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

Cardiac disease and cardiac death in AIDS patients is seldom reported. In recent years minor cardiac abnormalities have been demonstrated, especially by echocardiography. Cardiac pathology in AIDS patients is here reported from 60 consecutive autopsies where the heart was investigated either using single samples of ventricular myocardium (the first 21 cases) or by an examination of the whole heart (the last 39 cases). Myocarditis according to the Dallas criteria was seen in 25 of 60 cases (42%), and in seven of these cases a probable pathogen (Toxoplasma gondii, cytomegalovirus, fungi) was demonstrated. Diffuse myocardial fibrosis was seen in 40 of 60 cases (67%) and is considered to be partly due to repair after myocyte necrosis/myocarditis. A myocardium thus weakened might not be able to meet an increase in functional demand, and in 15 of the 39 cases (38%) where an examination of the whole heart was performed, there was dilation and/or hypertrophy of the right ventricle. This is in agreement with our knowledge that the main diseases and main causes of death in AIDS patients are pulmonary. Survival time in AIDS is increasing due to ever improving symptomatic treatment, and the results of this study indicate that the prevalence of especially right-sided heart failure will increase.
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PMID:Pathology of the heart in AIDS. A study of 60 consecutive autopsies. 156 20

Four years after an HIV infection and without any preceding illness characteristic of AIDS, a 24-year-old woman developed dyspnoea on exertion and peripheral oedema. She had for several years been an intravenous drug addict and contracted hepatitis A and B. There were no symptoms of the HIV infection. Clinical, radiological and echocardiographic examination demonstrated right ventricular failure caused by pulmonary hypertension not due to pulmonary embolism or another known aetiology. The patient died suddenly 9 months after the diagnosis from heart failure. Autopsy established primary pulmonary hypertension with pathognomonic plexogenic pulmonary arterial disease which had led to cor pulmonale with overload myocarditis. Although there had been no clinical signs of renal failure, there was histological evidence of mesangioproliferative glomerulonephritis and non-destructive interstitial nephritis. This case demonstrates that, in addition to the typical AIDS-associated diseases, other rarer syndromes may, in uncertain ways but connected with the HIV infection, decide the prognosis of such patients.
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PMID:[Primary pulmonary hypertension and mesangioproliferative glomerulonephritis in HIV infection]. 158 15

Male, 26-years old, with acquired immunodeficiency syndrome which was admitted in the hospital with focal neurologic disturbance, developed myocardial failure and echocardiographic pattern of ventricular dysfunction. Sudden death occurred 18 days after admission and the post mortem microscopic studies showed degenerative abnormalities of cardiac muscular fibers, focal lymphocytic and histiocytic infiltrate and the presence of T. gondii.
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PMID:[Myocarditis caused by Toxoplasma gondii in a man with acquired immunodeficiency syndrome]. 182 12

Cardiac involvement is being identified more often clinically and at autopsy in patients with AIDS. Recent estimates suggest that in the United States as many as 5000 patients per year may have cardiac complications resulting from HIV infection. Patients with AIDS may have pericardial, myocardial, and/or endocardial disease. Pericardial tamponade and/or constriction may be related to neoplasms, infections, or nonspecific effusions. Myocardial dysfunction may result from specific neoplastic infiltration or myocarditis. Particularly intriguing is the role of HIV-1 in the nonspecific myocarditis and dilated cardiomyopathy that occurs in patients with AIDS. As in other debilitating conditions patients with AIDS can have nonbacterial thrombotic endocarditis. Infective endocarditis may be a complication, especially in AIDS associated with intravenous drug abuse. Most patients with AIDS have no overt clinical evidence of cardiac disease. When cardiac dysfunction does develop, the signs and symptoms are often misinterpreted to be the result of noncardiac causes (pulmonary failure or infection) which can mimic heart failure. This review is intended to alert the reader to the cardiac manifestations of AIDS, which present a number of diagnostic and therapeutic challenges.
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PMID:Cardiac manifestations of acquired immune deficiency syndrome: a 1991 update. 185 38

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 pathologic study of the cardiac lesions in 25 persons who died of AIDS were studied from autopsies. Most of these patients were intravenous drug abusers (14 cases). Heart failure was symptomatic and lead to death in 4 cases. This study showed histological abnormalities in 76% of the cases. We observed 12 myocarditis. In 6 cases, pathogenes were found: Toxoplasma gondii (2), Cryptococcus neoformans (2), Candida (1), Aspergillus (1). A lymphocytic myocarditis was observed in 6 hearts. By immunohistochemical technique, we could distinguish 2 toxoplasmic myocarditis, and in 4 cases, solitary cysts in the myocardium without inflammation. The remaining lesions comprised respectively: 3 lymphocytic pericarditis, 2 marastic endocarditis and 1 dilated myocardiopathy.
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PMID:[Cardiac lesions in acquired immunodeficiency syndrome (AIDS). Apropos of an autopsy series of 25 cases]. 225 24

