Key result
HAART-naive HIV links to accelerated atherosclerosis, suggesting the virus per se is pro-atherogenic.
Why the study?
The relative contributions of HIV infection versus HAART to coronary heart disease risk remain unclear, with both implicated in pro-atherogenic metabolic derangements.
Case Report (n=1)
This case report suggests that HIV infection per se, independent of HAART, may contribute to accelerated atherosclerosis.
Should not yet change HIV management or screening; hypothesis-generating for infection as an independent atherosclerosis driver.
The pandemic spread of human immunodeficiency virus (HIV) has been the greatest challenge to public health in modern times. However today, people infected with HIV are living longer due to highly active antiretroviral therapy (HAART). This has resulted in age related complications like cardiovascular diseases, causing increased morbidity and mortality. The relative contributions of HIV infection versus potential adverse effects of HAART to coronary heart disease risk remains unclear. Recent reports implicate both HIV infection per se and HAART therapy to cause metabolic derangements which are pro-atherogenic. Here, we report a case of HIV infected young patient never exposed to HAART, presenting with accelerated atherosclerosis in aorta, coronary and carotid arteries.
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Kalyani et al. (2011) conducted a case report in HIV infection and accelerated atherosclerosis (n=1). HIV infection without HAART exposure was evaluated on Accelerated atherosclerosis in aorta, coronary and carotid arteries. A young HIV-infected patient never exposed to HAART presented with accelerated atherosclerosis in the aorta, coronary, and carotid arteries, suggesting HIV infection per se may be pro-atherogenic.
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