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

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.
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PMID:The cardiovascular and metabolic complications of HIV infection. 1117 4

The relationship between grade of pulmonary hypertension and factors associated with human immunodeficiency virus among patients with HIV infection is poorly documented. This report documents the most extensive attempt made thus far to determine whether a relationship exists between degree of pulmonary hypertension and the following conditions: HIV risk factor, degree of immunosuppression, presence or absence of AIDS, and presence or absence of liver cirrhosis. A retrospective study involving a search of the published literature on primary pulmonary hypertension among HIV cases from 1987 to 1998, using the Medline and Aidsline databases was conducted. Patients for whom secondary causes of pulmonary hypertension could be excluded were selected, and the following information for each was recorded: age, gender, risk factors for HIV infection, HIV disease stage according to the Centers for Disease Control, previous opportunistic and neoplastic diseases, CD4+ cell count (cells/L), presence or absence of liver cirrhosis, pulmonary systolic artery pressure level, and lung pathology specimens. Information about the patient's survival time was also recorded. Seventy-six patients were judged to have primary pulmonary hypertension and were included in the study. While no correlation was found between pulmonary systolic artery pressure level and CD4+ cell counts, a statistically significant difference was found between HIV-positive patients with and without AIDS as determined by the Centers for Disease Control criteria with regard to the degree of pulmonary hypertension, expressed as pulmonary systolic artery pressure level (85.4 +/- 17 mm Hg vs 71.8 +/- 15 mm Hg, p < 0.013). Although a higher PAPS was present in HIV cirrhotic patients, a statistically significant difference was not found between degree of pulmonary hypertension and evidence of hepatic cirrhosis (85 +/- 21 mm Hg vs 73.1 +/- 15 mm Hg, p < 0.062). Patients with AIDS and primary pulmonary hypertension present a higher degree of pulmonary hypertension than non-AIDS patients. Pulmonary hypertension associated with HIV seems to be related to a cytokine-related stimulation and proliferation of endothelium. High levels of cytokines present in AIDS patients can favor pulmonary hypertension, but the role of a host response to HIV--determined by one or more HLA subtypes--is suspected to enhance high cytokine production levels.
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PMID:Primary pulmonary hypertension in HIV patients: a systematic review. 1120 29

Attempts were made to infect human vascular smooth muscle cells derived from the pulmonary artery (hPASMC) with two different human immunodeficiency virus (HIV) vector systems. ADA/Luc or HXB2/Luc were generated by cotransfection of luciferase reporter gene vector, pNL4-3-Luc-E- R-, and one of two envelope expressing vectors, pSMADA (R5) or pSMHXB2 (X4). The VSV-G/Luc or VSV-G/GFP were produced by a three-plasmid expression system which consisted of vesicular stomatitis virus G protein (VSV-G) expressing vector, packaging plasmid, and one of two reporter genes (pHR'-CMV-Luc or pHR'-CMV-GFP). We used hPASMC, U87.CD4.CCR5 and U87.CD4.CXCR4 for infection. Neither ADA/Luc nor HXB2/Luc could infect hPASMC, though they could infect U87.CD4 with corresponding coreceptors. On the other hand, the transduction of both VSV-G/Luc and VSV-G/GFP to hPASMC was remarkable. At day 3, the relative proportion of positive cells of hPASMC infected with VSV-G/GFP was 15%. The above finding indicates a direct role of HIV-1 infection in pulmonary hypertension 'a rare complication of HIV-1 infection' and HIV-based vectors could introduce foreign genes into hPASMC for gene therapy of pulmonary hypertension.
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PMID:A VSV-G pseudotyped HIV vector mediates efficient transduction of human pulmonary artery smooth muscle cells. 1122 Jun 75

Pulmonary hypertension occurs with increased frequency among patients with human immunodeficiency virus (HIV) infection. Although the pathogenesis of HIV-associated pulmonary hypertension remains unknown, it appears to occur independently of other risk factors associated with pulmonary vasculopathy, such as chronic hepatitis C infection and intravenous drug use. Signs and symptoms are typical of those immunocompetent patients with primary pulmonary hypertension, but because many HIV-infected patients are receiving intensive medical supervision, the diagnosis of pulmonary hypertension is often made at an earlier stage. Acute responses to epoprostenol are similar to those among non-HIV-infected individuals, but the benefits of long-term, intravenous treatment with epoprostenol in HIV-infected patients is unknown. Future investigations should define the true incidence of pulmonary hypertension and the long-term effects of epoprostenol on survival among HIV-infected individuals. Physicians should be alert to possible pulmonary hypertension in persons infected with HIV.
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PMID:Pulmonary hypertension associated with HIV infection. 1144 Mar 33

Given the improved life expectancy with highly active antiretroviral therapy among patients with human immunodeficiency virus (HIV)-infection, the treatment of medical problems such as hypertension will become increasingly more important. Although HIV-infected patients are at increased risk for the development of pulmonary hypertension, there is little data to suggest they are at increased risk for systemic hypertension or secondary causes of hypertension. Multiple potential drug interactions exist between antiretroviral medications, particularly the protease inhibitors and antihypertensive medications. Additionally, certain antiretroviral medications have frequent and important side effects relating to the kidneys and urinary system. Knowledge of these interactions and side effects is essential toward caring for the patient with HIV-infection.
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PMID:Hypertension and medication-related renal dysfunction in the HIV-infected patient. 1145 27

