Table 2.

Summary of recent important developments in inflammatory markers of CHD in HIV

Outcome	Study	Major new findings	Summary of results
Mortality and HIV disease progression	SMART study [21••] (N=5472)	D-dimer and IL-6 levels associated with HIV progression and mortality	In an expanded case-control analysis (four controls per case), the OR (DC/VS) for mortality was 1.5 (95% CI, 0.8–2.8) and 1.4 (95% CI, 0.8–2.5) after adjustment for latest levels of IL-6 and D-dimer, respectively.
Mortality and HIV disease progression	FRAM [23••] (N=922)	Fibrinogen and hsCRP associated with a higher risk of all-cause mortality	Higher adjusted odds of death with: 2.6-fold higher with fibrinogen levels in the highest tertile (>406 mg/dL) and, 2.7-fold higher with higher CRP (>3 mg/L).
Subclinical atherosclerosis	Prospective cross-sectional study [36] (N=187)	Framingham risk score under predicts subclinical atherosclerosis	56% with low-risk Framingham risk scores had subclinical atherosclerosis associated with: MCP-1 (OR 1.027; 95% CI 1.004–1.050; P=0.020) oxidized LDL (OR 1.026; 95% CI 1.001–1.051; P=0.041).
cIMT and arterial stiffness	Prospective cross-sectional study [34] (37 subjects)	cIMT and femoral artery stiffness increased after initiation of antiretroviral therapy, but no correlation with biologic markers of inflammation	cIMT increased by 0.061±0.016 mm (P<0.001) in the ZDV/3TC/LPV/r arm and by 0.044±0.018 mm (P=0.012) in the NVP/LPV/r arm
cIMT, inflammation, endothelial activation	Prospective cross-sectional study [35••] (73 subjects; 21 controls)	Enhanced endothelial activation, inflammation, and increased cIMT occur in HIV-infected patients despite antiretroviral therapy	hsCRP, mg/L 5.43 (0.13–84.6) vs 1.53 (0.05–24.4) P<0.001 cIMT, 1.25 mm (0.75–3.23) vs 1.05 mm (0.75–1.35) P<0.001 IL-6, pg/mL 6.0 (0.8–270) vs 2.8 (1.0–8.2) P=0.008

CHD coronary heart disease; cIMT carotid intima media thickness; CRP C-reactive protein; hsCRP high-sensitivity CRP; IL interleukin; MCP-1 monocyte chemoattractant protein-1