NATAP: Subclinical Heart Disease in HIV-inflammation/activation

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Subject: NATAP: Subclinical Heart Disease in HIV-inflammation/activation'subclinical atherosclerosis in patients with HIV'......caused by inflammation due to activation in patients on HAART with 650 cd4s & undetectable viral load"These data have clinical relevance and suggest that patients with HIV with chronic infection have significant vascular inflammation, and thus added CVD risk, beyond that estimated by traditional risk factors.""This information should now be considered in determining optimal monitoring and CVD prevention strategies for this group""Future studies will be useful to further investigate unique immune-based mechanisms of arterial inflammation and potential agents to reduce the proatherogenic activation of monocytes and macrophages with hopes of reducing risk of atherothrombosis in patients infected with HIV."Arterial Inflammation in Patients With HIV - (07/25/12) JAMA. July 25 2012.....inflammation attracts plaque..."......data suggest a clinically relevant degree of added CVD risk due to increased arterial inflammation in the HIV population studied herein.....Our study demonstrates that HIV is associated with a high degree of inflammation within the arterial wall""One hundred percent of the patients with HIV studied were receiving ART and had been receiving such therapy for a long duration of approximately 12 years. A significant majority had undetectable HIV viral load......The patients we studied are similar to the majority of patients undergoing treatment with ART today, with well-controlled virus and absent history of CVD. Such patients.... are not considered to be at high risk for CVD, yet such patients have increased arterial wall inflammation, equal to that of patients without HIV with established CAD.""Participants infected with HIV vs noninfected control participants withsimilar cardiac risk factors had signs of increased arterial inflammation, which was associatedwith a circulating marker of monocyte and macrophage activation.....our data suggest monocyte and macrophage activation may be contributing""the signal that is observed likely reflects atherosclerotic inflammation with macrophage infiltration into arterial atheroma. The results from our study using the 18F-FDG-PET technique suggest that macrophage infiltration and resulting arterial inflammation, measured here in the aorta, are increased among patients infected with HIV.""Our observation that HIV infection is associated with increased arterial inflammation, even among relatively young patients with HIV with low FRS and undetectable viremia, is concordant with the epidemiological observations that patients with HIV have a higher risk of stroke and myocardial infarction than patients without HIV1 ,20 and demonstrates that this risk may not be measured adequately by traditional risk assessment tools, such as the FRS"