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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human immunodeficiency virus (HIV) disease is recognized as an important cause of dilated cardiomyopathy. Myocarditis and myocardial infection with HIV-1 are the best-studied causes of cardiomyopathy in HIV disease. HIV-1 virions appear to infect myocardial cells in a patchy distribution with no direct association between the presence of the virus and myocyte dysfunction. Myocardial dendritic cells seem to play a significant pathogenetic role by activating multifunctional cytokines (i. e., tumor necrosis factor-alpha) and the inducible form of nitric oxide synthase that contribute to progressive and late myocardial tissue damage. Coinfection with other viruses (usually, coxsackievirus B3 and cytomegalovirus) may also play an important etiopathogenetic role.The introduction of highly active antiretroviral therapy (HAART) has significantly reduced the incidence of myocarditis in HIV-infected patients living in developed countries. By contrast, in developing countries, where the availability of HAART is scanty and greater is the pathogenetic role of nutritional factors, the incidence of HIV-associated myocarditis and cardiomyopathy is increasing with a high mortality rate for congestive heart failure.A clinical diagnosis of myocarditis or congestive heart failure may be difficult in an HIV-infected patient due to masking of symptoms by concomitant bronchopulmonary disease and/or wasting syndromes, especially in a more advanced stage of HIV disease. Immunomodulatory therapy (intravenous immunoglobulins) may be helpful in adults and children with HIV-associated myocarditis and declining left ventricular function. Data on the role of HAART in the treatment of HIVassociated myocarditis and cardiomyopathy are lacking.
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PMID:HIV-associated cardiomyopathy etiopathogenesis and clinical aspects. 1617 Jun 79

Human immunodeficiency virus (HIV) infection is a global public health issue that is frequently associated with cardiovascular involvement. Left ventricular dysfunction, an independent predictor of mortality in HIV-infected patients, is the result of many causes in this population and may result in dilated cardiomyopathy and congestive heart failure in about 10% of patients. Antiinfective and highly active antiretroviral therapies may be particularly helpful in this population to reduce HIV-associated diseases. However, some of these drugs exhibit mitochondrial toxicity being expected to impair myocardial function. The HIV-associated cardiomyopathy is often clinically occult or attributed incorrectly to other noncardiac disease processes. Therefore, a heightened awareness and routine screening for cardiovascular involvement in HIV-infected patients would lead to earlier detection and the hope for a reduction in associated morbidity and mortality. In summary, cardiovascular complications, particular HIV-associated cardiomyopathy, are important contributors to morbidity and mortality in HIV-infected patients that can be detected early in many cases and may be treated effectively. The therapy of HIV-associated cardiomyopathy comprises standard medical treatment for heart failure.
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PMID:[HIV-associated cardiomyopathy]. 1617 Jun 87

More than one million Americans have been diagnosed with human immunodeficiency virus (HIV). Advances in prevention and treatment of HIV have led to an increased life expectancy for patients with HIV infection. Due to their increased life span, HIV+ patients are now presenting to hospitals with an increased number of diverse late-stage complications, such as cardiomyopathy and other cardiovascular conditions. These complications are as a direct or indirect result of HIV disease, HIV treatment modalities, comorbid conditions, dietary and lifestyle factors, and unknown etiologies. Cardiac complications, particularly HIV-related dilated cardiomyopathy, are potentially life-threatening diagnoses, with symptoms that may be minimized with appropriate cardiac-specific assessments and treatments, patient teaching, and collaboration among nurses caring for the HIV-positive client with cardiac disease.
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PMID:HAART to heart: HIV-related cardiomyopathy and other cardiovascular complications. 1646 5

