Beatriz Díaz-Pollán1, Vicente Estrada2, Manuel Fuentes-Ferrer3, Dulcenombre Gómez-Garré4, Jesús San Román-Montero5. 1. Medicina Interna, Hospital Universitario La Paz, Madrid, Spain. 2. Medicina Interna III, Hospital Clínico San Carlos, Madrid, Spain. 3. Preventive Medicine Department, Hospital Clínico San Carlos, Madrid, Spain. 4. Vascular Biology Research Laboratory, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain. 5. Departamento de Medicina y Cirugía, Universidad Rey Juan Carlos, Alcorcón, Spain.
Abstract
INTRODUCTION: HIV-infected patients show an increased risk of cardiovascular disease (CVD). In the general population, lipoprotein-associated phospholipase A2 (Lp-PLA2) appears to be an independent predictor of CVD. We aimed to study associations between Lp-PLA2 plasma levels and other risk factors for CVD in HIV patients. MATERIALS AND METHODS: A cross-sectional, comparative study of two series of cases (HIV patients, n=116 and age-matched non-HIV healthy controls, n=113) was conducted. Eighty-seven percent HIV patients on antiretroviral therapy (ART), 72.4% with HIV-1 viral load <50 cop/mL. Inflammatory biomarkers (CRP, Lp-PLA2) and internal carotid intima-media thickness (IMT) were measured and CVD risk (Framingham and SCORE algorithms) was calculated. Univariate and multivariable associations between these variables were performed. RESULTS: HIV patients presented higher Lp-PLA2 levels [276.81 ng/mL (209.71-356.58)] than uninfected healthy controls [220.80 ng/mL (172.70-256.90)], p≤0.01. In univariate analysis of the global sample, only cigarette smoking was associated with higher Lp-PLA2 levels, p≤0.001. In HIV group, female and smoker patients showed higher Lp-PLA2 levels, p≤0.05. No significant association was found between Lp-PLA2 levels and another CVD risk factors, carotid IMT, Framingham and SCORE algorithms, ART, HIV-1 viral load neither and CD4+ T lymphocyte count. In multivariate analysis, cigarette smoking remained significantly associated with Lp-PLA2 levels [β=64.8 (95% CI 10.8-118.9) ng/mL, p=0.020]. CONCLUSIONS: HIV-infected patients present higher Lp-PLA2 levels than healthy controls, and in this population, tobacco smoking is significantly associated with increased Lp-PLA2 levels. Smoking cessation should be a priority in CVD prevention in HIV-infected patients.
INTRODUCTION:HIV-infectedpatients show an increased risk of cardiovascular disease (CVD). In the general population, lipoprotein-associated phospholipase A2 (Lp-PLA2) appears to be an independent predictor of CVD. We aimed to study associations between Lp-PLA2 plasma levels and other risk factors for CVD in HIVpatients. MATERIALS AND METHODS: A cross-sectional, comparative study of two series of cases (HIVpatients, n=116 and age-matched non-HIV healthy controls, n=113) was conducted. Eighty-seven percent HIVpatients on antiretroviral therapy (ART), 72.4% with HIV-1 viral load <50 cop/mL. Inflammatory biomarkers (CRP, Lp-PLA2) and internal carotid intima-media thickness (IMT) were measured and CVD risk (Framingham and SCORE algorithms) was calculated. Univariate and multivariable associations between these variables were performed. RESULTS:HIVpatients presented higher Lp-PLA2 levels [276.81 ng/mL (209.71-356.58)] than uninfected healthy controls [220.80 ng/mL (172.70-256.90)], p≤0.01. In univariate analysis of the global sample, only cigarette smoking was associated with higher Lp-PLA2 levels, p≤0.001. In HIV group, female and smoker patients showed higher Lp-PLA2 levels, p≤0.05. No significant association was found between Lp-PLA2 levels and another CVD risk factors, carotid IMT, Framingham and SCORE algorithms, ART, HIV-1 viral load neither and CD4+ T lymphocyte count. In multivariate analysis, cigarette smoking remained significantly associated with Lp-PLA2 levels [β=64.8 (95% CI 10.8-118.9) ng/mL, p=0.020]. CONCLUSIONS:HIV-infectedpatients present higher Lp-PLA2 levels than healthy controls, and in this population, tobacco smoking is significantly associated with increased Lp-PLA2 levels. Smoking cessation should be a priority in CVD prevention in HIV-infectedpatients.
Authors: Udo Hoffmann; Michael T Lu; Borek Foldyna; Markella V Zanni; Julia Karady; Jana Taron; Bingxue K Zhai; Tricia Burdo; Kathleen V Fitch; Emma M Kileel; Kenneth Williams; Carl J Fichtenbaum; Edgar T Overton; Carlos Malvestutto; Judith Aberg; Judith Currier; Craig A Sponseller; Kathleen Melbourne; Michelle Floris-Moore; Cornelius Van Dam; Michael C Keefer; Susan L Koletar; Pamela S Douglas; Heather Ribaudo; Thomas Mayrhofer; Steven K Grinspoon Journal: JAMA Netw Open Date: 2021-06-01