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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The postoperative course in two children with extrahepatic biliary atresia and cardiovascular disease was reviewed and the correlation between biliary drainage and cardiac function was analyzed. Both patients obtained satisfactory biliary drainage after Kasai's hepatic portoenterostomy. One patient developed heart failure postoperatively due to severe viral myocarditis. This child's total serum bilirubin concentration remained elevated for eight months, despite adequate bilirubin excretion, until her cardiac function returned to normal. Another patient died of cardiac failure due to congenital heart disease 83 days after Kasai's operation, but his postoperative biliary drainage was satisfactory as long as cardiac function remained compensated. In both cases, fluid intake was restricted severely (30 to 70 ml/kg body weight/day), as titrated by echocardiographic assessment of cardiac function, but biliary excretion was satisfactory as long as the cardiac fractional shortening ratio was greater than 30% and the ejection fraction was greater than 55%. This suggests that cardiac decompensation affects postoperative biliary excretion in patients with biliary atresia; however, with careful medical management satisfactory biliary drainage can be achieved even in patients with severe heart diseases.
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PMID:Postoperative management of children with biliary atresia and heart failure. 161 Jul 49

Immunization with purified cardiac myosin induces autoimmune myocarditis in A strain mice. Because this disease parallels Coxsackievirus B3 (CB3)-induced myocarditis in many respects, we are now using the immunization model as a virus-free system to study certain forms of immunologically-mediated heart disease. In the present article we will describe several characteristics of the humoral and cellular autoimmune response acting in myosin-induced myocarditis. Furthermore, we discuss hypotheses which might explain how myosin-reactive T cells recognize and attack the heart tissue.
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PMID:Cardiac myosin-induced myocarditis as a model of postinfectious autoimmunity. 165 42

The authors present a clinico-pathological study on 21 patients who died in acute cerebrovascular diseases. The main myocardial lesions were focal hemorrhages, contraction band necroses and myocarditis. The ECG abnormalities and the pathogenesis of the cardiopathy are discussed on the basis of their investigations and dates of references. Their conclusions is that the heart damages are modulated by catecholamines. The occurrence of this cardiopathy should be prevented by beta-blockers, so the life-expectancy of patients and the number of heart donors could increase.
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PMID:[Heart damage associated with cerebrovascular accidents]. 167 28

There has been a resurgence of interest in immunologically-mediated heart disease, culminating in a recent meeting. This interest was sparked off by new experimental models of autoimmune myocarditis that have served two useful functions: first, as good models of human myocarditis and second, as paradigms of infection-induced autoimmune disease.
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PMID:Autoimmune myocarditis: concepts and questions. 168 Mar 35

The expression of leucocyte adhesion facilitating molecules on endothelia is a major stimulus for tissue inflammation and cell infiltration. Recently, specific receptor ligands have been identified that mediate cellular adhesion of lymphocytes or monocytes. In the present study, sequential changes in the expression of immune adhesion receptors (LFA-1, CD2) and their ligand molecules (ICAM-1, LFA-3) were studied in heart allografts during rejection. Consecutive endomyocardial biopsies (n = 157; d.3-1013) of 16 heart transplanted patients were studied using monoclonal antibodies and standard immunohistology. In biopsies that showed no rejection, immune adhesion molecules (ICAM-1) were weakly expressed on a few endothelial cells. ICAM-1 was induced on blood vessel and capillary endothelia during rejection. After treatment, expression declined, as did the clearance of infiltrates. Occasionally, ICAM-1 persisted on capillaries compared with class II MHC expression. Weak LFA-3 induction on endothelia was observed in acute rejection, similar to ICAM-1, however LFA-3 expression was more restricted. Infiltrating lymphocytes expressed the adhesion receptor molecules LFA-1 and/or CD2. The variability of expression of ICAM-1 and FA-3 ligand molecules was related to the inflammatory changes in the graft during acute rejection. It is likely that the induction of adhesion ligand molecules in tissue is regulated by systemic and local release of cytokines, and is an initiating step in graft infiltration. The demonstration of immune adhesion-molecule induction in heart graft rejection may also be applicable to inflammatory heart disease in viral myocarditis.
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PMID:Signs of endothelial inflammation in human heart allografts. 168 Jun 86

The adenine nucleotide translocator (ANT) and myosin have been shown to be major autoantigens in myocarditis and dilated cardiomyopathy. We studied the use of synthetic peptides, with sequences derived from ANT and myosin, as antigens in screening tests for autoantibodies in myocarditis (MC) and dilated cardiomyopathy (DCM) and as absorbents for specific elimination of autoantibodies from the sera of patients. Using computer prediction of the secondary structure of the ANT and myosin we identified two sequences of the ANT and three sequences of myosin as possible main antigenic determinants. Using overlapping synthetic peptides and antibodies against them, the antigenicity of the selected determinants was shown. Of 72 sera from patients with MC or DCM 45 (62.5%) bound to the peptides derived from ANT, 32 (44.4%) reacted with the sequences from myosin, in contrast to healthy controls. Using the peptides from the ANT or myosin immobilized on thiopropyl-sepharose, more than 95% of the autoantibodies could be removed specifically from the positive sera. The results demonstrate the usefulness of synthetic peptides as antigens in antibody screening tests in MC and DCM and offers a new approach to the therapy of inflammatory heart disease by specific elimination of autoantibodies.
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PMID:The possible value of synthetic peptides in the diagnosis and therapy of myocarditis and dilated cardiomyopathy. 171 75

