Artery
Elasticity Is Reduced in People with Untreated HIV Infection
 | Using
a non-invasive technique known as pulse waveform analysis, investigators determined
that elasticity of both small and large blood vessels is reduced -- an indicator
of atherosclerosis -- in untreated people with HIV, according to a report in the
September
2009 Journal of Acquired Immune Deficiency Syndromes. |
|
A
growing body of research indicates that people with
HIV have a higher risk of cardiovascular
disease, but it is not yet clear whether this is due to HIV infection itself,
antiretroviral therapy (ART),
or traditional cardiovascular risk factors in an aging population. Atherosclerosis,
or loss of elasticity and build-up of plaque within the arteries, can restrict
blood supply to the heart, leading to myocardial infarction. Recent research indicates
that HIV infection is an independent risk factor for atherosclerosis
based on measurement of carotid intima-media thickness, or thickness of the walls
of the major arteries in the neck. Now, a study using a different technique has
produced concordant results.
Jason
Baker and colleagues estimated large and small artery elasticity in 32 untreated
HIV positive study participants and 30 HIV negative control subjects by analyzing
radial pulse waveforms, a technique that reveals evidence of early, preclinical
atherosclerosis. Individuals with pre-existing clinical atherosclerotic disease
(e.g., previous myocardial infarction or chronic angina) were excluded. Differences
in elasticity were compared with and without adjustment for Framingham cardiovascular
risk. The researchers also took into account demographic characteristics and risk
factors including sex, age, race/ethnicity, smoking, injection drug use, hepatitis
C virus (HCV) coinfection, and high-density lipoprotein (HDL or "good")
and non-HDL cholesterol levels. Results  | HIV
infection was associated with reduced large artery elasticity (-2.55 mL/mm Hg
× 10; P = 0.02) and small artery elasticity (-1.50 mL/mm Hg × 100;
P = 0.02). |  | Associations
with traditional risk factors were often stronger for small compared with large
artery elasticity. |  | After
adjusting for other factors, artery elasticity differences between HIV positive
and HIV negative participants were similar regardless of method of analysis. |  | HCV
coinfection was associated with reduced small artery elasticity, but its effect
on large artery elasticity did not reach statistical significance. |  | Fasting
blood lipid levels were not significantly associated with large or small artery
elasticity. |  | CD4
cell count and HIV RNA level likewise were not associated with large or small
artery elasticity among HIV positive participants. |
"Untreated
HIV infection is associated with impaired arterial elasticity, of both the large
and small vasculature, after controlling for additional risk factors," the
study authors concluded. "The degree of HIV-related impairment reported in
arterial elasticity is clinically relevant." "Pulse
waveform analysis is a noninvasive technique to assess cardiovascular disease
risk that should be evaluated in larger studies of HIV-infected persons,"
they added. Large
artery elasticity reflects damage to major central arteries, while small artery
elasticity reflects the condition of the peripheral or distal circulation. "Our
findings suggest that HIV-mediated vessel damage and dysfunction are present throughout
the arterial vasculature," the researchers noted. While
the mechanisms underlying blood vessel damage and cardiovascular disease in HIV
positive people is not fully understood, the authors suggested that inflammation
and immune activation related to chronic viral infection likely plays a role. Department
of Medicine, Hennepin County Medical Center, Minneapolis, MN; School of Medicine
and Department of Biostatistics, School of Public Health, University of Minnesota,
Minneapolis, MN. 9/11/09 Reference JV
Baker, D Duprez, J Rapkin, and others. Untreated HIV Infection and Large and Small
Artery Elasticity. Journal of Acquired Immune Deficiency Syndromes 52(1):
25-31. September 2009. (Abstract).
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