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MI Risk Not Falling in HIV Group, as It Is in non-HIV Peers
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2022 CROI, February 12-16 and 22-24, 2022
Mark Mascolini
People with or without HIV had a similar myocardial infarction (MI) risk in 2005-2009, according to a comparison in two big healthcare systems in California and Massachusetts [1]. But in 2010-2017, the MI risk was 60% higher in the HIV group. Researchers attributed the growing difference to MI risk improvement in HIV-negative people but not HIV-positive people,
Abundant research documents higher MI risk in people with than without HIV, probably because of higher rates of classic MI risk factors, ongoing inflammation and immune activation with HIV, and the cardiovascular impact of certain HIV medications, Researchers who conducted this study in the Kaiser Permanente system in northern California and the Massachusetts General Brigham Partners group in Massachusetts noted that MI risk may be rising in people with HIV because of heart-related effects of increased integrase inhibitor use, consequent weight gain, and aging of the HIV population.
The Kaiser/Partners team aimed to chart changes in MI incidence (new diagnoses) over time in people with versus without HIV in the California and Massachusetts healthcare systems. They selected HIV and non-HIV groups that had similar initial MI risks when starting the study's observation period. The Kaiser Permanente Northern California system serves 4.5 million people in the San Francisco area, about 30,000 of them with HIV. The Boston-area Partners system serves 1.5 million people, about 7000 of them with HIV.
Study participants with HIV had to be at least 18 years old when starting observation between 2005 and 2017. They could not have cardiovascular disease when beginning study follow-up. For every 1 person with HIV the investigators picked 3 people without HIV from the Kaiser group and 4 without HIV from Partners. They based selection of HIV-negative people on a propensity score involving demographics (age, race, sex, year) and baseline Framingham heart risk components (total cholesterol, high-density lipoprotein [HDL] cholesterol, diabetes, systolic blood pressure, hypertension treatment, smoking).
The study baseline was the first year the Framingham components were measured. Follow-up lasted from baseline until an MI diagnosis, death, loss to follow-up (failing to return for visits), 5 years after baseline, or the end of the study observation period (2020)—whichever came first. The researchers used Cox proportional hazards models to estimate adjusted hazard ratios for the effect of HIV infection on MI risk within two periods, 2005-2009 and 2010-2017; the models adjusted for relevant demographics and Framingham risk components.
The analysis involved 4280 people with HIV versus 14,059 without HIV in 2005-2009, and 5121 with HIV versus 15,359 without HIV in 2010-2017. Those four groups each averaged about 44 years in age when starting observation, about 87% were men, about half white, and about 18% black. People with HIV included a higher proportion of smokers (about 28% versus 23%) and had marginally lower (worse) HDL cholesterol. The HIV and non-HIV groups were similar in systolic blood pressure and diabetes rate.
Among people with HIV in the 2005-2009 and 2010-2017 periods, antiretroviral use rose from 76% to 88%, proportions with a viral load above 400 copies fell from 39% to 23%, average CD4 count climbed from 470 to 587, average years with HIV rose from 7.8 to 9.1, protease inhibitor experience fell from 54% to 27%, and integrase inhibitor experience leapt from 3% to 40%.
In 2005-2009 MI incidence was similar in the HIV and non-HIV groups (about 1.1% in both). But in 2010-2017 the HIV group had a significantly higher MI incidence (1.2% to 0.9%, P = 0.031). In the more recent study period, MI rate per 100 person years was 0.25 in people with HIV and 0.16 in people without HIV, whereas in 2005-2009 those rates were virtually identical—0.21 with HIV and 0.22 without HIV.
Adjusted hazard ratios (HR) determined that HIV did not affect MI risk in 2005-2009 (HR 1.1, 95% confidence interval [CI] 0.8 to 1.5, P = 0.61), but in 2010-2017 HIV infection boosted MI risk about 60% (HR 1.6, 95% CI 1.1 to 2.4, P = 0.007). In 2010-2017 the greater MI risk with HIV was statistically significant in the Kaiser group (HR 1.6, 95% CI 1.1 to 2.4, P = 0.02) but not in the Partners group (HR 2.1, 95% CI 0.6 to 7.5, P = 0.28).
The Kaiser/Partner investigators noted that their analysis is limited by unmeasured confounders like diet and exercise and the relatively short 5-year follow-up. Also, the much higher proportion of men studied raises questions about whether results apply to women. They observed that the overall greater MI risk with HIV in 2010-2017 appeared to be driven by the drop in MI risk from 2005-2009 to 2010-2017 in people without HIV but not in those with HIV: MI rate per 100 person-years was 0.21 with HIV and 0.22 without HIV in 2005-2009; and MI rate per 100 person-years was 0.25 with HIV and 0.16 without HIV in 2010-2017.
The researchers surmised that "HIV-specific factors, such as longer HIV duration and newer antiretroviral therapy (for example, integrase inhibitors), may have prevented people with HIV from realizing the same improvement in MI risk as people without HIV."
Reference
1. Silverberg MJ, Lyass A, Hurley LB, et al. Trends in myocardial infarction risk by HIV status in two US healthcare systems. 2022 CROI, February 12-16 and 22-24, 2022. Abstract 39.
CROI: Trends in Myocardial Infarction Risk by HIV Status in Two US Healthcare Systems - (02/14/22)
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