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

Peripartum cardiomyopathy is an important cause for idiopathic heart failure associated with pregnancy. Current evidence suggests a potential role for myocarditis in the pathogenesis of this disease. About 3% to 4% of these patients present before delivery. Another group of patients with prior history of this disease request information about pregnancy prognosis. This article focuses on current concepts about peripartum cardiomyopathy and presents a reasonable approach to this clinical challenge during pregnancy.
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PMID:Clinical management of gravid women with peripartum cardiomyopathy. 194 54

Although most cases of viral myocarditis are subclinical, some patients develop overt symptomatic disease. These patients may present with findings that range from benign myopericarditis to frank heart failure. Furthermore, a growing body of evidence links viral myocarditis with idiopathic dilated cardiomyopathy, sudden death, and chronic arrythmias. The pathogenesis of the disease is currently incompletely understood in humans but is being investigated in animal models. A multifactorial process involving direct viral damage, autoimmunity, and possibly vascular damage is emerging. Breakthroughs in rapid diagnosis, such as the use of DNA probes, are occurring and may soon provide the opportunity for early intervention. Although there is currently no widely accepted standard of treatment, promising new therapeutic modalities are under investigation. These include the use of general immunosuppressive agents, T cell monoclonal antibody, interferon, specific immunization, and synthetic antiviral agents.
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PMID:Viral myocarditis. 196 11

Infectious heart diseases in childhood are--with less than 1% of hospital admissions--rare, but serious diseases. Among several causes of myocarditis in our region virus myocarditis plays the most important role. Besides of the acute course an autoimmune mediated chronic myocarditis and the transition to dilated cardiomyopathy are observed. The patho-histological assessment depends also on subjective influences. Clinical diagnosis is based on cardiac symptoms (Adams-Stokes, congestive heart failure, LV-dilatation), ECG-changes with increased enzyme levels and positive virus-serology or endomyocardial biopsy. Immunoserology and -histology as well as in-situ-hybridization can support diagnosis, echocardiography and eventually heart catheterization exclude other causes. In respect to therapy, ACE-inhibitors are a substantial improvement of conventional therapy of heart failure, while immunosuppressive therapy of chronic myocarditis has to assessed.
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PMID:[Myocarditis in childhood]. 202 60

Phosphodiesterase inhibitors that are selective for cAMP-specific cardiac and vascular PDE III comprise a new group of agents for the treatment of heart failure, which at present are limited to clinical shortterm intravenous use and research uses only. Although both intravenous amrinone and milrinone are FDA approved, only amrinone is available for general clinical use. Selective phosphodiesterase inhibition produces beneficial actions of positive inotropy and peripheral vasodilation that result from increased cardiac and vascular muscle concentrations of intracellular cAMP and ionic calcium. In addition, a positive lusitropic action (enhancement of cardiac relaxation) has been observed. Neither beta-adrenergic agonist activity nor inhibition of the sodium-potassium ATPase is produced by these agents. The magnitude of hemodynamic improvement generally exceeds that of the cardiac glycosides and is comparable with that of intravenous catecholamines such as dobutamine. The different pharmacodynamic profile of the PDE inhibitors is additive to the effects of cardiac glycosides, complementary and synergistic to the actions of catecholamines, and has been shown to have favorable effects on coronary hemodynamics. As a result there is continued enthusiasm for the short-term intravenous use of amrinone and potentially milrinone in the setting of acute heart failure resulting from systolic dysfunction (after myocardial infarction, open heart surgery, or infectious or toxic myocarditis), heart failure resulting from right ventricular systolic dysfunction, and when patients with severe heart failure await cardiac transplantation. Initiation of treatment with an intravenous bolus followed by a maintenance infusion provides prompt increases in stroke volume and cardiac output and simultaneous reductions in right and left ventricular filling pressures and systemic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute positive inotropic intervention: the phosphodiesterase inhibitors. 203 20

The diagnostic yield of endomyocardial biopsies in patients with chronic congestive heart failure of non-ischaemic aetiology remains questionable and, therefore, the use of endomyocardial biopsies under such circumstances is at stake. The present report documents the correlation between the histologic interpretation of endomyocardial biopsies and the corresponding cardiac explants in 13 patients who underwent cardiac transplantation. The biopsy diagnoses in these patients varied from 'compatible with dilated cardiomyopathy' (n = 6) to 'non-conclusive' (n = 4), 'ischaemia' (n = 2) and 'borderline myocarditis' (n = 1). Correlation with the corresponding cardiac explants revealed hypertrophy of myocytes as the leading histologic feature in the majority of cases. Because of the non-specific histopathology of dilated cardiomyopathy, the discrepancy between biopsy diagnoses and the leading explant diagnosis is mostly a matter of semantics. Ischaemia was present at high incidence, but is considered a result of imparied myocardial perfusion rather than the prime mechanism of heart failure. In four cardiac explants myocarditis was encountered, while the corresponding biopsies showed no cellular inflammation. In two, the cellular infiltrates suggested an early state of repair. One heart contained an active and extensive lymphocytic myocarditis. The fourth case showed an eosinophilic myocarditis, most likely acquired after the biopsy was taken. These discrepancies almost certainly relate to the sampling error and the time interval between biopsy and onset of symptoms. The immediate diagnostic yield of the biopsy, in this particular subset of patients, was minimal, particularly with respect to the diagnosis 'myocarditis'. Nevertheless, biopsy diagnoses such as 'compatible with' and 'non-conclusive' do contribute to the final categorization and management of these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic non-ischaemic congestive heart disease and endomyocardial biopsies. Worth the extra? 204 56

