Protease inhibitor treatment effect on aortic stiffness in normotensive patients with human immunodeficiency virus infection

Lopez‐Sublet, Marilucy; Honoré, P.; Bentata, M.; Bratis, Costas; Rougès, F.; Krivitzky, A; Dhôte, Robin; Mourad, Jean‐Jacques

doi:10.1016/j.jmv.2012.05.001

Cited by 13 publications

(18 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Conversely, several other studies found increased aortic stiffness in HIV-infected individuals [9][10][11]. Such discrepancies may be because of differences in study population characteristics, notably cART use, immunologic status, cardiovascular risk level, and variations in the methods used to evaluate aortic stiffness, particularly cardiac magnetic resonance [11], SphygmoCor [9,10,15,17,18] and Complior [12][13][14]16]. Our cross-sectional study provides additional information by observing that, among HIV-infected individuals, aortic stiffness is associated with both nadir CD4 þ T-cell count, a marker of past profound immunodeficiency, and traditional cardiovascular risk factors.…”

Section: Discussionmentioning

confidence: 99%

“…Carotid-femoral pulse wave velocity (cf-PWV) is the gold standard for measuring aortic stiffness [8]. Several cross-sectional studies have previously addressed the effect of HIV infection [9][10][11][12][13] or cART [14][15][16][17] on aortic stiffness using different methods of evaluation, including cf-PWV, radial PWV, and cardiac magnetic resonance. Certain studies found increased aortic stiffness among HIV-infected individuals when compared with controls [9][10][11], whereas others did not [12][13].…”

Section: Introductionmentioning

confidence: 99%

“…Certain studies found increased aortic stiffness among HIV-infected individuals when compared with controls [9][10][11], whereas others did not [12][13]. Contradictory results have also been reported concerning the effect of cART on aortic stiffness, observing either deleterious effects [14][15][16] or no association [17][18]. These discordant results may simply be because of population differences, differences in study design, or methodological approach.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Aortic stiffness aging is influenced by past profound immunodeficiency in HIV-infected individuals

Maia-Leite

Catez

Boyd

et al. 2016

Journal of Hypertension

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Aortic stiffness aging is influenced by past profound immunodeficiency in HIV-infected individuals

Maia-Leite

Catez

Boyd

et al. 2016

Journal of Hypertension

View full text Add to dashboard Cite

show abstract

“…It has been reported that ART, specially protease inhibitors (PI), deteriorate arterial function [28].…”

Section: Introductionmentioning

confidence: 99%

Aortic stiffness and central hemodynamics in treatment naïve HIV infection: A cross-sectional study.

Martínez-Ayala

Alanis-Sánchez

Gonzalez-Hernández

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Human immunodeficiency virus (HIV) infection is associated with a greater risk of cardiovascular disease (CVD). HIV infection causes a chronic inflammatory state and increases oxidative stress which can cause endothelial dysfunction and arterial stiffness. Aortic stiffness measured by carotid femoral-pulse wave velocity (cfPWV) and central hemodynamics are independent cardiovascular risk factors and have the prognostic ability for CVD. We assessed cfPWV and central hemodynamics in young individuals with recent HIV infection diagnosis and without antiretroviral therapy. We hypothesized that individuals living with HIV would present greater cfPWV and central hemodynamics (central systolic blood pressure and pulse pressure) compared to uninfected controls.Methods. We recruited 51 treatment-naïve individuals living with HIV (HIV(+)) without previous CVD and 51 age- and sex-matched controls (HIV negative (-)). We evaluated traditional CVD risk factors including metabolic profile, blood pressure (BP), smoking, HIV viral load, and CD4+ T-cells count. Arterial stiffness and central hemodynamics were evaluated by cfPWV, central systolic BP, and central pulse pressure (cPP) via applanation tonometry.Results. HIV(+) individuals presented a greater prevalence of smoking, reduced high-density lipoprotein cholesterol, and body mass index. 65.9% of HIV(+) individuals exhibited lymphocyte CD4+ T-cells count <500 cells/µL. There was no difference in brachial or central BP between groups; however, HIV(+) individuals showed significantly lower cPP. We observed a greater cfPWV (mean difference= 0.5 m/s; p<0.01) in HIV(+) compared to controls, even after adjusting for heart rate, mean arterial pressure and smoking.Conclusion: In the early stages of infection, non-treated HIV individuals present a greater prevalence of traditional CVD risk factors, arterial stiffness, and normal or in some cases central hemodynamics.

