Abstract P186: Plasma Ceramides Are Associated With HIV Treatment and Increased Risk of Carotid Artery Plaque in Two Prospective HIV Cohorts

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Wei Zhao ◽  
Simin Hua ◽  
Clary B Clish ◽  
Amy Deik ◽  
David B Hanna ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Hiv Infection ◽  
Hiv Treatment ◽  
Infection Status ◽  
Cvd Risk ◽  
Carotid Artery Plaque ◽  
Infected People ◽  
Increased Risk ◽  
Prospective Cohorts ◽  
Variance Estimates

Introduction: Ceramides, a family of bioactive sphingolipids on plasma membrane, have been implicated in inflammation, immune response, and HIV infection. Recent studies have related plasma ceramides with cardiovascular diseases (CVD), but data are sparse in HIV infected people who have excess CVD risk. Methods: We profiled baseline plasma ceramides C16:0, C22:0, C24:0 and C24:1 in 737 participants aged 35-55 years (520 HIV+, 217 HIV-) from two prospective cohorts (Women’s Interagency HIV Study and Multicenter AIDS Cohort Study) and examined their associations with the risk of incident carotid artery plaque (CAP), assessed by B-mode carotid artery ultrasound imaging over a 7-year period. Plasma levels of ceramides were inverse-normal transformed. We used robust variance estimates from Poisson regression to estimate risk ratios (RRs) on CAP per standard deviation increment in ceramides. We also compared ceramide levels by HIV infection status and antiretroviral therapy (ART) use. Results: Over a 7-year follow-up, 112 individuals developed CAP (90 HIV+, 22 HIV-). After multivariate adjustment, ceramides C16:0 (RR=1.40 [95% CI: 1.09-1.79]; P <0.001) and C24:1 (RR=1.32 [1.06-1.65]; P <0.001), but not ceramides C22:0 or C24:0, were significantly associated with increased risk of CAP in all participants. Ceramides C16:0 showed stronger association with CAP in HIV+ people compared to HIV- people ( Figure ), but there was no significant effect modification by HIV infection status ( P for interaction>0.05). Compared to HIV- group, plasma ceramides C16:0, C22:0 and C24:1 were significantly ( P <0.001) higher in HIV+ group. Further analyses in HIV+ group showed that ceramides were significantly ( P < 0.001) higher in people using ART than those not using ART. Conclusions: This study reported that elevated plasma ceramides, especially C16:0, are increased with ART use and associated with HIV-related atherosclerosis. Our data suggest that ceramides might be an intermediate link between HIV infection and CVD risk.

Abstract P322: Association of Hiv Infection With Carotid Artery Plaque Echomorphology in the Women’s Interagency HIV Study (wihs)

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Claudio A Bravo ◽  
Jee-Young Moon ◽  
Jean Claude Uwamungu ◽  
Robert Kaplan ◽  
Kathryn Anastos ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Carotid Artery ◽  
Hiv Infection ◽  
Carotid Plaque ◽  
Cd4 Count ◽  
Morbidity And Mortality ◽  
Hiv Care ◽  
Carotid Artery Plaque ◽  
Hiv Women ◽  
Hiv Negative

