Frequency of development of acute global left ventricular dysfunction in human immunodeficiency virus infection

Castro, S. De; d’Amati, Giulia; Gallo, Pietro; Cartoni, Domenico; Santopadre, Paola; Vullo, Vincenzo; Cirelli, A; Migliau, G

doi:10.1016/0735-1097(94)90864-8

Cited by 66 publications

(33 citation statements)

References 34 publications

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“…[4][5][6][7][8][9][10][11][12] Abnormally high levels of coagulation markers, endothelial activation markers, and platelet activation markers have also been documented in HIV-infected patients. [13][14][15] The SMART (Strategies for Management of AntiRetroviral Therapy) study confirmed that a mild-to-moderate hypercoagulable state exists in HIV infection.…”

Section: Introductionmentioning

confidence: 99%

“…We routinely checked for pathology similar to that seen in HIV-infected patients, including renal TMA, arteriopathy, myocardial hypertrophy and fibrosis, atherosclerosis (ATS), infarction, and myocarditis. [4][5][6][7][8][9][10][11][12] Four-micron paraffin sections were stained with H&E for routine histopathology diagnosis and with Masson trichrome for collagen detection.Immunohistochemical staining was performed on the formalin-fixed, paraffin-embedded tissues using an avidin-biotin complex HRP technique (Vectastain Elite ABC kit; Vector Laboratories) and a rabbit polyclonal antifibrinogen Ab (DAKO) as a primary Ab. …”

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confidence: 99%

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Coagulation biomarkers predict disease progression in SIV-infected nonhuman primates

Pandrea

Cornell

Wilson

et al. 2012

Blood

128

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HIV infection is associated with increased risk of cardiovascular complications, the underlying mechanism of which remains unclear. Plasma levels of the coagulation biomarker D-dimer (DD) correlate with increased mortality and cardiovascular events in HIV-infected patients. We compared the incidence of cardiovascular lesions and the levels of the coagulation markers DD and thrombin antithrombin in pathogenic SIV infections of rhesus and pigtailed macaques (PTMs) and in nonpathogenic SIV infection of African green monkeys (AGMs) and sooty mangabeys. Hypercoagulability and cardiovascular pathology were only observed in pathogenic SIV infections. In PTMs infected with SIV from AGMs (SIVagm), DD levels were highly indicative of AIDS progression and increased mortality and were associated with cardiovascular lesions, pointing to SIVagm-infected PTMs as an ideal animal model for the study of HIVassociated cardiovascular disease. In pathogenic SIV infection, DD increased early after infection, was strongly corre- IntroductionThere are increasing data demonstrating the significant impact of non-AIDS-defining comorbidities on the outcome of HIV infection. Cardiovascular disease (CVD) emerged as a major comorbidity during the era of highly active antiretroviral therapy (HAART), 1-3 especially in urban African-American and Hispanic populations, which are disproportionately affected by HIV and are also at high risk for CVD. CVD may be intrinsically related to HIV infection 2 or to long-term HAART, which may increase CVD risk by adverse metabolic effects (lipid changes) or vascular toxic effects. 3 To date, however, our understanding of the relationship among HIV infection, HAART, and CVD risk is unclear and incomplete, and this is a critical barrier preventing interventions that may reduce CVD mortality in these patients.CVD complications in HIV-infected subjects include thrombotic micrangiopathy (TMA), arteriopathy, dilated cardiomyopathy, abnormal coronary artery pathology (including atherothrombotic disease), and myocarditis. [4][5][6][7][8][9][10][11][12] Abnormally high levels of coagulation markers, endothelial activation markers, and platelet activation markers have also been documented in HIV-infected patients. [13][14][15] The SMART (Strategies for Management of AntiRetroviral Therapy) study confirmed that a mild-to-moderate hypercoagulable state exists in HIV infection. 2 This study also showed that increased levels of the coagulation biomarker D-dimer (DD) are associated with increases in inflammation markers (ie, IL-6), both being strongly linked to the loss of HIV/SIV control, disease progression, and death, 2 suggesting a causal relationship between immune activation/inflammation and CVD in HIVinfected patients.It is widely accepted that immune activation levels more accurately predict HIV disease progression to AIDS and death than do levels of viral replication or CD4 ϩ T cells. [16][17][18] This paradigm is supported by data from our group and others showing that natural hosts of SIV such as African green m...

