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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As more effective therapies have produced longer survival times for human immunodeficiency virus (HIV)-infected patients, new complications of late-stage HIV infection including HIV-related heart disease have emerged. Almost any agent that can cause disseminated infection in patients with acquired immunodeficiency syndrome (AIDS) may involve myocardium, but clinical evidence of cardiac disease is usually overshadowed by manifestations in other organs, primarily the brain and lungs. Cardiac abnormalities are found at autopsy in two-thirds of patients with AIDS, and more than 150 reports of cardiac complications have been published. Cardiac involvement in HIV disease includes pericardial effusion, myocarditis, dilated cardiomyopathy, and/or endocardial involvement at any stage of the disease. This review deals with all the cardiac manifestations of AIDS and serves to highlight two problems and one indication. First of all, there are very few clinical studies. Current knowledge is based almost exclusively on echocardiography and autopsy studies. Observational or clinical trials would be useful. Second, there exists very poor information on the impact of treatment; and epidemiologic and clinicopathologic studies are mandatory for obtaining detailed data concerning the mechanisms of myocardial damage in AIDS. Finally, because cardiac complications are often clinically inapparent or subtle in the initial stages, periodic screening of HIV-positive patients by electrocardiogram and echocardiogram is probably indicated. In addition, AIDS may also provide the opportunity to gain insights into the pathogenesis of little understood cardiac diseases such as lymphocytic myocarditis and dilated cardiomyopathy.
Clin Cardiol 1998 Jul
PMID:Cardiac involvement in acquired immunodeficiency syndrome--a review to push action. The Committee for the Study of Cardiac Involvement in AIDS. 966 54

AZT, a widely-utilized drug for the treatment of HIV infection, inhibits the polymerase responsible for mitochondrial DNA replication (mtDNA). The aim of this study was to assess myocardial alterations caused by this action. Ventricular muscle from rats treated for > or = 35 days with 1 mg/ml of AZT in their drinking water was analysed for cytochrome oxidase activity and the content of mRNAs for the nuclear-encoded cytochrome oxidase (COX) subunit VIc and the mitochondrial-encoded COX subunit III. In addition contractile protein expression was assessed by examining mRNA levels for alpha- and beta-myosin heavy chains (MHC). Changes in MHC mRNA levels were correlated with changes in alpha- and beta-MHC proteins and changes in myofibrillar ATPase activity. Results show that AZT caused a reduction in COX activity, COX subunit III mRNA, and mtDNA levels. There was no decrease in the COX subunit VIc mRNA. MHC expression was altered such that the relative content of beta-MHC protein and mRNA were increased. Accumulation of beta-MHC was reflected in the reduction of myofibrillar ATPase activity at pCa values of 5.875 and 6.125. These data demonstrate that AZT induces a reorganization of cardiac gene expression indicative of changes in cardiac contractile properties. The observed decreases in mtDNA levels along with mRNA for a mitochondrial-encoded protein and COX activity is consistent with the postulated mechanism whereby AZT induces a myopathy by diminishing mtDNA replication.
J Mol Cell Cardiol 1998 Oct
PMID:AZT decreases rat myocardial cytochrome oxidase activity and increases beta-myosin heavy chain content. 979 52

Recent reports have suggested a possible association between HIV-1 infection and "idiopathic" pulmonary hypertension (PH), but the pathogenetic role of the viral agent has not been fully defined yet. We report the cases of two white males positive for human immunodeficiency virus type 1 (HIV-1) who presented with clinical and hemodynamic diagnosis of pulmonary hypertension. They were heterosexual, non-hemophiliac, heroin abusers with no signs of clinical AIDS. Neither one of the patients had opportunistic lung infections or any other cause of secondary pulmonary hypertension. In one case, peculiar clinical and electrocardiographic features of PH were associated with signs of thrombotic thrombocytopenic purpura (TTP). The association between PH and HIV-1 infection might be explained by a severe alteration of pulmonary endothelial cell homeostasis secondary to HIV-1 viral infection.
G Ital Cardiol 1998 Dec
PMID:Pulmonary hypertension associated with human immunodeficiency virus infection. Report of two cases and review of the literature. 988 95