Human immunodeficiency virus-related cardiomyopathy is characterized by global left ventricular (LV) dysfunction commonly associated with biventricular dilation. Human immunodeficiency virus (HIV) cardiomyopathy carries a poor prognosis, and the role of antiretroviral therapy in the reversal of heart failure is not very clear. We report two patients with HIV infection who presented with severe right ventricular (RV) dysfunction in the absence of pulmonary parenchymal, pulmonary arterial and left ventricular myocardial involvement. During the period of intensive antiretroviral therapy, the symptoms of right heart failure progressively and remarkably improved. This was accompanied by normalization of right ventricular size and RV function documented by repeat echocardiograms. Given that the serologic tests for opportunistic infections were negative, and the RV function improvement correlated with a decrement in the viral load, it is likely that the cardiomyopathy was due to direct infection by HIV. These cases illustrate that there can be isolated involvement of the right heart in the absence of lung, significant pulmonary vascular and left ventricular disease, and also that the antiretroviral therapy might reverse the cardiomyopathy.
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PMID:Reversible right ventricular dysfunction in patients with HIV infection. 1655 85

Takotsubo cardiomyopathy (in Japanese language "takotsubo" is a fishing pot with a round bottom and a neck that is used for trapping octopuses) is a new syndrome, which is characterized by transient left ventricular dysfunction and by a typical left ventriculogram showing transient extensive akinesis of the apical and mid portions of the left ventricle with hypercontraction of the basal segment, from which this disease takes its name. Since 1990 sporadic cases of takotsubo cardiomyopathy were reported by Japanese authors, and only a few European reports are available. We report a case of takotsubo-like left ventricular dysfunction in an human immunodeficiency virus (HIV)-infected caucasian patient.
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PMID:Takotsubo-like left ventricular dysfunction in an HIV-infected patient. 1661 Oct 62

Doxorubicin remains a useful anti-cancer drug but as lifetime dose approaches 500 mg/m2 and particularly when this dose is exceeded, iatrogenic life-threatening cardiomyopathy becomes progressively more likely. This note reviews evidence indicating that doxorubicin induced cardiomyopathy is partly mediated by stimulation of Toll-like receptors (TLR) 2 and 4 which are expressed on cardiomyocytes. Indinavir, nelfinavir, ritonavir, and saquinavir are currently marketed protease inhibitors used to suppress human immunodeficiency virus. They have recently been shown to inhibit signalling at TLR 2 and 4 as well as intracellular events downstream from these receptors. It is possible that these FDA-approved anti-retroviral protease inhibitors could be used off-label to diminish likelihood of doxorubicin cardiotoxicity permitting higher doxorubicin doses. We suggest that currently marketed anti-viral protease inhibitors be investigated in animal models of doxorubicin cardiomyopathy and if such studies do indeed show protection, human studies be initiated.
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PMID:Doxorubicin cardiomyopathy via TLR-2 stimulation: potential for prevention using current anti-retroviral inhibitors such as ritonavir and nelfinavir. 1735 82

Chagas' disease, caused by the parasite Trypanosoma cruzi, remains the leading cause of cardiopathy in Latin America with about 12 million people infected. Classic clinical manifestations derive from infection of muscle cells leading to progressive cardiomyopathy, while some patients develop megacolon or megaesophagus. A very aggressive clinical course including fulminant meningoencephalitis has been reported in patients who contract Chagas' disease in the background of immunodeficiency. This includes patients with human immunodeficiency virus infection as well as patients receiving immunosuppressive therapy for organ transplant. Currently, only two drugs are approved for the treatment of Chagas' disease, nifurtimox and benznidazole. Both have significant limitations due to common and serious side effects as well as limited availability. A promising group of new drug leads for Chagas' disease is cysteine protease inhibitors targeting cruzain, the major protease of T. cruzi. The inhibitor N-methyl-Pip-F-homoF-vinyl sulfonyl phenyl (N-methyl-Pip-F-hF-VS phi) is in late-stage preclinical development. Therefore, the question arose as to whether protease inhibitors targeting cruzain would have efficacy in Chagas' disease occurring in the background of immunodeficiency. To address this question, we studied the course of infection in recombinase-deficient (Rag1(-/-)) and normal mice infected with T. cruzi. Infections localized to heart and skeletal muscle in untreated normal animals, while untreated Rag1(-/-) mice showed severe infection in all organs and predominantly in liver and spleen. Treatment with the dipeptide N-methyl-Pip-F-hF-VS phi rescued immunodeficient animals from lethal Chagas' infection. The majority (60 to 100%) of inhibitor-treated Rag1(-/-) mice had increased survival, negative PCR, and normal tissues by histopathological examination.
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PMID:A cysteine protease inhibitor cures Chagas' disease in an immunodeficient-mouse model of infection. 1769 25

