Among HIV-infected patients, high rates of myocardial infarction (MI) and sudden cardiac death have been observed. Exploring potential underlying mechanisms, we used multidetector spiral coronary computed tomography angiography (coronary CTA) to compare atherosclerotic plaque morphology in HIV-infected patients and non-HIV-infected controls.
Coronary atherosclerotic plaques visualized by CTA in HIV-infected (101) and non-HIV-infected (41) men without clinically apparent heart disease matched on cardiovascular risk factors were analyzed for three vulnerability features: low attenuation, positive remodeling, and spotty calcification.
Ninety-five percent of HIV-infected patients were receiving ART (median duration 7.9 years) and had well controlled disease (median CD4 cell count, 473 cells/μl; median HIV RNA <50 copies/ml). Age and traditional cardiovascular risk factors were similar in HIV-infected patients and controls. Among the HIV-infected (versus control) group, there was a higher prevalence of patients with at least one: low attenuation plaque (22.8 versus 7.3%, P = 0.02), positively remodeled plaque (49.5 versus 31.7%, P = 0.05) and high-risk 3-feature plaque (7.9 versus 0%, P = 0.02). Moreover, patients in the HIV-infected (versus control) group demonstrated a higher number of low attenuation plaques (P = 0.01) and positively remodeled plaques (P = 0.03) per patient.
Our data demonstrate an increased prevalence of vulnerable plaque features among relatively young HIV-infected patients. Differences in coronary atherosclerotic plaque morphology – namely, increased vulnerable plaque among HIV-infected patients – are here for the first time reported and may contribute to increased rates of MI and sudden cardiac death in this population.
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aProgram in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School
bCardiovascular Imaging Section, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
*M.V.Z. and S.A. contributed equally to the writing of this article.
Correspondence to Markella V. Zanni, MD, Program in Nutritional Metabolism, Massachusetts General Hospital, 55 Fruit Street, LON207, Boston, MA 02114, USA. Tel: +1 617 724 6926; fax: +1 617 724 8998; e-mail: email@example.com
Received 31 October, 2012
Revised 23 December, 2012
Accepted 9 January, 2013
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