Determining safe and effective antiarrhythmic therapy in paediatric patients requires definition of the mechanism of the arrhythmia, determination of associated risk factors for treatment (such as the presence of congenital cardiac defects, myocarditis or cardiomyopathy), and monitoring for potential drug side effects related to the treatment. A number of modalities for non-invasive evaluation of arrhythmias is available, including ECG, 24-hour ambulatory Holter monitoring, and transtelephonic ECG transmission. Arrhythmias requiring medical treatment in children with normal cardiac anatomy and function include supraventricular tachycardia (SVT), ventricular tachycardia (VT) and primary atrial tachycardias. SVT is treated acutely with vagal manoeuvres or drugs which slow AV conduction [adenosine (adenine riboside), edrophonium, phenylephrine or verapamil]. When medical conversion is not achieved, transoesophageal overdrive pacing or direct current (DC) cardioversion may be required. Long term drug therapy for SVT includes first-line treatment with digoxin, verapamil or propranolol. Ventricular tachycardia is managed acutely with DC cardioversion and intravenous lidocaine (lignocaine). Chronic drug regimens include mexiletine, propranolol or amiodarone. In children with structural congenital heart disease or myocardial dysfunction, hazards of drug therapy for arrhythmias include depression of cardiac function, proarrhythmia (drug-induced worsening of arrhythmias), and conduction abnormalities. Care must be taken to choose medication regimens which are likely to be effective with minimum risk of potentiating abnormal haemodynamics or conduction.
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PMID:Cardiac arrhythmias in childhood. Diagnostic considerations and treatment. 172 43

Between March 1982 and March 1991, 225 heart transplantations (HTx) have been performed in 220 patients suffering end stage cardiac disease. Thirteen percent were females and 87% were males. Age range was from 5 to 68 years. The underlying cardiac disease was ischemic cardiopathy in 51.5%, congestive dilated cardiomyopathy in 42%, valvular cardiomyopathy in 3.5%, toxic myocarditis (post-adriamycin) in 1.5% and chronic rejection in 2.5% (retransplantation). Selection of the recipients was done following the currently well established criteria also taking into account the absolute major contraindications for HTx. Due to the still increasing demand of donor organs, currently donor age has been extended up to 50 years for male and 55 years for female donors. One quarter of the grafts were harvested on site in our institution, two other quarters were harvested somewhere else in Belgium and the last quarter provided by other countries cooperating with Eurotransplant. All patients have undergone orthotopic cardiac transplantation using the standard Lower and Shumway technique. Immunosuppression protocols have changed four times throughout the years. Nevertheless all were based on the use of Ciclosporine variously combined with other current immunosuppressive drugs. Rejection monitoring relied on routine endocardiac biopsy and was diagnosed according to the Billingham criteria. The in-hospital mortality is currently 11%. Infection, early right heart graft failure and acute rejection were the leading causes of death. The major causes of early morbidity were several curable infections, reversible rejection episodes, transient acute renal failure and controllable arterial hypertension. Among the survivors followed for at least one month up to nine years, half of late mortality was caused by chronic rejection followed by infection, sudden death, metabolic disorders, stroke and malignancy. Late morbidity involves cases of mild coronary graft diseases, biological renal insufficiency, some degree of arterial hypertension, dislipidemia. Current actuarial survival rate is 87% at one year, 76% at 5 years up to 9 years. Our experience confirms that HTx represents today and effective therapy for selected patients suffering end stage cardiac disease.
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PMID:A survey of nine years heart transplantation at Erasme Hospital, University of Brussels. 178 50

Cardiac disease is usually the most serious complication of human infection with Trypanosoma cruzi in our country. This report studies the evolution of the chagasic cardiopathy in mice inoculated with low number of parasites during acute and indeterminate stages in different aspects: contractility, histopathology and pharmacological response. From 2-45 days post infection (p.i.) (acute stage) myocardium contractile force reached higher values than in controls, but norepinephrine (NE) response was significantly lower. Acetylcholine (ACh) caused a negative inotropic effect similar to the observed in control group. In this period cardiac damage evolved to an acute interstitial myocarditis. In the indeterminate phase (45-75 days p.i.) of this parasitosis NE produced either small inotropic effect, negative inotropic effect or had no effect on the ventricles tested. A significantly low ACh effect, sub-endocardiac perivascular fibrosis and necrosis in wall bases were also observed. The abnormal pharmacological response described could be ascribed to modifications in cardiac beta and muscarinic receptors number or affinity. The present results showed that in myocardium isolated from T. cruzi infected mice the histopathology, contractility and pharmacological response were altered from 48 h p.i. reaching a maximum disorder at 60 days p.i.
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PMID:Isometric developed tension and histopathology of myocardium of chagasic mice. I. 184 45

Carditis developed 7 days after the administration of murine cytomegalovirus to neonatal, young adult or aged mice of varying sensitivity to lethal infection with this virus. The inflammation persisted for up to 80 days, but infected myocardial cells were rare and were not seen after day 10. The inflammatory cells comprised macrophages (up to 30%) and T cells (up to 80%), with a high ratio of Lyt2+ to L3T4+ cells throughout. Although the H-2 genotype affects murine cytomegalovirus replication at the level of individual cells, and hence resistance to lethal infection, it did not determine resistance to cardiopathy per se. However BALB/c, BALB.B, and BALB.K mice developed persistent myocarditis regardless of age at infection, and age-related cardiopathy was frequent and severe in infected and uninfected mice. B10 and B10.BR mice also developed myocarditis after neonatal infection, but inflammation resolved rapidly after adult infection and age-related cardiopathy was correspondingly mild. C3H mice exhibited minimal carditis after neonatal or adult infection. However neonatal infection appears to accelerate age-related cardiopathy, which is severe in retired breeders of this strain.
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PMID:Genetic determination of cytomegalovirus-induced and age-related cardiopathy in inbred mice. Characterization of infiltrating cells. 184 66


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