Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study mice were treated with tumor necrosis factor alpha (TNFalpha) for 6 weeks to determine if chronic TNFalpha treatment could produce serum levels of TNFalpha similar to what has been observed in disease states (heart failure, HIV) and to determine if these levels of TNFalpha alter ventricular K(+) currents. Mice chronically treated with TNFalpha and sham treated mice were utilized for experiments. Serum levels were measured with a Searchlight protein array. Patch-clamp techniques, real-time PCR and Western blot analysis were used to study K(+) current densities and K(+) channel expression. Results showed that serum concentrations of TNFalpha were significantly higher in TNFalpha treated mice compared to controls (control: 9.5+/-1.5 pg/ml, TNFalpha: 27.4+/-5.0 pg/ml; p<0.05) and comparable to serum TNFalpha levels observed in heart failure and HIV models. In ventricular myocytes from TNFalpha treated mice the outward K(+) currents I(to) and I(Kur) were significantly reduced (at +30 mV: I(to): control: 45.0+/-2.9 pA/pF, TNFalpha: 34.5+/-2.9 pA/pF; p<0.05; I(Kur): control 34.1+/-2.7 pA/pF, TNFalpha: 25.0+/-2.2 pA/pF; p<0.05). Expression studies revealed that ventricular mRNA and protein expression for the channels underlying I(to) and I(Kur) did not differ between the two groups. However, the recovery from inactivation for I(Kur) was significantly longer in TNFalpha treated mice. Overall, this study shows that pathologically relevant levels of serum TNFalpha modulate K(+) currents in mouse ventricle. These findings could help to explain the role of TNFalpha in the pathogenesis of cardiac arrhythmia.
J Mol Cell Cardiol 2009 Aug
PMID:Ventricular K+ currents are reduced in mice with elevated levels of serum TNFalpha. 1928 15

Pulmonary hypertension is a pathophysiologic condition characterized by the increase of mean pulmonary arterial pressure > or =25 mmHg. A concomitant increase of pulmonary wedge pressure >15 mmHg may be present (post-capillary pulmonary hypertension) or not (precapillary pulmonary hypertension). The increase of pulmonary arterial pressure and of pulmonary vascular resistance and consequent elevation of the right ventricular afterload lead to right ventricular failure after variable periods of time. Pulmonary hypertension is present in multiple clinical conditions which have been classified in five groups. Pulmonary arterial hypertension (group 1) includes the familial and the idiopathic form and the forms associated with anorexigen drug use, connective tissue diseases, congenital heart diseases, HIV infection and portal hypertension. Group 2 includes all left heart diseases characterized by the increase of left atrial pressure and pulmonary wedge pressure (post-capillary pulmonary hypertension). Group 3 includes parenchymal lung diseases (chronic obstructive lung disease, lung fibrosis, ecc). Chronic thromboembolic pulmonary hypertension (group 4) is characterized by the obstruction of elastic pulmonary arteries at different levels by organized thromboembolism. Group 5 includes heterogeneous conditions such as sarcoidosis and histiocytosis X. These clinical groups are characterized by different pathobiologic and pathophysiologic mechanisms and therapeutic strategies. The exact pathobiologic mechanisms leading to pulmonary arterial hypertension (group 1) are unknown. Genetic factors (inheritable forms), predisposing factors (female gender) and exogenous factors (drugs, antibodies, viruses, congenital heart disease, etc). Endothelial dysfunction of lung microcirculation is invariably present and is characterized by the reduction of vasodilator and antiproliferative substances (prostacyclin, nitric oxide) and by the increase of vasoconstrictor and mitogenic factors (endothelin, thromboxane A2). Current approved therapies are targeted to the correction of this imbalance, which leads to the progressive increase of pulmonary vascular resistance. Different therapeutic strategies that are effective in diverse groups require an appropriate diagnostic algorithm in order to identify the precise group and specific conditions within the group. Evaluation of vasoreactivity and assessment of the severity of functional and hemodynamic changes are also required in pulmonary arterial hypertension for an appropriate therapeutic decision-making and estimate of results.
G Ital Cardiol (Rome) 2009 May
PMID:[Pulmonary arterial hypertension. Part I: pathobiologic, pathophysiologic, clinical and diagnostic aspects]. 1953 40

