Arterial disease in patients with human immunodeficiency virus infection: what has imaging taught us?
With advances in antiretroviral therapy (ART), individuals with human immunodeficiency virus (HIV) infection are living longer and increasingly die of non-HIV-related diseases, such as cardiovascular disease (CVD). Several observational studies suggest that HIV-infected patients on ART are at increased risk of CVD; however, the precise mechanisms underlying the association between HIV infection and CVD risk are uncertain. Atherosclerosis and arterial disease in HIV-infected individuals is a multifactorial process with several potential targets for research and therapeutic intervention. This paper critically reviews the contributions of imaging to our understanding of arterial disease, atherosclerosis, and CVD risk in HIV-infected individuals. In general, the findings of studies using carotid ultrasound, coronary computed tomographic angiography, and aortic positron emission tomography agree with those from observational studies of CVD events and suggest that HIV infection is associated with an increased risk of CVD. Observational studies of CVD outcomes and studies using carotid intima-media thickness suggest that there is a moderate increase in CVD risk related to HIV serostatus. Less can be said about the role of ART and specific ART therapies in CVD risk, mainly because imaging studies have had serious methodological limitations that diminish their generalizability. Brachial artery reactivity testing has been especially useful for elucidating the arterial pathophysiology of HIV infection and its treatments, as well as the arterial effects of interventions for treating HIV and dyslipidemia. Aortic positron emission tomography has been especially useful for evaluating arterial inflammation. Coronary artery calcium has not proven to be a useful marker of subclinical atherosclerosis in HIV-infected individuals. Imaging studies support the intriguing hypothesis that persistent inflammation and immune dysregulation contribute to increased CVD risk among treated and suppressed patients with HIV infection.
University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, Wisconsin. Electronic address: jhs@medicine.wisc.edu.
James H
JH
Stein
David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California.
Judith S
JS
Currier
Division of Cardiology, University of California-San Francisco, San Francisco, California.
Priscilla Y
PY
Hsue
D059168:Carotid Intima-Media Thickness; D002423:Cause of Death; D003952:Diagnostic Imaging / Q000379:methods*; D014943:Global Health; D006678:HIV; D015658:HIV Infections / Q000150:complications* / Q000401:mortality; D006801:Humans; D015994:Incidence; D058729:Peripheral Arterial Disease / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology; D018570:Risk Assessment; D012307:Risk Factors
HIV; carotid intima-media thickness; coronary arteries; endothelial function; ultrasound