CROI 2017 Abstract e-Book

Abstract eBook

Oral Abstracts

130 IMPACT OF SMOKING, HYPERTENSION & CHOLESTEROL ON MYOCARDIAL INFARCTION IN HIV+ ADULTS Keri N. Althoff 1 , Frank J. Palella 2 , Kelly Gebo 1 , Stephen J. Gange 1 , Charles Rabkin 3 , Jennifer E. Thorne 4 , Micheal A. Horberg 5 , Daniel B. Klein 6 , Mari Kitahata 7 , Richard D. Moore 8 1 The Johns Hopkins Univ, Baltimore, MD, USA, 2 Northwestern Univ, Chicago, IL, USA, 3 NCI, Rockville, MD, USA, 4 Kaiser Permanente Mid-Atlantic States, Rockville, MD, USA, 5 Kaiser Hosp, San Leandro, CA, USA, 6 Univ of Washington, Seattle, WA, USA Background: HIV-infected adults have a 1.5-to-2-fold increase in risk of myocardial infarctions (MIs) compared with uninfected adults. Our objective was to estimate the population attributable fractions (PAFs) of HIV-related and traditional MI risk factors, interpreted as the proportion of MIs that could potentially be avoided if HIV-infected adults were unexposed to these risk factors. Methods: We included adults from 7 contributing cohorts to the NA-ACCORD with validated first occurrence of a type 1 myocardial infarction, which are MIs from plaque rupture that would be most susceptible to traditional MI risk factors. Modifiable HIV-related risk factors included CD4 <200 cells/mm3, detectable plasma HIV RNA (≥400 copies/mL), and history of clinical AIDS. Modifiable traditional risk factors included tobacco smoking, treated hypertension (HTN), hypercholesterolemia (HC, defined as use of statins or a total cholesterol >240 mg/dL), type II diabetes, stage 4 chronic kidney disease (CKD), and hepatitis C virus (HCV) infection. Cox proportional hazard models with piecewise constant baseline hazard functions were used to estimate hazard ratios (adjusted for age, sex, race, and injection drug use). These hazard ratios were combined with the prevalence of the risk factor among persons with MIs to estimate adjusted PAFs for modifiable risk factors. Smoking and HCV infection were measured at study entry. All other variables were time-updated. Results: A total of 29,515 adults contributed 131,137 person-years and 347 MIs; median follow up was 3.5 years. At baseline, participants who subsequently had an MI were older, more likely to be black, have smoked, had HTN, HC, diabetes, stage 4 CKD, a low CD4, a clinical AIDS diagnosis, and HCV infection. Adjusting for demographics, eliminating smoking, HTN, and HC would avert 38%, 41% and 43% of MIs, respectively (Figure 1); eliminating all three would avert 86% of MIs. HIV-related risk factors and HCV infection had smaller PAFs. A subgroup analyses accounting for BMI showed similar results, with the exception of a reduction in the PAF for HC. Conclusion: Preventing smoking, hypertension, and HC each could result in a ~40% reduction in MIs among aging HIV-infected adults; further reductions in MIs can be achieved with aggressive antiretroviral management. These results underscore the need to implement traditional MI risk reduction interventions soon after prompt HIV treatment initiation in order to reduce excess MI burden among aging HIV-infected adults.

Oral Abstracts

131 CESSATION OF CIGARETTE SMOKING AND THE IMPACT ON CANCER INCIDENCE IN THE D:A:D STUDY Leah Shepherd 1 , Lene Ryom 2 , Kathy Petoumenos 3 , Camilla Ingrid Hatleberg 2 , Antonella d’Arminio Monforte 4 , Fabrice Bonnet 5 , Peter Reiss 6 , Jens D. Lundgren 2 , Amanda Mocroft 1 , for the D:A:D Study Group 1 Univ Coll London, London, UK, 2 CHIP, Copenhagen, Denmark, 3 Kirby Inst, Sydney, Australia, 4 Univ of Milan, Milan, Italy, 5 CHU de Bordeaux, Bordeaux, France, 6 Stichting HIV Monitoring and Academic Med Cntr, Amsterdam, Netherlands Background: Cancers are a major source of morbidity and mortality in the cART era. The prevalence of smoking in HIV+ people is 40–70% and the clinical benefits of smoking cessation on cancer risk have not been reported. We aimed to estimate cancer rates after smoking cessation in persons from the D:A:D study. Methods: Persons were followed from the latest of study entry or 1/1/2004 until earliest of first cancer diagnosis, last visit plus 6 months, death, or 1/2/2015. Three outcomes were considered: all cancers combined, lung cancer, and other smoking-related excluding lung cancer (OSRC; see footnote). Smoking status was defined as current and never smokers, those who stopped during follow-up (<1,1-2,2-3,3-5,5> years since stopping) and those who stopped prior to baseline. Adjusted rate ratios (aRR) were calculated using Poisson regression. Results: 39701 persons contributed 315327 person years of follow-up (PYFU) (median: 9 IQR: 6, 11 years per person). At baseline, 41% of people were current smokers, 17%were ex-smokers, 27% never smoked. 2230 developed cancer (IR 7.1/1000 PYFU, 95%CI: 6.8, 7.4), of which 251 were lung cancers (IR 0.8/1000 PYFU, 95%CI: 0.7, 0.9) and 516 were OSRC (IR 1.6/1000 PYFU 95%CI: 1.5, 1.8). Incidence of all cancers combined (Figure) was highest <1 year after quitting compared to those who had never smoked (aRR: 1.62 95%CI: 1.32, 1.99) and was similar to never smokers thereafter. Lung cancer incidence was over 11-fold higher <1 year after quitting (aRR: 11.72 95%CI: 4.81, 28.57) and remained >8-fold higher even after 5 years (aRR: 8.26 95%CI: 2.83, 24.09) with no evidence of decline when compared to non-smokers. OSRC incidence was almost 3-fold higher <1 year after quitting (aRR2.52 95%CI: 1.69, 3.74), but was similar to never smokers thereafter. Smoking duration was associated with the occurrence of all cancers combined (Per year longer aRR: 1.03 95%CI: 1.01,1.04), lung (aRR: 1.07 95%CI: 1.01, 1.12), but not OSRC (aRR: 1.03 95%CI: 0.99, 1.06). No significant interactions between smoking status and age, gender or CD4 were found. Conclusion: Overall cancer incidence declined to that of non-smokers after one year quitting except for lung cancer incidence, which did not decrease even >5 years after quitting. Smoking cessation efforts should be a priority to reduce the risk of cancer, however, surveillance and screening of lung cancer should not be stopped in patients who stop smoking.

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CROI 2017