Methamphetamine is a stimulant commonly abused in many parts of the United States. Most methamphetamine users are white men 18 to 25 years of age, but the highest usage rates have been found in native Hawaiians, persons of more than one race, Native Americans, and men who have sex with men. Methamphetamine use produces a rapid, pleasurable rush followed by euphoria, heightened attention, and increased energy. Possible adverse effects include myocardial infarction, stroke, seizures, rhabdomyolysis, cardiomyopathy, psychosis, and death. Chronic methamphetamine use is associated with neurologic and psychiatric symptoms and changes in physical appearance. High-risk sexual activity and transmission of human immunodeficiency virus are also associated with methamphetamine use. Use of methamphetamine in women who are pregnant can cause placental abruption, intrauterine growth retardation, and preterm birth, and there can be adverse consequences in children exposed to the drug. Treatment of methamphetamine intoxication is primarily supportive. Treatment of methamphetamine abuse is behavioral; cognitive behavior therapy, contingency management, and the Matrix Model may be effective. Pharmacologic treatments are under investigation.
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PMID:Methamphetamine abuse. 1799 Aug 40

The infection with the human immunodeficiency virus (HIV) is not only associated with a dysfunction of the immune system. Other organs are often affected in patients with HIV-infection, as well. In particular, an increased cardiovascular risk profile leads to an increasing rate of morbidity and mortality due to cardiac disorders, including heart failure and HIV-associated cardiomyopathy in this patient population. However, not only classic risk factors such as smoking, hypertension or dysregulation of lipid and glucose metabolisms are the reasons of HIV-associated myocardial dysfunction. Especially these subjects are also prone to opportunistic infections, side effects of antiretroviral therapy or the HI-virus itself.
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PMID:[HIV, AIDS and the cardiovascular risk]. 1830 15

The prognosis for patients with human immunodeficiency virus (HIV) infection has improved remarkably as a result of effective antiretroviral therapy. This has resulted in an increased awareness of cardiac complications from HIV infection, including cardiomyopathy and overt heart failure. Mechanisms responsible for HIV cardiomyopathy and heart failure are unknown, but may include direct effects of HIV proteins on the heart. We have previously reported that the HIV envelope glycoprotein, gp120, has a p38 MAP kinase-dependent negative inotropic effect on adult rat ventricular myocytes (ARVM). This signaling pathway presumably results from the binding of gp120 to a specific receptor on the surface of cardiac myocytes. HIV gp120 has been shown to bind to CD4, CXCR4, and CCR5 receptors on lymphocytes and macrophages. Accordingly, we sought to determine if HIV gp120 regulated its negative inotropic effect through activation of one of these binding sites on cardiac myocytes. AMD3100, a highly selective CXCR4 receptor antagonist, reversed HIV gp120-induced negative inotropic effect on ARVM. AMD3100 also blocked HIV gp120 phosphorylation of both p38 MAP kinase and Troponin I. The binding of gp120 to the CXCR4 receptor on ARVM was confirmed by co-immunoprecipitation. We conclude that the negative inotropic effect of HIV gp120 is mediated by a novel signaling pathway that begins with binding to a cardiac myocyte CXCR4 receptor, followed by phosphorylation of both p38 MAP kinase and Troponin I.
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PMID:CXCR4 receptor antagonist blocks cardiac myocyte p38 MAP kinase phosphorylation by HIV gp120. 1885 76


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