HIV infection is associated with a pro-inflammatory and thrombophilic state but little is known about the link between inflammation and thrombosis in treatment-naïve patients with acute coronary syndromes (ACS). Prospective single centre study was conducted in Soweto, South Africa, comparing markers of inflammation and endothelial cell activation in highly active anti-retroviral therapy-naïve HIV positive and negative patients presenting with ACS. Between March 2004 and February 2008, 30 consecutive black South African HIV patients with ACS were compared to 30 black HIV negative patients with ACS. The HIV patients were younger (43 ± 7 vs. 54 ± 13, p = 0.004) and besides smoking (73% vs. 33%, p = 0.002) and lower HDL levels (0.8 ± 0.3 vs. 1.1 ± 0.4, p = 0.001) had fewer risk factors than the control group. At baseline, HIV patients had higher levels of tumour necrosis factor-α [5.8 (1.7 - 15.0) vs. 0.19 (0.19 - 19.8) ng/ml, p = 0.0004] and vascular cell adhesion molecule-1 [263.3 (0.38 - 778.5) vs. 151.3 (80.6 - 416.3) ng/ml, p = 0.007] compared to HIV negative patients as well as higher levels of macrophage chemoattractant protein-1 at six months [70 (30 -130) vs. 50 (30 - 90) ng/L, p = 0.004]. Treatment-naïve black South African patients with HIV and ACS have evidence of a pro-inflammatory state and greater degree of endothelial cell activation compared to HIV negative patients, both of which may play a direct role in the pathogenesis of ACS in this otherwise low risk population. MCP-1 may play an important role in HIV-associated coronary artery disease.
Key words: Human immunodeficiency virus (HIV), acute coronary syndrome (ACS), inflammation, endothelial dysfunction, thrombosis.
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