Valve replacement, valvulectomy and valve repair are the alternatives for the surgical treatment of intractable tricuspid valve endocarditis. We present the case of a 24-year-old, HIV-positive Caucasian female, intravenous drug addict, with intractable tricuspid valve endocarditis, that was successfully treated with tricuspid valve repair. Advantages and major drawbacks of the different techniques are discussed and the appropriate literature is reviewed.
Rev Esp Cardiol 1999 Jan
PMID:[Valve repair in tricuspid endocarditis in the drug addict. Apropos a case]. 998 43

Human immunodeficiency virus (HIV, lentivirus) type-1 based vectors have a number of attractive features for gene therapy, including the ability to transduce non-dividing cells and long term transgene expression. We used a three-plasmid expression system to generate pseudotyped lentivirus-based vectors by transient transfection of human embryonic kidney 293T cells in the presence of sodium butyrate, which is known to activate the long terminal repeat-directed expression of HIV. Using this system we successfully generated versatile high titer lentivirus at titers of up to 2 x 10(8) transducing units/ml (TU/ml), and improved transduction efficiency in various cell types from seven to over twenty fold. We demonstrate its applicability of these vectors for the efficient transduction of non-dividing cells, including post mitotic beating rat cardiac myocytes and well-differentiated rat L6 myofibers. While both lentivirus-based and murine retrovirus-based vectors effectively transduced dividing cardiac fibroblasts and L6 muscle myoblasts in culture, lentivirus-based vectors also efficiently transduced cardiac myocytes and yielded titers of (6.3 +/- 1.2) x 10(5) TU/ml; however murine retrovirus-based vectors showed low transduction efficiency with titers reaching only (8.9 +/- 2.1) x 10(2) TU/ml. Furthermore, even 12 days after induction of differentiation of L6 myofibers, lentivirus-mediated transduction of beta-galactosidase (beta-Gal) at approximately 30-40% of the maximum expression levels achieved in replicating myoblasts. In contrast, the expression of beta-Gal following transduction of the myofibers by murine retrovirus-based vectors fell to less than 1% of an already reduced level of transduction in undifferentiated confluent myoblasts. These results demonstrate that lentivirus-based vectors can efficiently transduce both well-differentiated cardiac myocytes and differentiated myofibers. This appears to be an efficient method and provides a new tool for research and therapy for cardiovascular diseases.
J Mol Cell Cardiol 1999 Nov
PMID:A high-titer lentiviral production system mediates efficient transduction of differentiated cells including beating cardiac myocytes. 1059 Oct 30

Limited data are available on the electrocardiogram and ambulatory electrocardiogram recording (Holter) in children infected with the human immunodeficiency virus type 1 (HIV-1). The purpose of this study was to estimate the prevalence and cumulative incidence of rhythm and conduction abnormalities in HIV-1-infected children. Electrocardiograms and Holter monitoring studies were performed annually on 205 HIV-1-infected children enrolled after 28 days of life (group I), 93 HIV-1-infected infants enrolled during pregnancy or during the first 28 days of life (group IIa), and 463 HIV-1-uninfected infants enrolled during pregnancy or during the first 28 days of life (group IIb). The 5-year cumulative incidence in the group I children of second-degree atrioventricular block or supraventricular or ventricular tachycardia was 13.4%, and the 5-year incidence was higher for the older infected group I children (16.8% for children > or =4 years old at first study and 11.4% for children <4 years, p = 0.04). The mean corrected QT interval was also longer for the older infected group I children (p = 0.002) and prolonged in the HIV-1-infected compared to the HIV-1-uninfected group II children (p = 0.02). None of the children had atrial fibrillation or flutter. Arrhythmias are uncommon in children infected with HIV-1 and in children of HIV-1-infected mothers and the arrhythmias identified tend to be benign. Therefore, routine Holter monitoring does not appear to be indicated in asymptomatic children.
Pediatr Cardiol
PMID:Electrocardiography and 24-hour electrocardiographic ambulatory recording (Holter monitor) studies in children infected with human immunodeficiency virus type 1. The Pediatric Pulmonary and Cardiac Complications of Vertically Transmitted HIV-1 Infection Study Group. 1081 72

