute chest infection and signs of right heart congestion. PC was documented one year previously on a non-contrast CT chest. On this occasion, cardiac catheterisation confirmed hemodynamically significant CCP and cardiac magnetic resonance (cMR) study showed contiguous mass lesions in the pericardium, compression of the right ventricle, enlargement of the right atrium, hepatic enlargement and a pneumonic process in the left lung. He was commenced on antibiotics and anti-tuberculous therapy with a diagnosis of bacterial super-infection of tuberculous CCP. This was confirmed at pericardectomy along with an infected fistula into the left lung. Any finding of PC should be followed up with a thorough haemodynamic and anatomical assessment using any of a wide range of non-invasive imaging modalities.
Int J Cardiovasc Imaging 2010 Jan
PMID:Constriction infection. 1977 84

Tangier disease is one of the most severe forms of familial high-density lipoprotein (HDL) deficiency. Since its discovery it has been diagnosed in about 100 patients and is characterized by severe plasma deficiency or absence of HDL, apolipoprotein A-I (apoA-I, the major HDL apolipoprotein) and by accumulation of cholesteryl esters in many tissues throughout the body. The biochemical signs of this condition are plasma HDL concentrations less than 5 mg/dL, low total plasma cholesterol (below 150 mg/dL), and normal or high plasma triglycerides. Tangier disease is caused by mutations in the 'ATP-Binding Cassette transporter A1' (ABCA1) gene, which encodes the membrane transporter ABCA1. This transporter plays a key role in the first step of reverse cholesterol transport, through which the efflux of free cholesterol from peripheral cells is transferred to lipid-poor apoA-I. The Tangier disease clinical phenotype is inherited as an autosomal recessive trait, the biochemical phenotype is inherited as an autosomal co-dominant trait. Nearly all the children affected by Tangier disease were identified on the basis of large, yellow-orange tonsils, while half of the adult patients affected by Tangier disease came to medical attention because of symptoms of neuropathy. Diagnosis in the remaining subjects was related to the clinical features of hepatomegaly, splenomegaly, premature myocardial infarction (about 30% of Tangier disease cases) or stroke, thrombocytopenia, anemia, gastrointestinal disorders, corneal opacities, hypocholesterolemia, low HDL cholesterol, or following a familial screening of Tangier patients. To date there is no specific treatment for Tangier disease. Old and recently designed drugs, known to increase HDL levels, have been shown to be ineffective in Tangier patients. The possible and more realistic therapeutic strategy should be designed to obtain a selective increase of mature HDL concentration to restore cholesterol efflux. Recently designed drugs like the cholesteryl ester transfer protein (CETP) inhibitors dalcetrapib and anacetrapib and reconstituted forms of HDL could be considered until the development of gene therapy.
Am J Cardiovasc Drugs 2012 Oct 01
PMID:Tangier disease: epidemiology, pathophysiology, and management. 2291 75

Although dilated cardiomyopathy (DCM) is often caused by viral infections, it frequently involves autoimmune mechanisms associated with particular HLA-DR and DQ alleles. Our homozygous HLA-DQ8Ab(0) transgenic mice in the BALB/c background (HLA-DQ8(BALB/c)-Tg) developed early and progressive fatal heart failure from 4 to 5 weeks of age. Clinical signs of the disease included cyanotic eyes, tachycardia with dyspnea (from pale to cyanotic limbs), and terminal whole body edema. Sick mice had extremely dilated hearts, enlarged liver and spleen, and pleural/peritoneal effusion. Histology of the heart showed extensive heart muscle destruction with signs of fibrosis. The autoimmune nature of the disease was shown by high titers of antimyosin antibodies in the sera and IgG deposits in sick heart muscles, as well as focal neutrophil, T cell, and macrophage infiltration of the heart muscle. The sera of the sick mice showed a granular staining pattern on sections of healthy heart muscle. Quantitative analyses of DCM-specific gene expression studies revealed that sets of genes are involved in inflammation, hypoxia, and fibrosis. Treatment with FTY720 (Fingolimod/Gilenya) protected animals from the development of cardiomyopathy. HLA-DQ8(BALB/c)-Tg mice represent a spontaneous autoimmune myocarditis model that may provide a useful tool for studying the autoimmune mechanism of DCM and testing immunosuppressive drugs.
Cardiovasc Pathol
PMID:FTY720 (Gilenya) treatment prevents spontaneous autoimmune myocarditis and dilated cardiomyopathy in transgenic HLA-DQ8-BALB/c mice. 2728 45


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