Volume 27, Issue 3 pp. 173-179

Carotid intima–media thickness in HIV patients treated with antiretroviral therapy

Anne-Mette Lebech

Anne-Mette Lebech

Department of Infectious Diseases, Hvidovre University Hospital, Hvidovre

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Niels Wiinberg

Niels Wiinberg

Department of Clinical Physiology & Nuclear Medicine, Frederiksberg University Hospital, Frederiksberg

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Ulrik Sloth Kristoffersen

Ulrik Sloth Kristoffersen

Clinic of Clinical Physiology, Nuclear Medicine & PET

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Birger Hesse

Birger Hesse

Clinic of Clinical Physiology, Nuclear Medicine & PET

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Claus Leth Petersen

Claus Leth Petersen

Department of Clinical Physiology & Nuclear Medicine, Frederiksberg University Hospital, Frederiksberg

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Jan Gerstoft

Jan Gerstoft

Department of Infectious Diseases, Rigshospitalet University Hospital, Copenhagen

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Andreas Kjær

Andreas Kjær

Clinic of Clinical Physiology, Nuclear Medicine & PET

Cluster for Molecular Imaging, University of Copenhagen, Copenhagen, Denmark

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First published: 07 March 2007
Citations: 21
A. Lebech, Department of Infectious Diseases,
Hvidovre University Hospital, Kettegaard Allé 30,
DK 2650 Hvidovre, Denmark
E-mail: [email protected]

Summary

Introduction: Increased cardiovascular risk in HIV patients in antiretroviral therapy (ART) may be due to HIV infection, direct effect of ART or dyslipidaemia induced by ART. Our aim was to study the relative importance of HIV, ART and dyslipidaemia on atherosclerosis, assessed by the comparison of carotid artery intima–media thickness (IMT) in non-smoking HIV patients with high or low serum cholesterol levels as well as in healthy volunteers.

Methods : HIV patients in ART with normal cholesterol (≤5·5 mmol l−1; n = 13) or high cholesterol (≥6·5 mmol l−1; n = 12) as well as healthy controls (n = 14) were included. All were non-smokers and had never received medication for dyslipidaemia or hypertension. IMT was measured by ultrasonography.

Results : In HIV patients with normal cholesterol (≤5·5 mmol l−1), in HIV patients with hypercholesterolaemia (≥6·5 mmol l−1) and in controls (5·1 ± 0·9 mmol l−1) IMT were 683 ± 119, 656 ± 99 and 657 ± 99 μm, respectively. Thus no difference in IMT was found between the three groups. IMT values did not differ between patients receiving and not receiving protease inhibitors (658 ± 117 μm versus 687 ± 97 μm, P>0·05). In HIV patients IMT correlated inversely with HDL cholesterol levels (r = −0·50; P = 0·01), whereas no correlation was found with total cholesterol or LDL cholesterol.

Conclusions : In non-smoking HIV patients receiving ART no sign of accelerated atherosclerosis was found as assessed by IMT even not in hypercholesterolaemic HIV patients. IMT correlated with HDL cholesterol but not with LDL cholesterol. Based on these observations, one could speculate whether selective lowering of LDL cholesterol will be successful in reducing cardiovascular risk in non-smoking HIV patients.

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