show abstract

“…The results of the D:A:D study indicate that only half of the cardiovascular risk specifically associated with PI-based combination therapy is attributable to fasting dyslipidaemia. Postulated additional, PI-induced effects include endothelial dysfunction [3], impaired cholesterol efflux from macrophages [4], and vascular wall effects leading to greater arterial stiffness [5]. Arterial stiffness relates measurement of change in arterial diameter and pressure at the same site, and is positively correlated with premature coronary artery disease, and is a validated, independent predictor of cardiovascular mortality in HIV-uninfected populations [6].…”

Section: Introductionmentioning

confidence: 99%

Metabolic Effects of Ritonavir-boosted Atazanavir and Darunavir in HIVnegative Adults: A Randomised Comparison

Richardson¹

2014

J AIDS Clin Res

View full text Add to dashboard Cite

Objectives: The increased cardiovascular risk historically associated with protease inhibitor (PI) use in HIVinfected individuals is only partly attributable to fasting dyslipidaemia, and may not apply to the currently recommended PI drugs-atazanavir and darunavir. In this prospective pilot study, we aimed to describe the isolated metabolic differences between atazanavir/ritonavir and darunavir/ritonavir on circulating fasting and post-prandial lipids (primary objective), and arterial stiffness, glycaemic and inflammatory markers (secondary objectives) by administering them as monotherapy to healthy, HIV-uninfected adults. Methods: Participants were randomised 1:1 to receive open-label atazanavir (300 mg/day) or darunavir (800 mg/day), both boosted with ritonavir (100 mg/day), for 4 weeks. A standardised high-energy meal was consumed at weeks 0 and 4, with hourly post-prandial blood samples and arterial stiffness assessed for 4 hours. Mean fasting and post-prandial measurements were compared, the latter as the change in mean post-prandial incremental area under the curve. Results: Twenty participants (10 atazanavir/ritonavir, 10 darunavir/ritonavir; 50% male, mean age 38 years, mean blood pressure 113/72 mmHg, mean total cholesterol 4.4 mmol/L, mean triglycerides 0.9 mmol/L) completed the study. After four weeks, fasting total cholesterol rose more with darunavir/ritonavir than atazanavir/ritonavir (+0.8 mmol/L vs. +0.3 mmol/L, respectively; p=0.041), as did low-density lipoprotein cholesterol (+0.1 mmol/L vs. +0.7 mmol/L, respectively; p=0.017). Between-group differences in post-prandial lipid changes were non-significant. Postprandial decline in arterial stiffness was greater with atazanavir/ritonavir than darunavir/ritonavir (-27.6 h% vs. +0.1 h%, respectively; p=0.041). Bilirubin rose significantly with atazanavir/ritonavir but not darunavir/ritonavir (+29 µmol/L vs.-0.6 µmol/L, respectively; p=0.001). Changes in other parameters were similar. Conclusion: Atazanavir/ritonavir has modestly, but significant, favourable metabolic and haemodynamic profiles over darunavir/ritonavir, evident even after short-term monotherapy. Post-prandial lipid effects were similar, however. Further study of treatment-emergent cardiovascular event incidence with darunavir/ritonavir therapy is required to determine the clinical relevance of this between-group difference. J o ur nal o f A ID S & Cli n ic a l R es earc h

show abstract

Protease inhibitor treatment effect on aortic stiffness in normotensive patients with human immunodeficiency virus infection

Cited by 13 publications

References 39 publications

Aortic stiffness aging is influenced by past profound immunodeficiency in HIV-infected individuals

Aortic stiffness aging is influenced by past profound immunodeficiency in HIV-infected individuals

Aortic stiffness and central hemodynamics in treatment naïve HIV infection: A cross-sectional study.

Metabolic Effects of Ritonavir-boosted Atazanavir and Darunavir in HIVnegative Adults: A Randomised Comparison

Contact Info

Product

Resources

About