Atherosclerosis in HIV Patients: a New Face for an Old Disease?

As we have become more familiar with the pathogenesis of atheroma, it has become recognizedatherogenesis is mainly an inflammatory disease. Therefore, it is not surprising that a body of evidencedemonstrates that endothelium injury is associated with the progression and severity of HIVinfection. Another important question is: do antiretroviral drugs increase or reduce endothelial injury?Various studies support the hypothesis that HAART does induce activation of endothelial function.Thus, HIV virus as well as immune reconstitution and HAART itself promote premature endothelialactivation. Such a prominent role played by inflammatory events could affect the structure ofthe arterial lesions in HIV patients that could present different characteristics with respect to theclassical atheroma. In fact, in two HIV patients with severe stenosis of the carotid, histology revealedextensive inflammatory infiltration of the vascular wall. The characteristics of these lesions weresimilar to those of arteritis. Another study evidenced that the ultrasonographic structure of the lesionsin HIV patients substantially differ from those found in atherosclerosis, sharing similar characteristicswith arteritis.We hypothesize that the atherosclerotic lesions in HIV patients develop in two distinct phases: thefirst one characterized by an inflammation of the vascular wall, and subsequently, the lesions couldevolve towards the classic feature of the atheroma. The lesions in the first phase are probably determinedby immunodeficiency, immune reconstitution, and the same effect of HAART. In the secondphase they could be maintained by the classic risk factors.