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

Parasitic infections produce a wide spectrum of cardiac manifestations. They may involve various anatomic structures of the heart and are manifested clinically as myocarditis, cardiomyopathies, pericarditis, or pulmonary hypertension in many resource-constrained settings. However, many parasitic infections involving the heart may also be currently diagnosed in developed countries due to growing worldwide travel, blood transfusions, and increasing numbers of immunosuppression states such as organ transplantation, use of immunosuppressive agents, or HIV/AIDS. Clinicians anywhere in the globe need to be aware of the potential cardiac manifestations of parasitic diseases. This is part one of a three-part series discussing parasites of the heart. In this section, we provide a general overview and immunopathogenesis of parasitic infections of the heart.
Clin Cardiol 2007 Apr
PMID:Cardiac manifestations of parasitic infections part 1: overview and immunopathogenesis. 1744 54

There is controversy concerning the effectiveness of adjunctive corticosteroids in reducing mortality in tuberculous pericarditis. To assess the impact of this controversy on contemporary clinical practice, we studied the use of adjunctive corticosteroid in 185 consecutive patients with suspected pericardial tuberculosis from 15 hospitals in Cameroon, Nigeria, and South Africa. 109 (58.9%) patients received steroids with significant variation in corticosteroid use ranging from 0% to 93.5% per centre (P<0.0001). The presence of clinical features of HIV infection was the independent predictor of the non-use of adjunctive corticosteroids (OR 0.39, 95% CI 0.20-0.75, P=0.005). We have demonstrated marked variation in the use of corticosteroids by practitioners, with nearly half of all patients not receiving this intervention. Taken together with the statistical uncertainty regarding the effectiveness of adjunctive steroids in tuberculous pericarditis, these observations probably reflect a state of genuine uncertainty or clinical equipoise among practitioners who care for patients with tuberculous pericarditis in sub-Saharan Africa. These data provide a justification for the establishment of adequately powered randomised clinical trials to assess the effectiveness of adjunctive corticosteroids in patients with tuberculous pericarditis.
Int J Cardiol 2008 Mar 14
PMID:Contemporary use of adjunctive corticosteroids in tuberculous pericarditis. 1744 21

A 76-year-old woman was admitted to our hospital because of exertional dyspnea and leg edema during the previous month. Her systolic blood pressure on admission was 80 mmHg with 12 mmHg of pulsus paradoxous, and her pulse rate was 110 beats/min. Chest radiography revealed marked cardiomegaly and echocardiography showed massive pericardial effusion mainly behind the left ventricle and collapse of the right ventricle. The initial diagnosis was pericardial tamponade. Pericardiocentesis and pericardial drainage revealed bloody pericardial effusion. After drainage, her vital signs improved and her symptoms immediately disappeared. The cytological analysis of the pericardial effusion revealed numerous lymphoma cells. Computed tomography of the neck, chest and abdomen showed no evidence of tumor masses, lymph node enlargement, or hepatosplenomegaly. Infectious disease, collagen disease and aortic dissection were excluded. The final diagnosis was primary effusion lymphoma. The prognosis of primary effusion lymphoma is generally unfavorable because it is frequently accompanied by immunodeficiency disease. However, there was no human immunodeficiency virus infection in this patient. Fortunately, the effect of chemotherapy was excellent and the patient is doing well 1 year after the diagnosis.
J Cardiol 2007 Apr
PMID:[Primary effusion lymphoma complicating cardiac tamponade: a case report]. 1746 Aug 82

Human immunodeficiency virus (HIV) infection affects multiple organs including the cardiovascular system. Postmortem studies have revealed multiple abnormalities including abnormal coronary artery pathology, arteriopathy/endothelial dysfunction, hyperlipidemia and hypercoagulability prior to the use of protease inhibitors. With the introduction of antiretroviral medications, specifically protease inhibitor therapy, patients with HIV have been further noted to have premature coronary artery disease, hypercoagulability, hyperlipidemia, insulin resistance, fat redistribution syndrome and increased tendency to myocardial infarction. In this article, we report on one patient with HIV disease on protease inhibitor therapy that presented with non-Q-wave myocardial infarction and underwent percutaneous coronary intervention, and was later found to have stent thrombosis. A review of the literature showed no other previous reports of stent thrombosis secondary to acquired hypercoagulability due to protease inhibitor therapy. Possible predictors of stent thrombosis and hypercoagulability are also discussed.
J Invasive Cardiol 2007 May
PMID:HIV disease in thrombocardiology. 1747 40

Pharmacological agents used to treat patients with AIDS have been associated with QT prolongation and result in delayed repolarization. New evidence suggests that delayed repolarization can occur independently of pharmacological therapy. However, the effect of HIV on ventricular repolarization has not been investigated. Therefore, the objective of this study was to characterize cardiac repolarization in a mouse model of human HIV disease. All experiments were conducted on HIV transgenic mice (CD4C/HIV). These mice express the human HIV gene nef in cells of immune system and develop a severe AIDS-like disease that is similar to that observed in humans. ECG was recorded in conscious free moving mice and patch-clamp techniques were used to record action potentials and K+ current densities in single ventricular myocytes. Results showed that the QT interval and action potential duration were significantly prolonged in CD4C/HIV mice compared to wild-type littermates. This delay in repolarization was associated with a significant reduction in outward K+ currents. Echocardiography showed that cardiac structure and function were similar in CD4C/HIV and littermate control mice. This suggests that the changes in ventricular repolarization were not the result of heart failure or cardiac hypertrophy. Overall, this study shows that repolarization was delayed in CD4C/HIV mice and that this phenotype occurred in the absence of any pharmacological intervention. Thus, it appears that HIV may be responsible for the delayed ventricular repolarization phenotype observed in CD4C/HIV mice.
J Mol Cell Cardiol 2007 Aug
PMID:Cardiac repolarization is prolonged in CD4C/HIV transgenic mice. 1759 46