Introduction: Cardiovascular disease is a major contributor to morbidity and mortality among women living with HIV (WLWH). We previously found HIV infection to be associated with carotid artery plaque, a marker of subclinical atherosclerosis. Plaque morphology and composition may predict plaque rupture and cardiovascular disease events. We characterized the association of HIV-related factors with carotid plaque echomorphology in the WIHS. Methods: Using B-mode ultrasound, we characterized plaque (focal intima-media thickness >1.5 mm) at 6 locations in the right carotid artery in 1,722 participants (1,230 HIV+, 492 HIV-) of the WIHS, a cohort study of women with or at risk for HIV at 6 US sites. Plaque echomorphologic features included relative echogenicity (>50% of plaque is echolucent vs >50% of plaque is echogenic) and surface morphology (smooth vs irregular, i.e., height variations along contour of plaque). We used multinomial logistic regression to assess the odds of each feature vs no plaque comparing HIV+ and HIV- women, adjusting for demographic (e.g., age, race/ethnicity, socioeconomic status), behavioral (e.g., drug/alcohol use, smoking, HCV infection, smoking), cardiometabolic (e.g., systolic blood pressure, BMI, lipids, diabetes) and HIV-related risk factors (e.g., antiretroviral therapy use, current CD4+ T-cell count, AIDS). We further stratified WLWH by CD4+ count (<200, 200-499, 500+ cells/uL) and HIV-1 RNA suppression. Results: Among 1,722 women (median age 40, IQR 33-46, 59% black, 29% Hispanic, 71% HIV+), 160 (9%) had at least one carotid plaque (128 HIV+, 32 HIV-). In unadjusted analyses, WLWH had more echolucent plaque (5.3% vs 2.6%, p=0.02) and plaques with smooth surface (2.7% vs 0.6%, p=0.005) than HIV-negative women. After covariate adjustment, HIV serostatus remained significantly associated with smooth plaque (odds ratio [OR] 3.45, 95% CI 1.12-10.62) but not with echolucent plaque (OR 1.60, 95% CI 0.84-3.05). Stratified by HIV viremia, WLWH with unsuppressed HIV viremia had significantly more smooth plaque (OR 3.34, 95% CI 1.26-8.87) than HIV- women, whereas suppressed WLWH did not (OR 1.79, 95% CI 0.55-5.83). In a dose-response manner, lower CD4+ count among WLWH was associated with smooth plaque (e.g., OR for <200 cells/uL compared with HIV-negative women 7.43, 95% CI 1.46-37.87), and this association was of greater magnitude than that with irregular plaque (OR 2.46, 95% CI 1.14-5.32). Low CD4+ count was also associated with both echolucent (OR 3.36 for <200 cells/uL vs HIV-negative, 95% CI 1.29-8.77) and echogenic plaque (OR 2.65, 95% CI 1.18-5.96). Conclusions: Unsuppressed viremia and low CD4+ count, which are markers of suboptimal HIV care, were associated with certain echomorphologic features of carotid plaque. Further work should assess whether these features differentially lead to cardiovascular morbidity and mortality in WLWH.

scholarly journals Echocardiographic Assessment of Asymptomatic US Air Force Members with Early HIV Infection

2019 ◽  
Author(s):  
Gadiel Rafael Alvarado ◽  
Courtney Usry ◽  
Rosco Gore ◽  
James Watts ◽  
Jason Okulicz
Keyword(s):  
Hiv Infection ◽  
Air Force ◽  
Global Longitudinal Strain ◽  
People Living With Hiv ◽  
Hiv Diagnosis ◽  
Cvd Risk ◽  
Us Air Force ◽  
Increased Risk ◽  
Hiv Acquisition ◽  
Living With Hiv

Abstract Objective People living with HIV (PLHIV) are at increased risk for cardiovascular disease (CVD) and development of subclinical echocardiographic abnormalities. The pathogenicity of HIV induced cardiotoxicity has been described however the time to development of echocardiographic abnormalities after HIV acquisition remains unclear. In this study we describe the echocardiographic evaluations of asymptomatic US Air Force members who were diagnosed with HIV infection. Results Patients (n=50) were predominantly male (96%), mostly black (60%), with a mean age of 28 years. At HIV diagnosis, the mean viral load was 112,585 copies/mL and CD4 count was 551 cells/uL; 2 patients were diagnosed with AIDS. All were found to have normal systolic ejection fraction (EF) and global longitudinal strain (GLS) however evidence of right ventricular dilatation and cardiac remodeling was observed in 7 (14%) and 13 (26%) patients, respectively. Subgroup analyses showed no significant differences in echocardiographic findings by HIV disease severity or CVD risk factors (p >0.05 for all). This study suggests that untreated HIV may have a low impact on the development of echocardiographic abnormalities shortly after seroconversion. Longitudinal studies are warranted to determine the optimal CVD risk assessment strategies for PLHIV.

scholarly journals Echocardiographic Assessment of Asymptomatic US Air Force Members with Early HIV Infection

2019 ◽  
Author(s):  
Gadiel Rafael Alvarado ◽  
Courtney Usry ◽  
Rosco Gore ◽  
James Watts ◽  
Jason Okulicz
Keyword(s):  
Hiv Infection ◽  
Air Force ◽  
Ventricular Remodeling ◽  
Medical Center ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
People Living With Hiv ◽  
Cvd Risk ◽  
Us Air Force ◽  
Increased Risk

