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HIV-Infected Adults Are at Greater Risk for Myocardial Infarction (MI), End-stage Renal Disease (ESRD), and Non-AIDS-defining Cancers, But Events Occur at Similar Ages Compared to HIV-uninfected Adults (VA)
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Reported by Jules Levin
CROI 2013
Keri N Althoff1, Christina Wyatt2, Cynthia Gibert3, Kris Ann Oursler4, David Rimland5, Maria Rodriguez-Barradas6, Kathleen McGinnis7, Melissa Skanderson7, Kelly Gebo1, and Amy C Justice7 for the Veterans Aging Cohort Study (VACS)
1. Johns Hopkins University, Baltimore, MD; 2. Mount Sinai School of Medicine, New York, NY; 3. George Washington University Medical Center and Veterans Affairs Medical Center, Washington, DC; 4. University of Maryland and Veterans
Affairs Maryland Health Care System, Baltimore, MD; 5. Atlanta Veterans Affairs Medical Center and Emory University School of Medicine, Atlanta, GA; 6. Baylor College of Medicine and the Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX; 7.Yale University and the Veterans Affairs Connecticut Healthcare System, New Haven, CT
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Author Summary and Conclusions
Greater risk?
· HIV+ individuals had a greater rate of MI, ESRD, and HIV- ssociated cancers
- Prevention (diet, exercise, smoking cessation, diabetes
control, etc.) and screening are critical in protecting the health
of aging HIV+ adults
Premature aging?
· No difference in mean age or adjusted mean age at MI and
ESRD diagnosis, by HIV status
· Modest difference (≈6 months younger in HIV+) at age of non-
AIDS-defining cancers
No difference in the rate of other cancers, by HIV status
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This study is a retrospective cohort analysis looking at risk & the effect of "premature aging". An important point to keep in mind reflected in the slide below of the baseline patient demographics the HIV- vets had more diabetes, hypertension, hyperlipidemia, while the HIV+ had more HCV. With regards to MI they found an 81% increased risk, after adjustments for a number of things, among HIV+ vs HIV- in their VA cohort, which is similar to that found in the Triant 2007 published study in JCEM which these authors refer to although this VA cohort appears to look at more recent time period. However, this analysis did not find an affect of what they called "premature aging" - the crude & adjusted age differences for developing an MI were the same in HIV+ vs HIV, about 55 yrs of age. In the Q&A after the presentation several people came to the mic: Joe Eron said be careful how you use the term premature aging, he said there are so many factors potentially involved, he said even if HIV+ had MIs 5 yrs earlier vs HIV- it could be due to higher cholesterols, and that is a good point I agree, there could be other factors like immune activation & inflammation markers. This study did not consider these markers probably because the patients were not tested for these but if they had these markers my guess is there would be an association between these markers and the onset of MIs or CVD in general, as other studies find CVD associated with these markers. In fact, in this same oral session Wendy Post reported from the MACS they found an association between aging & certain parameters of heart disease which I wrote up in a separate report emailed yesterday: "HIV-infected men compared to HIV-uninfected men had a greater prevalence of - coronary artery calcium - non-calcified plaque - any plaque and a greater extent of non-calcified plaque, (2) Noncalcified plaque prevalence rose with age in HIV-positive men but not HIV-negative men". Steve Grinspoon also reported in his oral in the same session & in a publication in AIDS increased rate of subclinical heart disease in HIV+. So he was looking for subclinical heart disease & the VA is looking at disease events, and all these studies have different types of analyses so you have to be a bit creative in putting all the findings together. Grinspoon said in his presentation that immune activation "is very strongly related", the average age here is 44 in this study & we are looking at subclinical disease, in this young population the affects of smoking & lipids abnormalities have not yet have time to cause serious heart disease by immune activation & inflammation are the drivers of this subclinical disease concern, "even in virologically suppressed patients this is occurring". Daniel Pierce from Loma Linda went to the mic & mentioned his published paper from the Fall 2012 inAm J Cardiology which found there was an age difference in MI mortality between HIV+ vs HIV- (48 vs 54 yrs age) but he hound HIV+ were less likely to receive needed procedures, I will provide link to this paper in this email. Frank palella asked an important question at the mic during Q&A after the presentation, that there are a number of key factors that probably drive disease, its important to parse out the roles & associtaions, factors he said we have seen in other cohorts contribute mightily to the occurrence of comorbidities, so are theresubsets of patients who are truely driving earlier development of MI or other comorbidities, this is what Eron was referring to & what I would reinforce - with whether a patient was treated, when a person starts ART, nadir CD4, and i would add immune/activation markers. In response Althof the presenter said we have yet to parse this out in the VACS, but those steps are planned and often they are the very sick, the ones with the greatest burden of illness - to which I would add that other studies find an association with immune activation/inflammation markers - as did Grinspoon in his study. The august audience & myself agree we need a more scientific description of the phenomenon of "premature aging". Regarding end-stage renal disease, this VA analysis found the crude mean difference in age was 3.2 years (58 vs 55 yrs age) but after adjusting the mean difference in age was -0.23 yrs, no difference in age at diagnosis by HIV status. However look at the slides below, they found a greater risk among HIV+ looking at the crude risk ratio 1.88 vs 2.93 and after adjustment a 43$ increase in the rate in HIV+ vs HIV-, and looking at the graph in the slide below the author Athof said "the age stratified incidence rates show a slightly higher rate of ESRD [for HIV+] at all ages". For HIV-associated cancers, see the slide below, after adjusting there was a 5 month decrease in mean age at diagnosis in HIV+ vs HIV for "other cancers", "again this does support the hypothesis of premature aging for cancer". they found a slight decrease in HIV+ vs HIV- in the rate and after adjustment they found no difference in rates for risk of other cases for HIV+ vs HIV-. Age specific rates show similar incidence at all ages with "slightly higher incidence in HIV+ in the older groups". They looked at "other cancers" too. After adjusting there was a 5 month decrease in mean age at diagnosis in HIV+ vs HIV for "other cancers", see slide below, "again this does support the hypothesis of premature aging for cancer". they found a slight decrease in HIV+ vs HIV- in the rate and after adjustment they found no difference in rates for risk of other cases for HIV+ vs HIV-neg. Age specific rates show similar incidence at all ages with "slightly higher incidence in HIV+ in the older groups"
Comparison of In-Hospital Mortality From Acute Myocardial Infarction in HIV Sero-Positive Versus Sero-Negative Individuals - Am J Cardiology
http://www.natap.org/2012/ICAAC/ICAAC_14.htm
This study looked at reasons why HIV+ received worse care & less procedures which probably contributed to the worse outcomes: age 48 vs 54, MI mortality in hospital
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