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HIV Infection Is an Independent Risk Factor for Atherosclerosis Similar in Magnitude to Traditional Cardiovascular Disease Risk Factors
Carl Grunfeld*1,2, J Delaney3, C Wanke4, J Currier5, R Scherzer1,2, M Biggs3, S Sidney6, J Polak7, D O'Leary7, R Kronmal3, and FRAM Study
1Univ of California, San Francisco, US; 2VAMC, San Francisco, CA, US; 3Univ of Washington, Seattle, US; 4Tufts Univ Sch of Med, Boston, MA, US; 5Univ of California, Los Angeles, US; 6Kaiser Permanente, Oakland, CA, US; and 7Tufts Med Ctr, Boston, MA, US
Background: Atherosclerotic cardiovascular disease
(CVD) is an increasing cause of morbidity and mortality in HIV-infected
patients. However, it is unknown whether HIV infection contributes to
accelerated development of atherosclerosis independent of traditional CVD risk
factors. Therefore, we compared pre-clinical atherosclerosis quantified by
carotid intima medial thickness (IMT) among HIV-infected and control subjects
after adjustment for traditional CVD risk factors.
Methods: This was a cross-sectional study of
HIV-infected (n = 433) and control (n = 5749) subjects without previous CVD
events. Subjects were selected for common age range (37 to 78 years) from the
studies, Fat Redistribution and Metabolic Change in HIV Infection (Framingham
Study), Coronary Artery Risk Development in
Young Adults (CARDIA), and the Multi-Ethnic Study of Atherosclerosis
(MESA). Carotid scans were read by a single reading center and adjusted for
reader effect. The association between HIV infection and IMT was estimated using
a multivariable, linear generalized estimating equation.
Results: For internal carotid, mean maximal IMT was
1.17±0.50 mm for HIV-infected subjects and 1.06±0.58 mm for controls (p <0.0001).
After multivariable adjustment for demographic characteristics (age, gender,
and race), the adjusted mean difference of HIV-infected vs controls was +0.188 mm
(95%CI 0.113 to 0.263, p <0.0001). Further adjustment for traditional
CVD risk factors (smoking, diabetes, systolic and diastolic blood pressure,
total and HDL cholesterol) modestly attenuated the HIV effect (+0.148 mm, 95%CI
0.072 to 0.224, p = 0.0001). For the common carotid, HIV infection was also
independently associated with greater IMT (+0.033 mm, 95%CI 0.010, 0.056, p
= 0.005). The association of HIV infection with IMT was similar to that of
traditional risk factors such as smoking which was associated with greater IMT
(internal +0.173 mm, common +0.020 mm). The HIV association with IMT was
somewhat stronger among women than in men (HIV by gender interactions p =
0.046 and p = 0.003, for internal and common).
Conclusions: Even after adjustment for traditional
CVD risk factors, HIV infection was characterized by more severe
atherosclerosis as measured by carotid IMT. This study found an independent association
of HIV infection with carotid IMT similar in magnitude to that of traditional
CVD risk factors, such as smoking.
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