Abstract Objective People living with HIV (PLHIV) are at increased risk for cardiovascular disease (CVD) and development of subclinical echocardiographic abnormalities. However, there is scant evidence of the echocardiographic changes that occur shortly after seroconversion. In this study we describe the echocardiographic evaluations of asymptomatic US Air Force members who were diagnosed with HIV infection and evaluated at the San Antonio Military Medical Center between September 1, 2015 and September 30, 2016. Results Patients (n=50) were predominantly male (96%), mostly African American (60%), with a mean age of 28 years. At HIV diagnosis, the mean viral load was 112,585 copies/mL and CD4 count was 551 cells/uL. All were found to have normal left ventricular systolic ejection fraction (EF) and global longitudinal strain (GLS) however evidence of right ventricular dilatation and left ventricular remodeling was observed in 7 (14%) and 13 (26%) patients, respectively. Subgroup analyses showed no significant differences in echocardiographic findings by HIV disease severity or CVD risk factors (p >0.05 for all).This study suggests that untreated HIV may have a low impact on the development of echocardiographic abnormalities shortly after seroconversion. Longitudinal studies are warranted to determine the optimal CVD risk assessment strategies for PLHIV.

scholarly journals Echocardiographic assessment of asymptomatic US Air Force members with early HIV infection

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Gadiel R. Alvarado ◽  
Courtney R. Usry ◽  
Rosco S. Gore ◽  
James A. Watts ◽  
Jason F. Okulicz
Keyword(s):  
Hiv Infection ◽  
Air Force ◽  
Ventricular Remodeling ◽  
Medical Center ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
People Living With Hiv ◽  
Cvd Risk ◽  
Us Air Force ◽  
Increased Risk

Abstract Objective People living with HIV (PLHIV) are at increased risk for cardiovascular disease (CVD) and development of subclinical echocardiographic abnormalities. However, there is scant evidence of the echocardiographic changes that occur shortly after seroconversion. In this study we describe the echocardiographic evaluations of asymptomatic US Air Force members who were diagnosed with HIV infection and evaluated at the San Antonio Military Medical Center between September 1, 2015 and September 30, 2016. Results Patients (n = 50) were predominantly male (96%), mostly African American (60%), with a mean age of 28 years. At HIV diagnosis, the mean viral load was 112,585 copies/mL and CD4 count was 551 cells/μL. All were found to have normal left ventricular systolic ejection fraction (EF) and global longitudinal strain (GLS) however evidence of right ventricular dilatation and left ventricular remodeling was observed in 7 (14%) and 13 (26%) patients, respectively. Subgroup analyses showed no significant differences in echocardiographic findings by HIV disease severity or CVD risk factors (p > 0.05 for all).This study suggests that untreated HIV may have a low impact on the development of echocardiographic abnormalities shortly after seroconversion. Longitudinal studies are warranted to determine the optimal CVD risk assessment strategies for PLHIV.

scholarly journals Targeting thrombogenicity and inflammation in chronic HIV infection

2019 ◽  
Vol 5 (6) ◽  
pp. eaav5463 ◽  
Author(s):  
Meagan P. O’Brien ◽  
M. Urooj Zafar ◽  
Jose C. Rodriguez ◽  
Ibeawuchi Okoroafor ◽  
Alex Heyison ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Immune Activation ◽  
Platelet Reactivity ◽  
Coronary Thrombosis ◽  
Myocardial Infarctions ◽  
Cvd Risk ◽  
Activation Markers ◽  
Increased Risk ◽  
Underlying Mechanisms ◽  
Chronic Hiv Infection

Persons with HIV infection (PWH) have increased risk for cardiovascular disease (CVD), but the underlying mechanisms remain unclear. Coronary thrombosis is known to provoke myocardial infarctions, but whether PWH have elevated thrombotic propensity is unknown. We compared thrombogenicity of PWH on antiretroviral therapy versus matched controls using the Badimon chamber. Measures of inflammation, platelet reactivity, and innate immune activation were simultaneously performed. Enrolled PWH were then randomized to placebo, aspirin (81 mg), or clopidogrel (75 mg) for 24 weeks to assess treatment effects on study parameters. Thrombogenicity was significantly higher in PWH and correlated strongly with plasma levels of D-dimer, soluble TNF receptors 1 and 2, and circulating classical and nonclassical monocytes in PWH. Clopidogrel significantly reduced thrombogenicity and sCD14. Our data suggest that higher thrombogenicity, interacting with inflammatory and immune activation markers, contributes to the increased CVD risk observed in PWH. Clopidogrel exhibits an anti-inflammatory activity in addition to its antithrombotic effect in PWH.