Major causes of anaemia in pregnancy in tropical Africa are malaria, iron deficiency, folate deficiency and haemoglobinopathies: now there is added also the acquired immune deficiency syndrome (AIDS). Anaemia is often multifactorial, with the different causes interacting in a vicious cycle of depressed immunity, infection and malnutrition. Anaemia progresses through 3 stages: compensation, with breathlessness on exertion only; decompensation, with breathlessness at rest and haemoglobin (Hb) below about 70 g/litre; cardiac failure, with Hb below about 40 g/litre. Without treatment, over half of the women with haematocrit less than 0.13 and heart failure die. Maternal anaemia, malaria and deficiencies of iron and folate cause intrauterine growth retardation, premature delivery and, when severe, perinatal mortality. Surviving infants have low birthweights, immune deficiency and poor reserves of iron and folate. They have entered already the vicious cycle of infection, malnutrition and impaired immunity. Treatment with blood transfusions is even more hazardous since the advent of AIDS, and should be limited to saving the life of the mother. Treatment of malaria is complex as chloroquine-resistant strains are now common. Prevention remains relatively easy with proguanil and supplements of iron and folic acid and is highly cost-effective in the improvement of maternal and infant health; it is more important than ever as it avoids the unnecessary exposure of women and infants to HIV transmitted through blood transfusion.
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PMID:Tropical obstetrics and gynaecology. 1. Anaemia in pregnancy in tropical Africa. 269 76

Few data are available about cardiac involvement in AIDS. We examined 102 consecutive patients with AIDS diagnosed clinically and serologically (Walter Reed Stage 5 and 6), by means of TM and cross-sectional echocardiography with the aim of detecting cardiac abnormalities. None of the patients had overt clinical signs of heart failure. Fifty-five (54%) patients showed persistent tachycardia, diminished left ventricular (LV) wall thickness (mean 7.6 +/- 0.2 mm) and decreased percentage LV fractional shortening (27 +/- 5). In 42 (41%) there was a globular and poorly contracting LV. Thirty-nine (38%) patients had pericardial effusion which was moderate in 30 and small in nine. In four patients, valvular endocarditic vegetation was shown--on the tricuspid valve in three, on the aortic valve in one: all of them were drug addicts; in three (2.9%) patients a cardiac mass was found which proved to be a localization of Kaposi's sarcoma in two. Twenty-five (24.5%) patients died; necropsy showed cardiac chamber dilation, and thin LV walls in 18. On microscopic examination, myocardial fibrosis and lymphocyte infiltration with cell necrosis were observed. We conclude that cardiac abnormalities are common in AIDS. Impairment in LV contractility as assessed from fractional shortening appears to be the most common echocardiographic finding, followed by LV wall thinning, pericardial effusion and eventually by LV cavity dilation. This evolution is suggestive of myocardial damage and supports the hypothesis that dilated cardiomyopathy may be a cardiac complication of AIDS.
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PMID:Echocardiography detects myocardial damage in AIDS: prospective study in 102 patients. 318 Nov 75

20 Zambians with sickle cell anemia presented with generalized lymphadenopathy and other signs suggestive of the acquired immunodeficiency syndrome or the AIDS-related complex at the Arthur Davison Children's Hospital and the Ndola Central Hospital in Ndola, Zambia. All were found to have anti-HIV antibodies. 3 are known to have died within 10 months of diagnosis. Patients with this sickle cell anemia form a major group at risk for HIV infection through transfusion. The 1st step in prevention is to maintain the health of the patients, so avoiding the need to transfuse blood, and a call is make for the development of Sickle Cell Clinics. Secondly, blood transfusion should be confined to only those patients in danger of dying of anemic heart failure. These 2 steps should be taken, even when blood donors are screened for HIV.
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PMID:AIDS and AIDS-related complex in twenty Zambians with sickle cell anemia. 324

Emergency readmissions among patients discharged from the medical service of an acute-care teaching hospital were analyzed. Using the multivariate technique of recursive partitioning, the authors developed and validated a model to predict readmission based on diagnoses and other clinical factors. Of the 4,769 patients in the validation series, 19% were readmitted within 90 days. Twenty-six per cent of the readmissions occurred within ten days of discharge, and 57% within 30 days. Readmitted patients were older, had longer hospitalizations, and had greater hospital charges (p less than 0.01). The discharge diagnoses of AIDS, renal disease, and cancer were associated with increased risks of readmission regardless of patients' demographics or test results. The relative risks (95% confidence interval) associated with these diagnoses were: AIDS, 3.3 (1.4-7.8); renal disease, 2.3 (1.7-3.0); cancer, 2.8 (2.4-3.4). Other patients at increased risk were those with diabetes, anemia, and elevated creatinine (2.1; 1.6-2.8) and those with heart failure and elevated anion gaps (2.2; 1.7-2.8). For patients without one of these diagnoses, a normal albumin and no prior admission within 60 days identified patients at reduced risk for readmission (0.4; 0.3-0.4). Thus, commonly available clinical data identify patients at increased risk for emergency readmission. Risk factor profiles should alert physicians to these patients, as intensive intervention may be appropriate. Future studies should test the impacts of clinical interventions designed to reduce emergency readmissions.
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PMID:Predicting emergency readmissions for patients discharged from the medical service of a teaching hospital. 369


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