Oxidation-reduction (redox) coupled mechanisms play an important role in the regulation of cell surface adhesion molecule expression. In endothelial cells membrane-bound NADH/NADPH oxidase is a significant source of intracellular superoxide (O(2)(-)) production. We explored the role of flavin containing proteins such as NADH/NADPH oxidase in the induction of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) gene expression in human aortic endothelial cells (HAECs) and human dermal microvascular endothelial cells (HMECs). Treatment of HAECs by tumor necrosis factor- alpha (TNF- alpha, 100 U/ml) for 1 h induced a 31% increase in O(2)(-)production within 5 min as determined by lucigenin chemiluminescence analysis of whole cells (n=4, P<0.05). Pretreatment with the NADH/NADPH oxidase inhibitor diphenylene iodonium (DPI, 40 microm) for 1 h inhibited O(2)(-)production. DPI also inhibited TNF and LPS-induced VCAM-1 and ICAM-1 cell surface expression and TNF- alpha, LPS, or IL-1 beta induced VCAM-1 and ICAM-1 mRNA accumulation. However, DPI did not inhibit TNF- alpha -induced activation of nuclear NF- kappa B-like binding activity in HAECs and HMECs. Furthermore, DPI did not inhibit TNF- alpha induced transactivation of NF- kappa B-driven VCAM-1 and HIV-LTR promoter gene constructs in transiently transfected HMECs. These data suggest that flavin binding proteins such as NADH/NADPH oxidase can regulate VCAM-1 gene expression independent of NF- kappa B. Furthermore, intracellular O(2)(-)generation is not necessary for NF- kappa B activation or for transactivation of NF- kappa B driven promoters.
J Mol Cell Cardiol 2000 Aug
PMID:NF- kappa B independent suppression of endothelial vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 gene expression by inhibition of flavin binding proteins and superoxide production. 1090 Jan 76

Polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes (POEMS) syndrome, a plasma cell dyscrasia associated with pulmonary hypertension, has been treated in the past with anticytokine strategies with a poor outcome. A patient is described who had POEMS syndrome with precapillary pulmonary hypertension and Raynaud's phenomenon, and who responded well to a short course of corticosteroids and long term nifedipine. POEMS syndrome, like anorexigens, cocaine, portal hypertension and human immunodeficiency virus infection, may be another trigger for the pulmonary vascular occlusive process found in primary pulmonary hypertension.
Can J Cardiol 2000 Aug
PMID:Reversible pulmonary hypertension in POEMS syndrome--another etiology of triggered pulmonary vasculopathy? 1097 36

With the advent of more effective therapies for human immunodeficiency virus (HIV) infection, HIV-infected patients are living longer and cardiovascular disease is becoming more obvious in this population. Patients with HIV infection represent one of the most rapidly developing groups with cardiovascular disease globally. Cardiovascular disease complicating HIV infection is likely to contribute to burgeoning healthcare costs. Pericarditis, myocarditis, cardiomyopathy, atherosclerotic coronary vasculopathy, arterial aneurysms, pulmonary hypertension, and endocarditis occur with increased frequency in these patients. Pericardial tamponade, dilated cardiomyopathy, endocarditis, and vasculopathy can lead to fatal outcomes in this population. The advent of cardiomyopathy heralds a very poor prognosis in patients infected with HIV. Coronary vasculopathy without obvious risk factors can lead to myocardial ischemia in young patients infected with the virus. Moreover, the protease inhibitors used to treat HIV infection induce a syndrome of lipodystrophy and dyslipidemia that may be associated with accelerated atherosclerosis as well as insulin resistance. All these factors contribute to increased cardiovascular morbidity and mortality in the HIV-infected population. HIV infection, opportunistic infections, secreted viral proteins such as gp120 (envelope protein) or Tat (transactivator of viral transcription), and cytokines elaborated during the course of HIV infection of the immune system all contribute to pathogenesis of these disorders. Further basic and clinical studies are required to understand the pathogenesis of cardiovascular complications and develop appropriate management strategies for these patients.
Cardiol Rev
PMID:The cardiovascular and metabolic complications of HIV infection. 1117 4

Both cocaine use and human immunodeficiency virus (HIV) infection alone have been associated with an increased incidence of cardiac dysfunction. Concomitant exposure to cocaine and HIV infection may exacerbate the cardiac toxicity of either agent alone, a hypothesis that is examined in this review article. A possible unifying hypothesis based on enhancement of adrenergic stimulation is proposed.
Clin Cardiol 2001 Mar
PMID:Can cocaine abuse exacerbate the cardiac toxicity of human immunodeficiency virus? 1128 61


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