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Telomere Length, Traditional Risk Factors, HIV-related Factors and Coronary Artery Disease Events in Swiss Persons Living with HIV
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CROI 2020 Isabella C. Schoepf1a, Tanja Engel1a, Marieke Raffenberg1a, Neeltje Kootstra2, Peter Reiss3, Christian Thorball4, Jacques Fellay4,5, Roger Kouyos6, Huldrych G√ľnthard6, Bruno Ledergerber6, Philip E. Tarr1, and the Swiss HIV Cohort
1Medizinische Universitätsklinik, Kantonsspital Baselland, University of Basel, Bruderholz, Switzerland; 2Department of Experimental Immunology, Amsterdam University Medical Centers, University of Amsterdam, Netherlands; 3Department of Global Health and Division of Infectious Disease, Amsterdam University Medical Centers, Location AMC, University of Amsterdam, Netherlands; 4EPFL School of Life Sciences and Swiss Institute of Bioinformatics; Lausanne, Switzerland; 5Precision Medicine Unit, CHUV, University of Lausanne, Switzerland; 6Division of Infectious Diseases, University Hospital Zurich, University of Zurich, Switzerland a=equal contribution
In the general population, leukocyte telomere length (TL) shortening, as occurs with advancing age, is associated with coronary artery disease (CAD) events. The relative contribution of TL, HIV-related and traditional risk factors to CAD has not been quantified in HIV-positive persons.
We measured TL in stored peripheral blood mononuclear cells (PBMC) as previously described (Cobos Jimenez J Infect Dis 2016) by quantitative PCR, using the single copy albumin gene as control. Relative TL was estimated using a standard curve prepared from healthy blood donors. Study participants were white Swiss HIV Cohort Study participants. Cases had a 1st CAD event during the study period (1.1.00-31.12.17). We used incidence density sampling and matched 1-3 controls (CAD event-free) on gender, age, and date of registration. We obtained univariable and multivariable odds ratios (OR) for a first CAD event from conditional logistic regression analyses, including as variables TL, age, gender, smoking, family history, hypertension, diabetes, hypercholesterolemia, and HIV-related factors (recent exposure to abacavir, exposure >1 year to indinavir, lopinavir/ritonavir, darunavir; ART discontinuation; on ART but HIV RNA>50 copies/mL).
We included 333 cases (median age at CAD event, 54 years; 14% women; 83% with HIV RNA<50) and 745 controls. Median (IQR) time of TL measurement was 9.4 (5.9-13.8) years prior to CAD event. Participants in the 5th (longest) TL quintile, compared to the 1st (shortest) TL quintile had univariable CAD odds ratio of 0.56 (95% confidence interval, 0.35-0.91; p=0.02), and a multivariable OR of 0.47 (0.26-0.86; p=0.01; Figure). In comparison, the OR for current smoking was 2.28 (1.46-3.56), hypercholesterolemia 1.84 (1.33-2.55), diabetes 3.92 (2.26-6.78), on ART/HIV RNA>50 1.80 (0.95-3.42); recent abacavir, cumulative lopinavir, indinavir, darunavir exposure 1.84 (1.28-2.64), 1.87 (1.23-2.84), 3.22 (1.99-5.21), and 1.68 (1.01-2.78), respectively.
HIV-positive persons with the longest telomeres (measured >9 years prior to CAD event) had approx. half the odds of developing CAD of those with the shortest telomeres. TL measurement may, in addition to traditional and HIV-related risk factors, provide prognostic information with respect to CAD risk.





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