In 1984-88 the authors examined in 813 subjects with the chest pain syndrome of varying aetiology (acute myocardial infarction, myocarditis, pericarditis, vertebrogenic algic syndrome, embolism of the pulmonary artery, patients lacking detectable organic causes of pain) the trend of myoglobin serum levels. They found significantly elevated values only in patients with myocardial infarction and myocarditis whereby the two diseases differ in particular as regards the shape of the curve of myoglobin values. In chest pain with another aetiology the myoglobin levels rose only rarely or not at all. From the differential diagnostic aspect it is particularly valuable that myoglobin was not elevated in any patient with embolism of the pulmonary artery and only very rarely in angina pectoris. Where in exceptional instances the myoglobin levels were elevated in patients with other investigated causes of chest pain, this increase was always due to another basic disease (right-sided cardiac failure, renal insufficiency, neuromuscular disease), whereby for these conditions prolonged persistence of the elevated serum myoglobin values was typical and the levels were never above 8 nmol/l.
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PMID:[The significance of myoglobin determination in the differential diagnosis of chest pain syndrome]. 205 2

In a 63-year-old patient presenting with signs of classical diphtheria including membranous pharyngotracheobronchitis and myocarditis, Corynebacterium ulcerans was isolated in pure culture from the membranes. The strain produced a toxin specific for C. ulcerans but no diphtheria toxin. The patient was discharged after a complicated hospital course including respiratory and cardiac failure. Besides Corynebacterium diphtheriae, which has very rarely been isolated in Switzerland in recent years, Corynebacterium ulcerans should be considered as a cause of classical diphtheria.
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PMID:[Classical pseudomembranous diphtheria caused by Corynebacterium ulcerans]. 208 36

There is a complex network of collagen throughout the heart. It is composed of a hierarchy of fibrils and fibers ranging from 10 nm to 2-3 microns in diameter. This network can be broken down by ischemia, adriamycin administration, or disulfide administration in laboratory animals. Following loss due to coronary artery ligation, the ischemic area begins bulging within 3 h. General loss of portions of the collagen matrix is induced by intravenous oxidizing glutathione, and results in marked diffuse ventricular dilatation. Generalized collagen loss in the ventricles, as induced by disulfide administration or adriamycin infusion, persists for 6 months at which time evidence of some replacement is visible, and evidence of diffuse fibrosis is present. In humans, cardiac dilatation occurs in a variety of disease states without overstretch of sarcomeres. This presumes rearrangement of the muscle bundles, which can only occur with marked alterations of the collagen matrix. Ventricular dilatation, associated with viral myocarditis or puerperal cardiomyopathy, may persist for months, suggesting the collagen loss, as with the experimental animals, takes many months to repair. The cardiac dilatation may ameliorate, or, in some patients, deteriorate into heart failure. The animal experiments with loss of the collagen matrix, ventricular dilatation, and failure to replace the matrix for many months provide an explanation for persistent cardiac dilatation in various human diseases.
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PMID:Myocardial connective tissue alterations. 209 Dec 28

A 70-year-old woman with active hypereosinophilic myocarditis presented with high fever and heart failure. Repeated right ventricular endomyocardial biopsies and 201-T1 myocardial scans before and after steroid therapy suggested that this treatment reversed the cardiac injury. Patients with hypereosinophilia may die from complications of eosinophilic infiltration and fibrosis in target organs, especially the heart. The findings in this patient suggest that steroids have benefit in this disease, at least in the short term.
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PMID:Hemodynamic and scintigraphic improvement after steroid therapy in a case with acute eosinophilic heart disease. 209 21

A 65-year-old man with idiopathic myocarditis is described. He was admitted with symptoms of acute heart failure. Examination revealed left ventricular hypokinesis. Results of an endomyocardial biopsy showed "resolving myocarditis". Immunological studies of the peripheral blood showed a low helper-suppressor (CD4/CD8) ratio on admission and depressed natural killer (NK) cell activity coincident with the onset of myocarditis. We considered that this immunological imbalance may have occurred during the progression of myocarditis to dilated cardiomyopathy.
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PMID:Idiopathic myocarditis associated with T-cell subset changes and depressed natural killer activity. 212 66


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