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HIV infection and low CD4 count associated with hardening of arteries
Michael Carter, 2015-05-06 10:20:00
HIV infection is
associated with an increased risk of hardening of the arteries, investigators
report in the online edition of Clinical
Infectious Diseases. The US study compared changes in carotid artery
thickness and new plaque formation between HIV-positive and HIV-negative men
and women with similar demographic and cardiovascular risk factors.
infection was not associated with changes in carotid artery thickness. However, people with HIV were more likely to have new plaque formation, even when
their viral load was undetectable.
that HIV-infected women and men had a 61% greater risk of new focal carotid
artery plaque formation over seven years compared with uninfected controls,”
comment the researchers. “The HIV-associated risk was higher than that
associated with smoking. Furthermore, the elevated risk persisted among ART
[antiretroviral therapy]-treated individuals with persistent HIV viral suppression,
suggesting that sustained suppression of circulating HIV RNA to below
detectable limits does not eliminate excess CVD [cardiovascular disease risk]
in the treated HIV-infected population.”
encouragingly, people living with HIV whose CD4 count was above 500 cells/mm3
had a similar risk of new plaque formation to HIV-negative individuals.
disease is now an important cause of morbidity and mortality in people with
HIV. Investigators from the United States wanted to see if HIV was
associated with progression of subclinical atherosclerosis – hardening of the
arteries – over seven years of follow-up.
population comprised 1011 women (74% HIV positive) enrolled in the Women’s
Interagency HIV Study and 811 men (65% HIV positive) in the Multicenter AIDS
Cohort Study. All had repeat carotid artery ultrasound investigations –
thickness and new plaque formation –
between 2003 and 2013. Two-thirds of women with HIV and
three-quarters of men with HIV were taking ART.
Changes in carotid
artery thickness did not differ according to HIV status in either men or women.
Factors associated with increased thickening were black and Hispanic
ethnicity and use of crack/cocaine. Use of anti-hypertensive medications was
associated with a reduction in carotid artery thickness.
The prevalence of
carotid arterial plaques increased from 8 to 15% in women and 25 to 34% in
men during follow-up. Overall, people with HIV were 61% more likely to
experience new plaque formation compared to HIV-negative individuals (OR =
1.61; 95% CI, 1.12-2.32). The association between HIV infection and plaque
formation was present in both men and women.
increased the risk of new plaque accumulation by 42%. Other risk factors were
higher total cholesterol and older age.
identified 199 people with HIV who were taking ART with persistent viral
suppression (16% of women with HIV; 29% of men with HIV). These
patients had an increased risk of new plaque formation compared to the
HIV-negative group (aRR = 1.77; 95% CI, 1.13-2.77).
“Our finding that
participants who maintained HIV suppression still had an increased risk of new
focal plaque formation suggests that vigilance with respect to the long-term
adverse consequences of ART remains warranted for all HIV-infected
individuals,” write the authors.
between immune status and plaque formation was then examined.
People living with HIV who had a baseline CD4 count above 500 cells/mm3 had a
comparable risk of new plaque formation to HIV-negative controls. The highest
risk of new plaque accumulation was observed in people with HIV who had a
CD4 count below 200 cells/mm3 (aRR = 2.57; 95% CI, 1.48-4.46).
Longer duration of
therapy with a protease inhibitor was a risk factor for plaque accumulation in
men with HIV (aRR = 1.12 per year of cumulative use; 95% CI, 1.01-1.25) but
not women with HIV.
“Our data support
earlier ART initiation, before CD4 counts decline, which may mitigate
HIV-associated increased CVD risks,” conclude the authors. “Better
understanding of these processes is necessary, both to prevent or delay CVD
development and to improve treatment strategies in the growing and increasingly
older HIV-infected population.”