The advent of highly active antiretroviral therapy has led to a significant decline in the incidence of mortality and progression to AIDS in HIV-infection. With increased life expectancy, HIV-infected individuals are being affected by cardiovascular disease. Research studies have identified an increased prevalence of traditional coronary risk factors in HIV-infected patients. Additional investigations suggest that the virus itself may independently result in atherosclerosis. Further studies have linked the use of highly active antiretroviral therapy to the atherosclerotic processes. These findings suggest the need to reconsider HIV as one of the traditionally accepted risk factors for coronary artery disease, with treatment aimed at prevention of myocardial infarction.
Cardiol Rev
PMID:Human immunodeficiency virus and atherosclerosis. 1969 Apr 71

Endothelin-1 is a potent vasoconstrictor and mitogen that is primarily synthesized and released from vascular endothelial cells. Bosentan is a dual endothelin-receptor antagonist that initially received approval for treatment of WHO group I pulmonary arterial hypertension (PAH) for patients in functional classes III and IV. Analysis of a study conducted in functional class II patients (Endothelin Antagonist Trial in Mildly Symptomatic PAH Patients [EARLY] trial) suggest its efficacy for these less symptomatic patients. In addition, bosentan has demonstrated efficacy in patients with congenital heart disease and Eisenmengers syndrome with right to left shunting and in HIV-related PAH. Studies of bosentan in inoperable or residual chronic thromboembolic pulmonary hypertension suggest possible efficacy. Bosentan appears promising in patients with idiopathic pulmonary fibrosis who do not have pulmonary hypertension. Combinations of bosentan with other PAH therapies such as iloprost and sildenafil may have incremental benefit over monotherapy.
Future Cardiol 2008 Sep
PMID:Bosentan for pulmonary hypertension and other pulmonary diseases: emerging evidence. 1980 40

Cardiac involvement in children with human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS) is known but less often considered. Our objectives were to determine cardiac manifestations in pediatric HIV/AIDS and estimate the cardiac isoform of alpha-2 macroglobulin [CA2M] among them. We recruited 67 pediatric HIV/AIDS patients, 37 with cardiac involvement (group A) and 30 without (group B); 30 cardiac patients without HIV infection (group C); and 30 healthy control subjects without any comorbid illness (group D). Their sociodemographic and clinical information were collected along with echocardiogram and blood for CA2M. Patterns of cardiac involvement in HIV/AIDS (group A) were pericardial effusion, left ventricular dysfunction, pulmonary hypertension, and cardiomyopathy and observed in 43, 30, 16, and 11% of subjects, respectively. CA2M levels among groups A, B, C, and D were 132.67 +/- 5.01, 41.25 +/- 3.33, 65.99 +/- 2.48 and 29.59 +/- 2.76 microgm/ml, respectively. It was elevated significantly in group A (P = 0.001; 95% confidence interval [CI] 87.27-95.55) compared with group B and was independent of sex and CD4 count among HIV/AIDS subjects. Although CA2M was elevated in HIV-negative patients with cardiac involvement, it was much less than in HIV/AIDS subjects with cardiac involvement (P = 0.001; 95% CI 62.54-70.82). Because CA2M is a cardiac biomarker, further research with larger population is needed to ascertain the role of CA2M as a diagnostic/therapeutic/prognostic marker in cardiac patients with and without HIV infection.
Pediatr Cardiol 2010 Feb
PMID:Cardiac isoform of alpha 2 macroglobulin: a marker of cardiac involvement in pediatric HIV and AIDS. 1991 89

Over 30 million people are currently living with human immunodeficiency virus (HIV) infection, and over 2 million new infections occur per year. HIV has been found to directly affect vascular biology resulting in an increased risk of cardiovascular disease compared to uninfected persons. Although HIV infection can now be treated effectively with combination antiretroviral medications, significant toxicities such as hyperlipidemia, diabetes, and excess cardiovascular co-morbidity; as well as the potential for significant drug-drug interactions between HIV and cardiovascular medications, present new challenges for the management of persons infected with HIV. We first review basic principles of HIV pathogenesis and treatment and then discuss relevant clinical management strategies that will be useful for cardiologists who might be involved in the care of HIV infected patients.
Curr Cardiol Rev 2008 Aug
PMID:The Relationship Between HIV Infection and Cardiovascular Disease. 1993 97

