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

A case of a 19-year-old man with congenitally acquired HIV infection who was found to have a large intracardiac mass is presented. Presurgical imaging studies and subsequent pathologic findings and histology are discussed.
Cardiol Rev
PMID:An intracardiac mass in a young man with congenitally acquired HIV. 1507 79

HIV-related pulmonary hypertension (HIV-PH) is a cardiovascular complication of HIV infection that has been recognized in the last years with increasing frequency. HIV-related pulmonary hypertension is a clinical disorder which carries a bad prognosis. While a direct HIV infection of the pulmonary vessels in the pathogenesis of this disorder was not demonstrated, currently a multifactorial pathogenesis of this disease could be hypothesized. Echocardiography has been found to be the most useful screening imaging modality for the diagnosis of HIV-PH, with a high predictive negative value and a low positive predictive value. For this reason Doppler echocardiography is not the gold standard in the diagnosis of HIV-PH. The treatment of HIV-PH is complex and controversial. To date, no study determining the agent of choice for the treatment of this disease exists. Different studies have shown variable results in patiens with HIV-PH treated with highly active antiretroviral therapy (HAART) but only HAART seems not to be effective in lowering pulmonary hypertension in these patients, and in some patients, HIV-PH develops in spite of a previous HAART. It seems reasonable in HIV-PH patients that a treatment with oral vasodilator drugs can improve the adherence of a long-lasting and complex antiretroviral therapy.
Acta Cardiol 2004 Jun
PMID:HIV-related pulmonary hypertension. From pathogenesis to clinical aspects. 1525 66

We describe a 54-year-old man who was HIV-positive, admitted for cardiogenic shock complications inferior myocardial infarction. He was treated with primary percutaneous transluminal angioplasty (PCTA) and stent deployment in mid right coronary artery. After a few days thrombotic occlusion of the stent occurred, and the problem recurred during implantation of a new stent in the course of a second PTCA. We detected coinheritance of factor V Leiden, primary antiphospholipid syndrome and antithrombin deficiency. We discuss the role of these coagulation disorders in acute myocardial infarction as well as the treatment and course of the coronary syndrome in this context.
Rev Esp Cardiol 2004 Oct
PMID:[Recurrent coronary thrombosis, factor V Leiden, primary antiphospholipid syndrome and HIV]. 1546 99

Primary pulmonary hypertension carries a grim prognosis, therefore, it is imperative that prior to reaching this diagnosis, a thorough search be made for all possible causes of pulmonary hypertension. An uncommon cause of pulmonary hypertension amenable to treatment may occasionally be identified. This case report describes a young woman who presented with rapidly progressive right heart failure. Work up for the common secondary causes of pulmonary hypertension was negative, including, congenital intracardiac shunts, left-sided atrial or ventricular heart disease, left-sided valvular heart disease, disorders of the respiratory system including hypoxemia and pulmonary thromboembolic and venoocclusive disease, collagen vascular disease, portal hypertension, HIV infection as well as pulmonary hypertension secondary to drugs and toxins. The only concurrent illness identified was Graves disease. After treatment of hyperthyroidism there was complete resolution of the right heart failure, tricuspid regurgitation, and the pulmonary hypertension. Only a few cases of reversible pulmonary hypertension and right heart failure associated with hyperthyroidism have been reported worldwide. In these patients, the most striking feature has been the normalization of the cardiovascular findings after adequate treatment of hyperthyroidism. The exact reasons for the development of pulmonary hypertension in hyperthyroidism are unclear. Proposed mechanisms include high cardiac output-induced endothelial injury, increased metabolism of intrinsic pulmonary vasodilating substances resulting in elevated pulmonary vascular resistance, and autoimmune phenomenon. Hyperthyroidism should be included in the causes of secondary pulmonary hypertension and/or otherwise unexplained right heart failure. This is especially important because hyperthyroidism is a treatable entity and its cardiac manifestations may be completely reversible.
Cardiol Rev
PMID:Reversible pulmonary hypertension, tricuspid regurgitation and right-sided heart failure associated with hyperthyroidism: case report and review of the literature. 1547 66