scholarly journals Relationship between Progression to AIDS and Thrombophilic Abnormalities in HIV Infection

2008 ◽  
Vol 54 (7) ◽  
pp. 1226-1233 ◽  
Author(s):  
Willem M Lijfering ◽  
Herman G Sprenger ◽  
Rita R Georg ◽  
Piet A van der Meulen ◽  
Jan van der Meer
Keyword(s):  
Hiv Infection ◽  
Factor Viii ◽  
Arterial Thrombosis ◽  
Protein S ◽  
Hiv Treatment ◽  
Repeated Measurements ◽  
Healthy Population ◽  
Free Protein ◽  
Cell Counts ◽  
Increased Risk

Abstract Background: HIV-infected patients are at increased risk of venous and arterial thrombosis. We hypothesized that acquired thrombophilic abnormalities that could predispose to thrombosis are most pronounced in patients in advanced stages of HIV infection. Methods: We included 109 consecutive HIV-infected patients in the study and tested them twice for currently known thrombophilic abnormalities at an interval of at least 3 months (median, 3 months; range, 3–12 months). Detailed information was collected about the date of diagnosis of HIV infection, HIV treatment, and previous episodes of venous and arterial thrombosis. Results: After HIV infection was diagnosed, 16% of the patients experienced symptomatic thrombosis (venous, 10%; arterial, 6%). Repeated measurements established protein C deficiency in 9% of the patients, increased factor VIII concentrations in 41%, high fibrinogen concentrations in 22%, and free protein S deficiency in 60%. Median factor VIII concentrations were higher in patients with AIDS (CD4 cell counts &lt;2 × 108/L) than in patients with a non–AIDS-defining illness (2260 IU/L vs 1 490 IU/L; P &lt; 0.001), whereas median free protein S concentrations were lower (450 IU/L vs 580 IU/L; P &lt; 0.001). Developing AIDS was associated with increasing factor VIII concentrations and decreasing free protein S concentrations. Increasing factor VIII concentrations were correlated with increasing fibrinogen concentrations and decreasing free protein S concentrations. Conclusions: Multiple acquired and persistent thrombophilic abnormalities are more frequently observed in HIV-infected patients than in the healthy population. The frequencies of these thrombophilic abnormalities increase with the progression to AIDS. These findings may contribute to the high prevalence of venous and arterial thrombosis in HIV-infected patients.

scholarly journals KIDNEY DISEASE IN THE SETTING OF HIV INFECTION: CONCLUSIONS FROM A KIDNEY DISEASE: IMPROVING GLOBAL OUTCOMES (KDIGO) CONTROVERSIES CONFERENCE

2018 ◽  
Vol 22 (6) ◽  
pp. 84-100 ◽  
Author(s):  
C. R. Swanepoel ◽  
M. G. Atta ◽  
V. D. D’Agati ◽  
M. M. Estrella ◽  
A. B. Fogo ◽  
...  
Keyword(s):  
Antiretroviral Therapy ◽  
Kidney Disease ◽  
Hiv Infection ◽  
Prolonged Exposure ◽  
Opportunistic Infections ◽  
Kidney Injury ◽  
Hiv Treatment ◽  
Hiv Positive ◽  
Treatment And Prevention ◽  
Increased Risk

HIV-positive individuals are at increased risk for kidney disease, including HIV-associated nephropathy, noncollapsing focal segmental glomerulosclerosis, immune-complex kidney disease, and comorbid kidney disease, as well as kidney injury resulting from prolonged exposure to antiretroviral therapy or from opportunistic infections. Clinical guidelines for kidney disease prevention and treatment in HIV-positive individuals are largely extrapolated from studies in the general population, and do not fully incorporate existing knowledge o f the unique HIV-related pathways and genetic factors that contribute to the risk of kidney disease in this population. We convened an international panel of experts in nephrology, renal pathology, and infectious diseases to define the pathology of kidney disease in the setting of HIV infection; describe the role of genetics in the natural history, diagnosis, and treatment of kidney disease in HIV-positive individuals; characterize the renal risk-benefit of antiretroviral therapy for HIV treatment and prevention; and define best practices for the prevention and management of kidney disease in HIV-positive individuals.

