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

Myocardial involvement in lupus erythematosis takes the form of an interstitial myocarditis with cellular infiltration and fibrinoid necrosis. The most lesions are perivascular, and involve the arterioles. The myocardial fibres are involved secondarily to the vascular lesions, or by grossly, damaging sclerosis. The clinical features are variable:--no clinical features, but haemodynamic evidence of abnormal ventricular function, and perhaps sudden death;--arrhythmias and disorders of atrio-ventricular conduction;--cardiac failure, which may be due to a genuine cardiomyopathy (a part may be played by hypertension, pulmonary hypertension, renal failure, constrictive pericarditis or haemodynamically major valve disorders);--abnormalities of the coronary trunk in a certain number of cases. If anti-nuclear antibodies are present in a cardiomyopathy, the presence of DLE or of a drug-induced lupus syndrome must be suspected. There remain some awkward cases which defy classification, and which systematic use of echocardiography and pericardial and myocardial biopsy may be able to define more accurately.
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PMID:[The myocardiopathies of systemic lupus erythematosus]. 9 56

17 patients with severe chronic heart failure (class III and IV) were prescribed hydralazine, an arterial vasodilatator, orally at doses of 150 mg to 400 mg/day. Considerable clinical improvement was observed in most patients. After 24 to 48 hours the cardiac index rose 79 p. 100, the systolic index by 67 p. 100 and left ventricular work by 73 p. 100, whilst systemic and pulmonary resistances fell by 51 p. 100 and 34 p. 100 respectively. There was no significant change in systemic blood pressure or in heart rate. These results were confirmed at 4 months. Mean pulmonary capillary pressure varied little at the start of treatment but decreased by 52 p. 100 at medium term (4 and 12 months) in this series. No cases of systemic lupus erythematosis were observed. The main, but not the only, indication of therapy with dihydralazine is low output heart failure with little elevation in the pulmonary capillary pressure, especially in primary cardiomyopathy and valvular regurgitation. At present, treatment should be based on the results of cardiac catheterisation and the dosage adjusted according to the rate of hepatic acetylation.
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PMID:[Treatment of severe chronic cardiac insufficiency with dihydralazine. Short-and median-term results]. 11 37

Seven patients with myasthenia gravis developed clinical signs of arthropathy. In two patients, the symptoms were due to a deforming rheumatoid arthritis and the myasthenic symptoms appeared as a transitory phase during the course of the disease. Muscle antibodies of IgG class were demonstrated with sera from both patients. Autoreactivity between muscle antibodies and rheumatoid factor was detected in one patient. Both patients died from sudden cardiac failure. Necropsy was performed in one and revealed a spotty myocardial necrosis. One patient had juvenile rheumatoid arthritis. Two patients had mild articular symptoms with indices of multivisceral disease and serological findings indicating a systemic lupus erythematous. One patient had classical ankylosing spondylitis, and one, unspecified arthropathy.
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PMID:Arthritis in myasthenia gravis. 110 89

A 46 year old woman presented with fever and normochromic anaemia followed rapidly by severe myocardial failure, unresponsive to maximum inotropic support and broad spectrum antibiotics. There were no classical clinical stigmata of systemic lupus erythematosus (SLE) but a possible immunological cause was looked for, and on the basis of her immuno-serology a diagnosis of SLE-like disease was made. She responded rapidly to high dose steroids. The importance of considering the possibility of SLE or 'lupus overlap' in an acutely ill 'undiagnosed' patient is emphasized. The relevance of instigating appropriate immuno-serological tests in the course of such an illness is discussed.
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PMID:Sub-clinical systemic lupus erythematosus presenting with acute myocarditis. 143 35

Over the last 10 years, our knowledge of immunologically mediated processes involving the myocardium appears to have made quantum leaps. New and important disease entities such as AIDS have appeared and the cardiologist now becomes an important member of the "AIDS team." Our understanding of "older diseases" such as sarcoidosis, Lyme disease, systemic lupus and other connective tissue syndromes has significantly increased. The concept of high-dose steroid therapy for these processes may, in fact, turn out to be futile and more selective, as less dangerous immunosuppression is being introduced. This concept has significantly advanced in the field of cardiac transplantation where immunosuppression has now been usurped by specific immunotherapy aimed at selective aspects of the immune sequence. New and exciting concepts will emerge from the molecular biology laboratory that will have direct bearing on the management of patients with cardiovascular disorders. This information explosion will force the cardiovascular physician to become more in tune with the world of immunology and molecular biology. Many obvious, significant problems remain, such as accelerated atherosclerosis in the transplant patient and the role of myocarditis in the patient with heart failure. However, it will truly be an exciting decade in which to work and watch the unraveling of these mysteries and hopefully, the study of today's problems will give way to solutions and a clearer understanding of the heart as a target of immune injury.
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PMID:The heart as a target organ of immune injury. 191 12