The Long QT syndrome is a disorder characterized by abnormalities of cardiac repolarisation, resulting in a propensity to polymorphic ventricular tachycardia (torsades de pointes) and sudden cardiac death. It remains unclear whether cardiac involvement with the HIV virus itself can cause QT prolongation. We report a case of a HIV infected young female presenting with recurrent syncope due to torsades de pointes.
Int J Cardiol 2009 Mar 20
PMID:HIV and Long QT syndrome--cause or coincidence. 1806 38

Although cardiotoxic effects of highly active antiretroviral therapy (HAART) are a growing concern, there is a lack of prospective studies of subclinical involvement of the heart in human immunodeficiency virus (HIV)-infected patients. This study evaluated noninvasively cardiac morphologic characteristics and function in HIV-positive (HIV(+)) men receiving HAART for > or =2 years with no clinical evidence of cardiovascular disease. Echocardiography at rest, including tissue Doppler imaging and exercise testing, were performed in 30 HIV(+) men (age 42.1 +/- 4.7 years, duration of HIV infection 10.4 +/- 4.7 years, duration of HAART 5.3 +/- 2.1 years) and 26 age-matched healthy controls. At rest, HIV(+) patients had similar left ventricular (LV) mass indexed to height(2.7) (40.6 +/- 9.5 vs 37.5 +/- 9.3 g/m; p >0.05), but a higher prevalence of LV diastolic dysfunction (abnormal relaxation or pseudonormal filling pattern in 64% of patients vs 12% of controls; p <0.001). LV systolic function indexes were significantly lower (ejection fraction 60.4 +/- 8.7% vs 66.9 +/- 6.9%; p <0.01, and tissue Doppler imaging peak systolic velocity 11.4 +/- 1.6 vs 13.5 +/- 2.2 cm/s; p <0.001). Pulmonary artery pressure was higher in patients compared with controls (32.1 +/- 5.4 vs 26.1 +/- 6.5 mm Hg; p <0.001). Exercise testing showed decreased exercise tolerance in HIV(+) patients, with no case of myocardial ischemia. In conclusion, subclinical cardiac abnormalities are frequently observed in HIV(+) patients on HAART. The usefulness of systematic noninvasive screening in this population should be considered. GECEM study no. 30: National Agency for AIDS Research (ANRS).
Am J Cardiol 2008 Apr 15
PMID:Subclinical cardiac abnormalities in human immunodeficiency virus-infected men receiving antiretroviral therapy. 1863 12

Since the advent of antibiotics, bacterial pericarditis has become relatively rare. Cardiac tamponade is a potentially lethal complication, especially when caused by methicillin-resistant Staphylococcus aureus (MRSA). In the intensive care setting other predisposing factors for purulent pericarditis, besides immunosuppression, are the high incidence of nasal and skin colonization and invasive techniques such as indwelling catheters. We present two case reports of cardiac tamponade in young patients, with underlying immunosuppression of different etiologies (HIV infection and liver transplantation). In both, clinical evolution was complicated by severe sepsis, with MRSA being isolated in various biological products, followed by bacterial pericarditis and tamponade. The authors highlight the need for a high degree of suspicion for the diagnosis of bacterial pericarditis in immunosuppressed patients, an ever-growing population, as well as the importance of echocardiographic monitoring during clinical evolution.
Rev Port Cardiol
PMID:Cardiac tamponade secondary to methicillin-resistant Staphylococcus aureus pericarditis. 1895 91

After more than two decades of AIDS epidemic, the spectrum of HIV-associated vascular diseases has mainly evolved from infectious and inflammatory vasculitides to premature atherosclerosis, its related contributing conditions (metabolic syndrome, dyslipidemia, insulin resistance syndrome) and complications (acute coronary and cerebrovascular syndromes). Today, as the AIDS epidemic further progresses worldwide and as the life expectancy of HIV-infected patients treated with effective antiviral regimens has dramatically increased, more than 10% of patients experience cardiovascular manifestations. The complex interplay between viral infection, inflammatory and cytokines pathways, protease inhibitors-induced hyperlipidemia and direct effects on endothelial cells has not, by far, been integrated in a single comprehensive pathogenesis network. However, recognition of its main components has resulted in a broader appreciation of cardiovascular risk and risk factors in HIV-infected/treated patients. Cardiovascular prevention is required in more than one half of HIV-infected/treated patients to achieve a reliable effectiveness of modern antiretroviral therapy. As the prognosis of HIV patients improves continuously, this rate is also likely to increase in the future.
Int J Cardiol 2009 Apr 17
PMID:HIV-associated vascular diseases: structural and functional changes, clinical implications. 1913 Nov 30

Heart muscle involvement associated with human immunodeficiency virus (HIV) infection may present as myocarditis, dilated cardiomyopathy or as isolated left or right ventricular dysfunction. Histopathological and ultra structural findings with different degrees of cardiac-chamber dilation have been described and an important role of the cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1) and IL-6 has been suggested. We present a case of myocarditis in a 47-year-old woman with HIV associated cardiomyopathy, focussing attention on heart muscle involvement in HIV disease.
Int J Cardiol 2011 Feb 03
PMID:Myocarditis and cardiomyopathy HIV associated. 1918 30


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