scholarly journals Echocardiographic Assessment of Asymptomatic US Air Force Members with Early HIV Infection

2019 ◽  
Author(s):  
Gadiel Rafael Alvarado ◽  
Courtney Usry ◽  
Rosco Gore ◽  
James Watts ◽  
Jason Okulicz
Keyword(s):  
Hiv Infection ◽  
Air Force ◽  
Ventricular Remodeling ◽  
Medical Center ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
People Living With Hiv ◽  
Cvd Risk ◽  
Us Air Force ◽  
Increased Risk

Abstract Objective People living with HIV (PLHIV) are at increased risk for cardiovascular disease (CVD) and development of subclinical echocardiographic abnormalities. In this study we describe the echocardiographic evaluations of asymptomatic US Air Force members who were diagnosed with HIV infection and evaluated at the San Antonio Military Medical Center between September 1, 2015 and September 30, 2016. Results Patients (n=50) were predominantly male (96%), mostly black (60%), with a mean age of 28 years. At HIV diagnosis, the mean viral load was 112,585 copies/mL and CD4 count was 551 cells/uL. All were found to have normal left ventricular systolic ejection fraction (EF) and global longitudinal strain (GLS) however evidence of right ventricular dilatation and left ventricular remodeling was observed in 7 (14%) and 13 (26%) patients, respectively. Subgroup analyses showed no significant differences in echocardiographic findings by HIV disease severity or CVD risk factors (p >0.05 for all).This study suggests that untreated HIV may have a low impact on the development of echocardiographic abnormalities shortly after seroconversion. Longitudinal studies are warranted to determine the optimal CVD risk assessment strategies for PLHIV.

Abstract P201: Associations of Plasma Acylcarnitines With Incident Carotid Artery Plaque in Individuals With or at Risk of HIV Infection

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Simin Hua ◽  
Clary Clish ◽  
Justin Scott ◽  
David Hanna ◽  
Sabina Haberlen ◽  
...  
Keyword(s):  
Viral Load ◽  
Hiv Infection ◽  
Carotid Plaque ◽  
Short Chain ◽  
Cvd Risk Factors ◽  
Hiv Viral Load ◽  
Cvd Risk ◽  
Medium Chain ◽  
Increased Risk ◽  
Long Chain

Introduction: Altered acylcarnitine concentrations may reflect impaired mitochondrial metabolism and are implicated in cardiovascular disease (CVD). Disturbances in carnitine metabolism have been observed in HIV infection, but it is unknown whether this is related to CVD risk in HIV infected people. Methods: Twenty-six acylcarnitine species were profiled with ultrahigh-performance liquid chromatography/tandem mass spectrometry in 705 men and women with or at risk of HIV infection in the Multicenter AIDS Cohort Study and the Women’s Interagency HIV Study. Using a weighted score approach to define aggregate levels of plasma acylcarnitines, we assessed the associations of short-chain (C2-C7), medium-chain (C8-C14) and long-chain acylcarnitine (C16-C26) with incident carotid plaque, over 7-year follow-up, defined as a carotid artery region with focal intima-media thickness>1.5mm among those with no baseline carotid plaque. Results: The mean age was 45 years and 70% were non-white. The majority (70%) had HIV, and 68% of 394 participants on antiretroviral therapy (ART) had undetectable HIV viral load. Over 7 years, 108 participants developed carotid plaque. Comparing HIV-infected with HIV-uninfected participants, some individual acylcarnitines were higher (C3, C16, C20, C26) while others were lower (C8, C10, C20:4) (all P <0.05), but no significant differences were found in aggregate levels of short-chain, medium-chain, or long-chain acylcarnitines. After adjusted for demographic, behavioral, and HIV infection related factors (HIV serostatus, CD4 cell count and ART), plasma levels of short-chain (risk ratio [RR] = 1.26 [95% CI 1.06-1.50] per standard deviation increment; P=0.008), medium-chain(RR=1.20 [1.01-1.43]; P=0.04) and long-chain acylcarnitines (RR=1.18 [1.00-1.40]; P=0.05) were associated with increased risk of carotid plaque. After further adjusting for traditional CVD risk factors (BMI, total- and HDL-cholesterol, blood pressure, lipid-lowering medication and antihypertensive medication use), the association of short-chain acylcarnitines, but not medium-chain or long-chain acylcarnitines, with carotid plaque remained significant (RR=1.23 [1.04-1.46]; P=0.01). Results were consistent between men and women. Further analyses indicated that the association of short-chain acylcarnitines and carotid plaque was stronger in individuals with HIV infection (RR=1.29 [1.08-1.54]) than those without HIV infection (RR=0.98 [0.66-1.45]), and stronger among HIV+ individuals with detectable viral load (RR =1.42 [1.15-1.75]) than those who had continuous virus suppression (RR =1.02 [0.71-1.47]). Conclusion: Plasma short-chain acylcarnitines were associated with increased risk of carotid plaque formation, independent of traditional CVD risk factors, especially in HIV-infected individuals and those with poor control of HIV viral load.