One of the most recent phenomena related to the acquired immunodeficiency syndrome (AIDS) is the emergence of a new vulnerable population: the elderly. One of the factors that account for this increase is the development of combination antiretroviral therapy (ART), which has provided better quality of life and life expectancy for HIV-positive patients. However, ART is associated with adverse effects such as dyslipidemia, diabetes mellitus and insulin resistance, which are risk factors for cardiovascular disease. Due to the impact of ART on lipid and glucose metabolism, many studies were published involving HIV infection and cardiovascular disease, as well as their risk factors and the use of ART, but few of them reported on the cardiotoxicity of this therapy in the elderly. The objective of this study is to review the main metabolic changes caused by the use of antiretroviral therapy and its impact on an increased risk of cardiovascular disease in elderly people with HIV.
Arq Bras Cardiol 2009 Nov
PMID:Metabolic abnormalities, antiretroviral therapy and cardiovascular disease in elderly patients with HIV. 2008 20

HIV/AIDS (Human immunodeficiency virus/ Acquired immuno deficiency syndrome) is a growing global problem, in terms of its incidence and mortality. Patients with HIV/AIDS are living much longer with HAART (Highly active antiretroviral therapy) therapy so much so that HIV/AIDS has now become a part of the chronic disease burden, like hypertension and diabetes. Patients with HIV/AIDS and symptoms suggestive of cardiac disease represent a diagnostic and therapeutic challenge in clinical practice; Cardiologists are more frequently encountering this problem. An algorithmic, anatomic approach to diagnosis, localizing disease to the endocardium, myocardium and pericardium can be useful. An intimate knowledge of opportunistic infections affecting the heart, effects of HAART therapy and therapy for opportunistic infections on the heart is needed to be able to formulate a differential diagnosis. Effects of HAART therapy, especially protease inhibitors on lipid and glucose metabolism, and their influence on progression to premature vascular disease require consideration. Treatment of cardiac disease, in HIV/AIDS patients can vary from non-HIV patients, based on drug interactions, differences in responsiveness, and other factors; and this area requires further research.
Curr Cardiol Rev 2009 May
PMID:Heart Disease in Patients with HIV/AIDS-An Emerging Clinical Problem. 2043 55

Vaccination against tuberculosis is not an obligation anymore in France, except for children at risk, but this disease remains not so rare, including its extrapulmonary forms. The authors report the case of a 27-year-old Madagascan HIV seronegative patient, who developed a pericardial effusion when coming back from a long stay in Madagascar. An anti-inflammatory treatment and then a probabilistic antibiotic treatment were ineffective, and at the same time echocardiographic signs of tamponade appeared. As a consequence, it was decided to perform a surgical pericardial drainage and a biopsy, and to introduce an antituberculosis chemotherapy, given the epidemiologic status. The course was then quickly favorable. The presence of granulomatous inflammation on the biopsy and an elevated pericardial adenosine deaminase activity level retrospectively supported the diagnosis of tuberculous pericarditis.
Ann Cardiol Angeiol (Paris) 2010 Aug
PMID:[Tuberculous pericarditis: still a relevant disease]. 2051 Sep 15

Pulmonary hypertension is a heterogeneous hemodynamic and pathophysiological state that is observed in a number of clinical conditions, which have been divided into six diagnostic groups. Although the increase in pulmonary pressure observed in these clinical groups may be similar, underlying disease mechanisms, diagnostic methods, and prognostic and therapeutic consequences are completely different. Pulmonary arterial hypertension is associated with several rare conditions that have comparable clinical and hemodynamic characteristics and exhibit virtually identical anatomical and pathological alterations in the lung microcirculation. These conditions include idiopathic and familial forms of the disease and disease forms associated with connective tissue disease, congenital heart defects involving systemic-to-pulmonary arterial shunts, portal hypertension, and HIV infection. It has been shown that treatment with specific drugs (e.g. prostanoids, endothelin-receptor antagonists and phosphodiesterase type-5 inhibitors) is effective in these patients and that these drugs can also be administered in various combinations. An evidence-based treatment algorithm has been developed for these patients. In patients with pulmonary hypertension due to left heart disease or lung disease, treatment focuses on the underlying condition and there is no convincing evidence that agents approved for pulmonary arterial hypertension are effective. For patients with chronic thromboembolic pulmonary hypertension, the treatment of choice is pulmonary endarterectomy. However, drugs intended specifically for the treatment of pulmonary arterial hypertension may be considered in inoperable cases or after suboptimal surgery.
Rev Esp Cardiol 2010 Jun
PMID:Current therapeutic approaches to pulmonary arterial hypertension. 2051 28


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