 |
|
|
| |
HIV Has as Much Impact on Heart Health as Traditional Risk Factors
|
| |
| |
16th Conference on Retroviruses and Opportunistic Infections,
February 8-11, 2009, Montreal
Mark Mascolini
HIV itself emerged as an atherosclerosis risk factor as potent at age, male gender, smoking, and diabetes [1]. Carl Grunfeld and FRAM colleagues also uncovered an important clue to why some studies show a higher HIV-related atherosclerosis risk by measuring carotid intima media thickness (IMT) and some do not.
FRAM investigators focused on carotid IMT because it reliably predicts cardiovascular disease. Grunfeld noted that studies of IMT in people with HIV disagree: While two studies tied HIV infection to increased IMT, 5 did not. The two positive studies evaluated IMT in both the common carotid and the internal/bulb region, whereas the five negative studies looked only at the common carotid, which is easier to assess.
Comparing HIV-infected people in the US with uninfected controls, the original FRAM study isolated peripheral and central fat atrophy as the hallmark of HIV lipodystrophy [2]. The second FRAM exam, conducted in 2005-2007, included carotid IMT measurement. The new analysis involved HIV-infected FRAM participants, FRAM's original HIV-negative controls, and a second set of uninfected US controls. All told, there were 433 people with HIV and 5749 controls without HIV, all of whom had carotid ultrasound of both the common carotid and the internal/bulb region.
The HIV group was younger than the control group (median 49 vs 60 years) and included a higher proportion of men (70% vs 47%). The FRAM HIV group was 51% white, 42% black, and 7% Hispanic, compared with proportions of 44%, 32%, and 24% in the control group. The HIV-infected contingent had a much higher proportion of current smokers (36% vs 15%) and a bigger share of people taking lipid-lowering therapy (24% vs 16%). Average triglycerides were higher in the HIV group than in controls (198 vs 130 mg/dL). Slightly higher proportions of controls had diabetes (13.5% vs 8.7%) and were taking antihypertensives (33% vs 27%).
When measured in the internal/bulb carotid, average IMT proved significantly wider in the HIV group than in controls (1.17 vs 1.06 mm, P < 0.0001). After statistical adjustment for demographics (age, race, gender), the mean difference between the HIV group and controls was 0.19 mm, still a highly significant difference (P < 0.0001). After further adjustment for cardiovascular risk factors (smoking, diabetes, lipids, blood pressure), the difference waned to 0.15 mm but remained highly significant (P = 0.0001).
When measured in the common carotid, mean IMT was 0.88 mm with HIV and 0.86 mm without HIV, a nonsignificant difference (P = 0.17). Mean common carotid IMT difference between HIV-infected people and controls reached statistical significance after adjustment for demographics and cardiovascular risk factors, but the differences were much smaller than when measuring IMT in the internal/bulb carotid.
In multivariate analysis, HIV infection had an estimated impact on internal/bulb carotid IMT thickness equivalent to the impact of numerous classic heart risk factors: male gender, current smoking, diabetes, and each 10 years of age:
• HIV infection: internal carotid IMT 0.15 mm (P < 0.001)
• Male gender: internal carotid IMT 0.13 mm (P < 0.0001)
• Current smoking: internal carotid IMT 0.17 mm (P < 0.0001
• Diabetes: internal carotid IMT 0.12 mm (P < 0.0001)
• 10 years of age: internal carotid IMT 0.16 mm (P < 0.0001)
In this analysis, HIV had a substantially greater estimated effect on internal carotid IMT than systolic blood pressure (0.05 mm) or total cholesterol (0.009 mm).
The estimated impact of HIV on internal/bulb IMT was greater in women (0.20 mm) than in men (0.13 mm) (P = 0.046), whereas current smoking and diabetes had equivalent estimated impacts on internal/bulb IMT in men and women.
Grunfeld concluded that the association between HIV and carotid IMT "is similar in magnitude to that of traditional cardiovascular risk factors such as smoking, diabetes, and gender." That HIV link may be more robust in women than in men. Finally, he suggested that the stronger correlation between HIV and IMT in the internal/bulb region than in the common carotid could explain apparent discrepancies in earlier studies of HIV and IMT.
From Jules: I asked Grunfeld at the microphone about separating out the effects of HIV and HAART as patients in this study were on HAART. He said the signal for carotid IMT was of greater magnitude than expected from ARTs so therefore HIV must play a role. In response I would say both HIV and HAART could be at play.
References
1. Grunfeld C, J Delaney J, Wanke C, et al. HIV infection is an independent risk factor for atherosclerosis similar in magnitude to traditional cardiovascular disease risk factors. 16th Conference on Retroviruses and Opportunistic Infections, February 8-11, 2009, Montreal. Abstract 146.
2. Bacchetti P, Gripshover B, Grunfeld C, et al. Fat distribution in men with HIV infection. Study of Fat Redistribution and Metabolic Change in HIV Infection (FRAM). J Acquir Immune Defic Syndr. 2005;40:121-31.
|
| |
|
|
|
|
|
