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  51th ICAAC
Chicago, IL
September 17-20, 2011
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HCV and Homocysteine Boost Risk of Covert
Atherosclerosis in Spanish HIV Group

  51st Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC), September 17-20, 2011, Chicago

Mark Mascolini

Exposure to hepatitis C virus (HCV) and high homocysteine levels independently raised the risk of subclinical atherosclerosis (detected by pulse wave velocity) in a Spanish HIV population [1]. But rates of subclinical atherosclerosis were equivalent in this HIV group and the general Spanish population.

Researchers from the University Hospital Virgen de las Nieves in Granada noted that Spain is a relatively low cardiovascular risk area. But because HIV-positive people typically run a higher risk of cardiovascular disease than the general population, the investigators planned this cross-sectional study of 132 consecutive HIV-positive adults, using pulse wave velocity (a measure of arterial stiffness) to detect subclinical atherosclerosis, defined as a value at or above than 12 m/s. They compared findings in this group with published results on the general Spanish population.

The HIV group included 90 men and 42 women with average ages of 43 and 42 years. Time since HIV diagnosis averaged 119 months, and 70 people (53%) had AIDS. Equivalent proportions got infected with HIV during heterosexual sex (29.5%), sex between men (29.5%) and injection drug use (27.3%). The others were infected via transfusion or unrecorded routes.

Only 6 people (4.5%) had a family history of cardiovascular disease and only 7 (5%) had type 2 diabetes. But 43 people (33%) were being treated for hypertension, and 26 (20%) had high lipids. Eighty-six people (65%) smoked and 35 (26.5%) met criteria for metabolic syndrome. Fifty-one people (39%) had anti-HCV antibodies and 9 (7%) had chronic HBV infection.

CD4 count on enrollment in the study cohort averaged 549 and viral load averaged 19,685 copies. Viral load at HIV diagnosis stood at 210,887 copies, and nadir CD4 count averaged 233.5. Thirty people (23%) had never taken antiretrovirals. Among the 102 who had, treatment duration averaged 23 months and only 20 (20%) had a record of virologic failure.

Total cholesterol averaged 186.5 mg/dL, low-density lipoprotein cholesterol 107.75 mg/dL, and triglycerides 157.75 mg/dL. Fasting glucose averaged 97.2 mg/dL, creatinine clearance 92.5 mL/h, and homocysteine 12.4 umol/L. Ten-year Framingham cardiovascular risk score averaged 15.6.

Pulse wave velocity averaged 9.56 +/- 2.03, and 15 people (11.4%) had a pulse wave velocity above 12 m/s, indicating subclinical atherosclerosis. Pulse wave velocity did not correlate with Framingham-calculated cardiovascular risk, and prevalence of pulse wave velocity indicating subclinical atherosclerosis in the HIV group did not differ from prevalence in the general Spanish population.

Age averaged 51.9 in HIV-positive people with a pulse wave velocity at or above 12 m/s and 41.5 in people with a lower pulse wave velocity. Among the 15 people with a pulse wave velocity at or above 12 m/s, 10 (67%) were anti-HCV positive, while 41 of 117 (35%) with a lower pulse wave velocity were anti-HCV positive. Multivariate analysis determined that older people had a 15% higher risk of subclinical atherosclerosis (odds ratio [OR] 1.15, 95% confidence interval [CI] 1.06 to 1.25, P = 0.001). Anti-HCV positivity raised the risk of subclinical atherosclerosis more than 6 times (OR 6.57, 95% CI 1.41 to 30.60, P = 0.016).

Among the 51 people coinfected with HIV and HCV, homocysteine level averaged 13.87 +/- 4.83 umol/L. Among the 81 people infected only with HIV, homocysteine averaged 11.2 +/- 4.23 umol/L. Multivariate analysis determined that higher homocysteine raised the risk of subclinical atherosclerosis almost 25% (OR 1.24, 95% CI 1.084 to 1.43, P = 0.02).

High homocysteine can reflect alcoholism or deficiencies in folic acid (B9), pyridoxine (B6), or cobalamin (B12). Elevated homocysteine is associated with a higher risk of heart disease, but homocysteine-lowering therapies have failed to reduce cardiovascular event rates [2].

Numerous studies have assessed arterial stiffness determined by pulse wave velocity as a cardiovascular risk marker in treated and untreated people with HIV [3-5].


1. Hidalgo Tenorio C, Jarilla F, Pasquau J, et al. The relationship between subclinical atherosclerosis in HIV patients and cardiovascular risk factors. 51st Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC). September 17-20, 2011. Chicago. Abstract H1-1392.

2. Abraham JM, Cho L. The homocysteine hypothesis: still relevant to the prevention and treatment of cardiovascular disease? Cleve Clin J Med. 2010;77:911-918. http://www.ccjm.org/content/77/12/911.long.

3. Ho JE, Deeks SG, Hecht FM, et al. Initiation of antiretroviral therapy at higher nadir CD4+ T-cell counts is associated with reduced arterial stiffness in HIV-infected individuals. AIDS. 2010;24:1897-905. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903431/?tool=pubmed.

4. Schillaci G, De Socio GV, Pucci G, et al. Aortic stiffness in untreated adult patients with human immunodeficiency virus infection. Hypertension. 2008;52:308-313. http://hyper.ahajournals.org/content/52/2/308.long.

5. Schillaci G, De Socio GV, Pirro M, et al. Impact of treatment with protease inhibitors on aortic stiffness in adult patients with human immunodeficiency virus infection. Arterioscler Thromb Vasc Biol. 2005;25:2381-2385. http://atvb.ahajournals.org/content/25/11/2381.long.