The radiological manifestations of asbestos-related visceral pleural changes are described. Generally, visceral pleural reactions follow the mesothelial cells response to various injurious substances, including asbestos, and even saline. The changes are nonspecific. They may occur subsequent to pleural reactions associated with many conditions, which include tuberculosis, viral pleurisy, malignancy and lymphoma, lupus, or rheumatoid-induced effusions, cardiac failure, and pulmonary embolism, among other etiologies. The failure to absorb the fibrinous exudate on the visceral pleural surface can lead to the development of diffuse fibrosis of the serosal surface, interlobar pleural thickening, localized pleural filaments (strands), subpleural wedge, and lenticular-shaped masses, and could be the forerunner of lobular atelectasis (pseudotumor) formation. Some of the features are recognized on posteroanterior chest radiographs and the counterparts corroborated with the use of routine and high-resolution computed tomography studies.
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PMID:Radiological features of asbestos-related visceral pleural changes. 200 21

The study of drug distribution in pregnancy was limited by ethical, technical and medico-legal considerations as samples of body fluids could only be taken at delivery. In recent times fetal blood samples have been taken with the fetoscope and will provide a new tool to monitor fetal concentrations and metabolic pathways. The advanced technology of ultrasound allows non invasive study of the fetal circulation and early experience of sympathomimetic drugs administered to the mother will be discussed. Auto immune disorders carry high perinatal wastage. New drugs have made reproductive life possible and when used prudently can improve maternal state and increase fetal salvage. The author has personally managed nearly 52 cases of systemic lupus erythematosus and 16 cases of idiopathic thrombocytopenic purpura. The use of steroids and low dosage aspirin therapy with elevated lupus anticoagulant levels will be described. Two cases of early hydrops in the fetus owing to heart failure due to supraventricular tachycardia were treated with digoxin given to the mother. The potential of therapeutic agents in fetal medicine will be discussed as it recognises the fetus as a patient and provides effective intra uterine therapy.
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PMID:Drugs in feto maternal medicine. 331 58

SLE affects most aspects of cardiac function, and recent studies have reported increasing cardiovascular morbidity and mortality. Pathologically, SLE is characterized by a pancarditis involving pericardium, myocardium, endocardium, and coronary arteries. In autopsy series, pericarditis has been found in 43% to 100% (mean 62%, Table I), and myocarditis was found in 8% to 78% (mean 40%, Table II), but both have been underdiagnosed clinically. Libman-Sacks lesions have been noted in 25% to 100% (mean 43%) and infective endocarditis in 1.1% to 4.9% of clinical and autopsy studies (Table III). Coronary disease may be due to arteritis, which should be treated with high-dose steroids, or it may be due to atherosclerosis, which is amenable to medical or surgical therapy. Valvular disease has been treated surgically, but with a combined surgical mortality as high as 25%. Aortic insufficiency and mitral regurgitation are the most common valvular problems, although aortic and mitral stenosis have also been reported. Hypertension has been noted in 14% to 69%, and heart failure in 5% to 44%. Evidence for a lupus cardiomyopathy, which may be subclinical, is reviewed. While steroids may ameliorate SLE pancarditis, they have also been associated with hypertension, LV hypertrophy, purulent and constrictive pericarditis, mitral regurgitation, and perhaps accelerated atherosclerosis. It remains to be seen if improved diagnosis and treatment of the cardiovascular manifestations of SLE can enhance survival.
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PMID:Cardiovascular manifestations of systemic lupus erythematosus. 390 17

We report a case of a newborn with a congenital heart-block. Clinical picture began with bradycardia and heart failure from birth. The mother had a systemic lupus erythematosus in remission during pregnancy suffering a reactivation after delivery. This report deals about the greater incidence of congenital heart-block in the lupus-mother's newborns and we expose some etiopathogenic hypothesis. Also we point-out the easy clinical and electrocardiographic diagnosis that shows a third degree heart-block with atrioventricular dissociation and atrial frequency two or three times greater than ventricular. It's established the differential diagnosis among neonatal bradycardias and congenital heart-blocks. The treatment with isoproterenol was ineffective. A pacemaker was need.
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PMID:[Congenital heart block in a newborn infant born to a mother with lupus erythematosus]. 668 91

In the last two years, six studies using prazosin in doses of 3-32 mg/day for two and 16 months have shown a persistent but variable benefit in 50-80% of those who initially responded favorably. However, serious side-effects occurred in up to 40% and, in many cases, tolerance developed. Mortality was 25-38% in 3-6 months, 50% by one year. In five studies using hydralazine (sometimes combined with long acting nitrates), 150 patients observed from six up to 29 months showed sustained benefit in 26 to 59%, while in many cases hemodynamic values returned to pretreatment values. Again side-effects were considerable, with worsening of angina, fluid retention, gastrointestinal symptomatology and, rarely, lupus erythematodes. Mortality was 28-41% in 10-12 months, higher in non-responders than in responders. Although exercise capacity increased in responders, no data are available today to prove that these vasodilators allow heart failure patients to live longer. Prudence is indicated in patients with congestive heart failure due to coronary artery disease. Furthermore, tolerance development, which only may be surmountable if discontinuation for a few weeks or switching to another drug is possible, is a serious problem limiting chronic vasodilator application.
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PMID:A review of the long-term effects of prazosin and hydralazine in chronic congestive heart failure. 684 Jan 21


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