During chemotherapy with anthracyclines, attenuated neuregulin signaling by the erbB2 receptor inactivating antibody Trastuzumab enhances the heart failure risk. We compared the effects of attenuated neuregulin/erbB signaling and of daunorubicin on splicing of the Bcl-x gene and on mitochondrial activation of apoptosis in cardiomyocytes. Attenuating erbB signals in cultured neonatal rat cardiomyocytes by the erbB2 antagonist tyrphostin AG825, by the erbB1/4 antagonist AG1478 or by antisense-induced lowering of erbB2 receptors resulted in an augmented Bcl-xS/Bcl-xL ratio, mitochondrial release of cytochrome c, activation of caspase 9 and caspase 3, and nucleosome-sized DNA fragmentation. A similar DNA fragmentation and caspase 3 activation was induced by TNF-alpha, but without Bcl-xS/Bcl-xL increase, cytochrome c release or caspase 9 activation. A BH4-domain containing HIV TAT fusion protein added to cardiomyocytes under attenuated erbB signaling lowered the enhanced Bcl-xS/Bcl-xL ratio, the cytochrome c release, the caspase 3 activation and the DNA fragmentation, while apoptosis was not modified by the fusion protein in TNF-alpha treated cardiomyocytes. Enhancement of Bcl-xS/Bcl-xL by reducing Bcl-xL via siRNA transfection mimicked the mitochondrial apoptotic activation due to erbB signal attenuation. Daunorubicin also caused Bcl-xS/Bcl-xL enhancement and mitochondrial apoptotic activation in cultured cardiomyocytes; this was attenuated by BH4-fusion protein or by neuregulin-1 and augmented by siRNA-mediated Bcl-xL lowering. We conclude that activation of mitochondrial apoptosis due to altered Bcl-x splicing contributes as a common mechanism of anthracyclines and erbB signal attenuation to the enhanced heart failure risk under this combination.
J Mol Cell Cardiol 2005 Mar
PMID:Apoptosis-modulating interaction of the neuregulin/erbB pathway with anthracyclines in regulating Bcl-xS and Bcl-xL in cardiomyocytes. 1573 8

Recent improvements in survival from AIDS have been accompanied by an increased recognition of the potential importance of other manifestations of HIV infection, including cardiomyopathy. Mechanisms responsible for HIV cardiomyopathy are unknown, but may include direct effects of HIV proteins on the heart. We previously provided support for direct effects of HIV proteins by demonstrating a negative inotropic effect of the HIV coat protein, gp120, on isolated adult rat ventricular myocytes (ARVM). We now report that this negative inotropic effect of HIV gp120 is mediated by a signaling pathway involving p38 MAP kinase, iPLA2 and troponin I. Exposure of ARVM to HIV gp120 resulted in maximal activation of iPLA2 by 60 min as reflected in hydrolysis of arachidonyl thiophosphatidylcholine that was completely blocked by the iPLA2 inhibitor, bromoenol lactone (BEL) or the p38 MAP kinase inhibitor, SB203580. The negative inotropic effect of gp120 was blocked by BEL, as well as SB203580. BEL did not block gp120 stimulated phosphorylation of p38 MAP kinase itself, and/or its downstream effectors, ATF2 or MAPKAP2. However, BEL did block gp120-stimulated phosphorylation of troponin I. Thus, the negative inotropic effect of HIV gp120 requires activation of p38 MAP kinase and iPLA2; as well as troponin I phosphorylation. Activation of this novel p38 MAP kinase-iPLA2-troponin I signaling pathway may contribute to HIV cardiomyopathy.
J Mol Cell Cardiol 2006 Jan
PMID:iPLA2 inhibitor blocks negative inotropic effect of HIV gp120 on cardiac myocytes. 1631 60

We report a case of recurrent myocardial infarction occurring in two different coronary territories in a man with HIV-1 infection. On each occasion, clinical and angiographic success was obtained by intracoronary stent placement.
J Interv Cardiol 2006 Feb
PMID:Interventional approach to recurrent myocardial infarction in HIV-1 infection. 1648 47

