**8. Coronary artery disease in HIV**

HIV-infected patients are known to be at risk for premature coronary artery disease (CAD) [78]. Different factors related to HIV can lead to development atherosclerosis, including immune dysfunction, proliferation of T-cells, inflammation, endothelial dysfunction, and lipid abnormalities [79, 80]. During atherogenesis, HIV promotes monocyte penetration of the vascular intima to promote secretion of cytokines and expression of endothelial cell adhesion molecules [81]. The process of endothelial dysfunction in HIV patients may be driven by HIV transcription factors [82]. Increased risk of CVD in HIV infected patients is directly related to lower CD4 T-cell counts [83]. Higher number of activated CD8 T-cells is observed in relation to increased rates of coronary artery plaque and carotid artery stiffness [84].

In the early stage of HIV infection both total cholesterol and high-density lipoprotein cholesterol are decreased [85]. Lower levels of apolipoprotein B and smaller low-density lipoprotein cholesterol have been reported in more advanced stages of HIV infection [86]. In addition, deleterious metabolic effects such as dyslipidaemia and insulin resistance after exposure to certain ART treatments have been reported [79]. Recent studies observed that HIV infected patients presented with large thrombus burden than atherosclerotic plaques suggesting *de novo* arteriothrombosis and thrombophilia as possible causes of CAD events [87, 88].
