As we have become more familiar with the pathogenesis of atheroma, it has become recognized atherogenesis is mainly an inflammatory disease. Therefore, it is not surprising that a body of evidence demonstrates that endothelium injury is associated with the progression and severity of HIV infection. 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 endothelial activation. Such a prominent role played by inflammatory events could affect the structure of the arterial lesions in HIV patients that could present different characteristics with respect to the classical atheroma. In fact, in two HIV patients with severe stenosis of the carotid, histology revealed extensive inflammatory infiltration of the vascular wall. The characteristics of these lesions were similar to those of arteritis. Another study evidenced that the ultrasonographic structure of the lesions in HIV patients substantially differ from those found in atherosclerosis, sharing similar characteristics with arteritis. We hypothesize that the atherosclerotic lesions in HIV patients develop in two distinct phases: the first one characterized by an inflammation of the vascular wall, and subsequently, the lesions could evolve towards the classic feature of the atheroma. The lesions in the first phase are probably determined by immunodeficiency, immune reconstitution, and the same effect of HAART. In the second phase they could be maintained by the classic risk factors.
|Number of pages||6|
|Publication status||Published - Oct 2006|
- Antiretroviral therapy
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