The use of highly active antiretroviral therapy (HAART) in patients with HIV infection has improved survival. This improvement combined with the metabolic effects of treatment has increased cardiovascular risk and the need for cardiac surgery in these patients. We compared morbidity and mortality in HIV-infected patients (cases, n=7) and non-HIV-infected patients (controls, n=21) who underwent isolated coronary artery surgery between 1997 and 2004. The durations of extracorporeal circulation and aortic cross-clamping were shorter in HIV-infected patients (P=.002 and P=.014, respectively). The percentage of patients who experienced complications was similar, at 57.1% in both groups, but there was a slightly higher number of complications per patient in non-HIV-infected individuals. The mean length of total hospitalization was greater in HIV-infected patients (27.1 [13.3] versus 8.8 [5.3] days; P=.003), as was that of postoperative hospitalization (18.2 [15.4] vs 7.9 [4.2] days; P=.08). No HIV-infected patient died or needed a repeat cardiac operation. No progression of the HIV infection was observed. Isolated coronary artery surgery in HIV-infected patients produces good results, and there is no increase in morbidity or mortality. Extracorporeal circulation did not influence disease progression.
Rev Esp Cardiol 2006 Mar
PMID:[Mortality and morbidity in HIV-infected patients undergoing coronary artery bypass surgery: a case control study]. 1671 53

Pericardial inflammation secondary to Mycobacterium tuberculosis infection is a rare condition, but its incidence is increasing in parallel with human immunodeficiency virus infection. Recrudescence of various types of tuberculosis should alert the clinician to the possibility of tuberculous pericarditis. The authors present the case of a 27-year-old white male, seropositive for the human immunodeficiency virus, presenting with large volume pericardial effusion and unusual echocardiographic features, global heart failure and clinical suspicion of tuberculosis. After anti-tuberculous chemotherapy and systemic corticosteroids there was some clinical improvement but evolution to constriction. The patient underwent pericardiectomy with good results. The authors present a literature review on constrictive tuberculous pericarditis in human immunodeficiency virus seropositive and seronegative patients, discussing the role of corticosteroids and the contribution of different diagnostic tools.
Rev Port Cardiol 2006 Nov
PMID:Constrictive pericarditis of tuberculous etiology in the HIV-positive patient: case report and review of the literature. 1727 59

Among the multiple cardiac manifestations occurring in HIV-infected patients, cardiomyopathy is one of the most challenging. Its incidence has only slightly decreased since the introduction of highly active antiretroviral therapy (HAART). Also, its pathogenesis remains relatively unclear. Although several studies demonstrated the presence of HIV genome in the heart of patients, more recent developments found that viral infection plays an indirect role only, as well as they recognized the contribution of proinflammatory cytokines in the progression of the disease. Experimental studies on animals and cultured myocytes have established the signalling pathway triggered by proinflammatory cytokines in heart failure and cardiomyopathy. Tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1) and IL-6 promote expression of inducible nitric oxide synthase (iNOS) in cardiomyocytes through activation of p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor kappaB (NFkappaB). TNF-alpha and high concentrations of NO also induce cardiomyocyte apoptosis by TNF type 1 receptor activation. This biological framework, which is also involved in progression of cardiomyopathy in humans, is more pronounced in HIV-infected patients, in whom proinflammatory cytokines TNF-alpha, IL-1 and IL-6 are increased, resulting in an enhanced expression of cardiac iNOS, especially in patients with a low CD4 T cell count. This may account for the worse outcome of heart failure in HIV-infected patients. However, there are only few data today to support future therapeutic implications of cytokines antagonism in treatment of HIV-infected patients with cardiomyopathy. Whether modulation of TNF production or selective inhibition of p38 MAPK pathway could be useful approaches remains uncertain.
Int J Cardiol 2007 Aug 21
PMID:Cytokines in HIV-associated cardiomyopathy. 1733 7


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