scholarly journals Cardiovascular Diseases Associated Inflammatory Biomarker Levels in a Small Cohort of HIV-1 Infected Patients Deintensificated from Abacavir/Lamivudine/ Dolutegravir to Lamivudine Plus Dolutegravir Running Head: Risk of Cardiovascular Diseases and Abacavir Use

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Be G ◽  
◽  
Lattuada E ◽  
Gibellini D ◽  
Diani E ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Diseases ◽  
Hiv Infection ◽  
Hiv Positive ◽  
Biological Mechanism ◽  
Cvd Risk ◽  
Increased Risk ◽  
Small Cohort ◽  
Hiv 1 ◽  
Hiv Negative

Following the successful introduction of combined Antiretroviral Therapy (cART), a dramatic decrease in viral burden and opportunistic infections along with a consistent increase in life expectancy has been observed in Human Immunodeficiency Virus (HIV) infected patients [1]. This deep change in the HIV disease evolution has determined that HIV positive subjects were effectively monitored for several alterations of many tissue and organs due to HIV chronic disease and antiretroviral treatment for example, cardiovascular system, bone, adipose tissues, kidney and central nervous system represent the major target of these structural and functional damages during HIV infection. In particular, Cardiovascular Diseases (CVD) were considered important clinical complications in the HIV patient and represent a leading cause of death among HIV-positive patients, accounting for approximately 11% of the total deaths in this population [2]; the risk of CVD is higher in HIV positive individuals compared with HIV negative people, and particularly the reported Myocardial Infarction (MI) incidence in cohort study ranges from 3 to 11 cases per 1000 patients a year in HIV- positive individuals against 2 to 7 cases per 1000 patients-years in HIV-negative population [3,4]. Although initial studies indicated a higher prevalence of traditional CVD risk factors in HIV infected population [5,6] as a possible cause, the molecular mechanisms of increased CVD risk in HIV still remain incompletely defined and should be probably attributable to a combination of multiple factors, including both direct and indirect effects of HIV infection on metabolism. Evidence from experimental and observational studies [7,8] in recent years suggested a more important role of HIV itself in contributing to CVD. Endothelial dysfunction due to gp120, Tat and Nef proteins have been identified as a critical link between infection, inflammation, immune activation, atherosclerosis and cardiovascular system. Moreover, ART may play a role in the exacerbation of risk factors for CVD [9]; since the presentation of findings from the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study in 2008 demonstrating a 90% increased risk of MI in HIV- positive individuals receiving ART regimens including Abacavir (ABC), subsequent studies, conducted by FDA [10], GlaxoSmithKline [11] and independent researchers [12], to investigate this risk have yielded conflicting results. Although more recent studies have shown an effective increased risk of CVD associated with use of ABC, many results did not reach statistical significance [13-17]. The absence of a demonstrated underlying biological mechanism for such a risk added interest and confusion about the question, as well as the higher prevalence of risk factors for CVD, such as renal impairment and substance abuse among abacavir recipients; in addition, a recent meta analysis suggests that Relative Risk (RR) for MI is increased within a 6 months exposure to ABC (RR=1.61; 95% confidence interval: 1.48–1.75) and in cART-naive population [18]. While the published evidence remains conflicting and a plausible biological mechanism for this potential association has not yet been identified, in the following study we have tried to verify whether, after introduction of ABC and its discontinuation in the contest of HAART deintensification, common metabolic markers CVD related such as glucose, LDL, HDL, total cholesterol and triglycerides and inflammatory biomarkers such as IL-6 and D-dimer could change in a small cohort of HIV-1 infected patients.

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