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

Coagulation biomarkers predict disease progression in SIV-infected nonhuman primates

Pandrea

Cornell

Wilson

et al. 2012

Blood

128

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“…One consequence of the increased survival is the emergence of new manifestations of HIV infection, including cardiac dysfunction. [1][2][3][4][5][6][7] Dilated cardiomyopathy and associated symptoms of congestive heart failure are being recognized with increasing frequency, with estimates that 10% to 18% of HIV seropositive individuals will manifest evidence of left ventricular dysfunction giving rise to 21 000 to 40 000 new cases of symptomatic heart failure each year by the year 2000. Despite this clinical recognition, the pathogenesis of HIV cardiomyopathy remains unclear, limiting application of both specific treatments and preventive strategies.…”

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Dilated Cardiomyopathy Associated With Simian AIDS in Nonhuman Primates

et al. 2000

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Background-Cardiomyopathy is being recognized with increasing frequency in patients with AIDS, yet the relationship between HIV infection and cardiac contractile dysfunction remains obscure. The purpose of the present study was to determine if infection with simian immunodeficiency virus (SIV) in nonhuman primates is associated with cardiac dysfunction and myocardial injury. Methods and Results-Left ventricular size and function were determined by 2D echocardiography in 16 rhesus macaques before and at weekly intervals following infection with cloned pathogenic SIV mac 239 or the highly attenuated SIV mac 239 nef deletion mutant. A second group of 15 rhesus macaques chronically infected with pathogenic (nϭ6) or nonpathogenic (nϭ9) virus were studied at Ͼ2 years following infection. Cardiac tissues from 24 rhesus macaques chronically infected (Ͼ2 years) with pathogenic SIV were reviewed for evidence of cardiac pathology. Acute infection (Ͻ6 weeks) with either pathogenic or nonpathogenic SIV caused neither contractile dysfunction nor cardiac pathology. However, LV ejection fraction was significantly (PϽ0.05) depressed (43Ϯ7%) in rhesus macaques chronically infected with pathogenic SIV compared with rhesus macaques chronically infected with nonpathogenic SIV (61Ϯ3%). Furthermore, two thirds of rhesus macaques that succumbed to simian AIDS had myocardial pathology including lymphocytic myocarditis (nϭ9) and coronary arteriopathy (nϭ6), with complete vessel occlusion (nϭ4) and associated myocardial infarction and necrosis. Conclusions-This unique model is valuable in understanding the pathogenesis of cardiac injury associated with retroviral infection in a relevant nonhuman primate model of AIDS.

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“…In addition, echocardiography may distinguish between fulminant and acute myocarditis by identifying near-normal left ventricular diastolic dimensions and increased septal thickness in fulminant myocarditis (versus increased left ventricular diastolic dimensions and normal septal thickness in acute myocarditis), with marked improvement in systolic function in time [Tang et al, 2009]. De Castro et al, in 1994 performed a study of 136 HIV-infected patients without clinical, electrocardiographic or echocardiographic evidence of cardiovascular dysfunction on admission who were prospectively studied with serial echocardiograms; 93 of these patients had AIDS. During a mean follow-up period of 415 days, seven patients, all in the AIDS subgroup, developed clinical and echocardiographic findings of acute global left ventricular dysfunction; six of these seven patients died of congestive heart failure.…”

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confidence: 99%

Myocarditis in HIV Positive Patients

Cambrea¹

2011

Myocarditis

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Frequency of development of acute global left ventricular dysfunction in human immunodeficiency virus infection

Cited by 66 publications

References 34 publications

Coagulation biomarkers predict disease progression in SIV-infected nonhuman primates

Coagulation biomarkers predict disease progression in SIV-infected nonhuman primates

Dilated Cardiomyopathy Associated With Simian AIDS in Nonhuman Primates

Myocarditis in HIV Positive Patients

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