Human Immunodeficiency Virus Associated Large Artery Disease

Abstract

Advances in human immunodeficiency virus (HIV) therapy with highly active antiretroviral agents has increased the longevity of patients afflicted with this disease. HIV vasculopathy is a unique disease entity presenting as aneurysms, dissections and vascular occlusion amongst others due to HIV related vasculitis. A few studies have investigated the pathogenesis of HIV related vasculopathy. This chapter provides a brief overview of aortic aneurysms in general. Further, the current understanding of the pathogenic mechanisms underlying HIV vasculopathy with an emphasis on inflammatory mediators, histology, clinical presentation and imaging are discussed. Finally, a summary regarding management of HIV associated large vessel disease is presented.

HIV-Positive Patient With Non-Percutaneous Coronary Intervention (PCI)-Amenable Left Coronary Artery Aneurysms Presenting With ST-Elevation Myocardial Infarction (STEMI)

“…Molecular mimicry is less understood but may play a part in aneurysm formation as it is theorized that the virus and its toxic by-products share ligands that are characterized by DNA sequence similarities to the viral envelope glycoprotein gp41 and gp120. This may result in autoimmune-mediated cell damage during infection and direct viral invasion of the aortic fibroblasts at the level of the adventitia [9]. Furthermore, external causes can also lead to the propagation of premature CAD and aneurysmal formation in HIV-positive patients given comorbidities associated with HIV with the aforementioned conditions exacerbated by daily habits including smoking and illicit drug use [11][12][13].…”

“…The reason for coronary aneurysms and atherosclerosis in HIV-positive patients stems from three main mechanisms and the vasculopathy associated with: inflammation and endothelial injury, smooth muscle cell proliferation and migration, and molecular mimicry [ 7 ]. Inflammation and endothelial cell dysfunction begin with an increase in inflammatory mediators such as interleukins and tumor necrosis factor-alpha, increased oxidative stress, and a decrease in CD4 count all of which lead to an increase in inflammation and immune dysfunction [ 8 - 9 ]. The inflammatory and endothelial changes lead to dyslipidemia, thrombosis, and endothelial dysfunction, all of which increase the risk of atherosclerosis and coronary aneurysms [ 9 - 10 ].…”

“…Inflammation and endothelial cell dysfunction begin with an increase in inflammatory mediators such as interleukins and tumor necrosis factor-alpha, increased oxidative stress, and a decrease in CD4 count all of which lead to an increase in inflammation and immune dysfunction [ 8 - 9 ]. The inflammatory and endothelial changes lead to dyslipidemia, thrombosis, and endothelial dysfunction, all of which increase the risk of atherosclerosis and coronary aneurysms [ 9 - 10 ].…”

“…Smooth muscle cell proliferation and migration occur as the muscularis media possess surface receptors facilitating the entry of the HIV virus into host cells, which would lead to infiltration, disorder, and thinning of the medial layer. The entry of the viral envelope protein also has been reported to activate tissue factor 2, which is a potent pro-coagulant inducing thrombosis and ligand production thought to be instrumental in promoting atherogenesis [ 9 ]. Molecular mimicry is less understood but may play a part in aneurysm formation as it is theorized that the virus and its toxic by-products share ligands that are characterized by DNA sequence similarities to the viral envelope glycoprotein gp41 and gp120.…”

Spectrum of ascending aortic aneurysms at a peri-urban tertiary hospital: an echocardiography-based study

“…In terms of the main aetiologies causing TAA aneurysms, it is well documented that atherosclerosis, hypertension, connective tissue and inflammatory disease, congenital heart disease, and infectious causes such as syphilis and human immunodeficiency virus (HIV) can cause TAA aneurysms ( 5 ). Further to this, ethnicity, geography, and burden of risk factors can also dictate the pattern of aneurysmal disease of the aorta ( 4 ).…”