Human immunodeficiency virus (HIV)-related pulmonary hypertension (HRPR) is a cardiovascular complication of HIV infection that has been recognized in the last years with increasing frequency. The etiology of HRPH is unknown. All the attempts to isolate HIV on pulmonary vessels in HRPH patients failed, and an indirect role for HIV in this disease has been hypothesized. Current theories on the pathogenesis focus on abnormalities of endothelial and smooth muscle cells of pulmonary vasculature. Endothelial and smooth muscle cell injury could be due to a high production or to a reduced clearance of cytokines in these patients. In fact, in several studies high levels of ET-1, IL-1alpha, IL-6 and PDGF in primary pulmonary hypertension (PPH) and in HRPH have been found. HIV gp 120 could induce the production of these cytokines by a stimulation of monocytes/macrophages. A high alpha1-adrenoreceptors stimulation of pulmonary vessels could be also implicated in the pathogenesis of HRPH. Chronic hypoxia is observed with increased frequency in HIV patients, and this could induce a chronic stimulation of alpha1-receptors of pulmonary vasculature with typical pathological changes. However, only a small percentage of HIV- patients develop HRPH. This observation suggests the existence of an idiosyncratic susceptibility to the development of vascular disease. This susceptibility could have a genetic basis, and might be determined by particular major histocompatibility complex alleles.
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PMID:Pathogenesis of HIV-related pulmonary hypertension. 1176 97

The authors describe two cases of pulmonary hypertension (PHT). In the first case it is secondary to pulmonary thromboembolism, a frequent and serious occurrence, witch is well known as a cause of PHT. In the second case the PHT is probably secondary to infection by human immunodeficiency virus, also a serious and frequent condition in clinical practice but which was only recently identified as a cause of PHT. Formerly these patients were considered as suffering from primary PHT. The authors make a brief review of the literature on pulmonary hypertension.
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PMID:[Pulmonary hypertension. Topic review. 2 clinical cases]. 1196 87

Five cases of human immunodeficiency virus-related pulmonary hypertension and their imaging manifestations are reported. The radiologic findings vary from mild enlargement of the pulmonary trunk or the central pulmonary arteries at early stages to marked dilatation of the central pulmonary arteries and massive cardiomegaly due to right ventricular and right atrial enlargement at later stages of the disease.
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PMID:Imaging findings in human immunodeficiency virus-related pulmonary hypertension: report of five cases and review of the literature. 1203 55

This case illustrates the reopening of foramen ovale in a young patient with chronic pulmonary hypertension caused by bronchiectasis and chronic pulmonary fibrosis, which resulted in a prominent right-to-left shunt and severe hypoxia. Her clinically unsuspected right-to-left shunt was discovered during ventilation-perfusion scan, which was performed for the evaluation of pulmonary embolism. She had common variable immune deficiency, a primary immunodeficiency disease in which B-lymphocytes produce few or no antibodies. Most patients with this syndrome have an intrinsic defect in their B-lymphocytes that results in reduced immunoglobulin production. In these patients, recurrent respiratory tract infections are common and may result in chronic lung disease, fibrosis, particularly bronchiectasis (20-30%) and even cor pulmonale as happened in our patient [J. Clin. Immunol. 9 (1989) 22-33.].
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PMID:Lung scan in the diagnosis and management of patent foramen ovale pulmonary embolism, paradoxical embolism. 1221 71

With more effective prophylactic treatment and an increased time of survival, noninfectious conditions associated with human immunodeficiency virus (HIV) disease are being recognized with increasing frequency in HIV patients. Cardiac involvement in HIV-infected patients varies from clinically silent to a fatal disease with a direct cardiac cause of mortality estimated at 1% to 6%. Pericardial effusion, pericarditis, myocarditis, cardiomyopathy, endocarditis, and pulmonary hypertension are known cardiac manifestations associated with HIV infection. Coronary artery disease (CAD) has not been a recognized complication of HIV disease, although some recent case reports have suggested occurrence of premature CAD and accelerated atherogenesis in HIV-infected patients. The role of protease inhibitors have been suggested in the development of this complication. After reviewing records of the last 7 years, the authors found 10 cases of acute coronary syndrome in HIV-infected patients who had no other risk factor for CAD except smoking. The presence of CAD was confirmed by angiography or autopsy. The mean CD4 count was 380 cells/mm3, and the mean duration between the diagnosis of HIV infection and CAD was 7.5 years. Four patients had single-vessel disease, 1 patient had 2-vessel disease, and 5 patients had 3-vessel disease. Three patients underwent coronary bypass surgery and 1 patient died of cardiogenic shock. CAD may be associated with HIV disease.
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PMID:Acute coronary syndrome in patients with human immunodeficiency virus disease. 1236 61


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