Relation of Oxidative Biomarkers, Vascular Dysfunction, and Progression of Coronary Artery Calcium

Ahmadi, Naser; Tsimikas, Sotirios; Hajsadeghi, Fereshteh; Saeed, Anila; Nabavi, Vahid; Bevinal, Manzoor A.; Kadakia, Jigar; Flores, Ferdinand; Ebrahimi, Ramin; Budoff, Matthew J.

doi:10.1016/j.amjcard.2009.09.052

« Previous Next »American Journal of Cardiology
Volume 105, Issue 4 , Pages 459-466, 15 February 2010

Relation of Oxidative Biomarkers, Vascular Dysfunction, and Progression of Coronary Artery Calcium

Naser Ahmadi, MD
- Los Angeles Biomedical Research Institute, Harbor UCLA Medical Center, Torrance, California
Sotirios Tsimikas, MD
- Vascular Medicine Program, University of California, San Diego, San Diego, California
Fereshteh Hajsadeghi, MD
- Los Angeles Biomedical Research Institute, Harbor UCLA Medical Center, Torrance, California
Anila Saeed, MD
- Los Angeles Biomedical Research Institute, Harbor UCLA Medical Center, Torrance, California
Vahid Nabavi, MD
- Los Angeles Biomedical Research Institute, Harbor UCLA Medical Center, Torrance, California
Manzoor A. Bevinal, MD
- Los Angeles Biomedical Research Institute, Harbor UCLA Medical Center, Torrance, California
Jigar Kadakia, MD
- Los Angeles Biomedical Research Institute, Harbor UCLA Medical Center, Torrance, California
Ferdinand Flores, MD
- Los Angeles Biomedical Research Institute, Harbor UCLA Medical Center, Torrance, California
Ramin Ebrahimi, MD
- Veterans Affairs Greater Los Angeles Health Care System, University of California, Los Angeles, Los Angeles, California
Matthew J. Budoff, MD
- Los Angeles Biomedical Research Institute, Harbor UCLA Medical Center, Torrance, California
- Corresponding author: Tel: (310) 222-4107; fax: (310) 787-0448

Received 21 August 2009; received in revised form 25 September 2009; accepted 25 September 2009.

The relation between oxidative stress and coronary artery calcium (CAC) progression is currently not well described. The present study evaluated the relation among the biomarkers of oxidative stress, vascular dysfunction, and CAC. Sixty asymptomatic subjects participated in a randomized trial evaluating the effect of aged garlic extract plus supplement versus placebo and underwent measurement of CAC. The postcuff deflation temperature-rebound index of vascular function was assessed using a reactive hyperemia procedure. The content of oxidized phospholipids (OxPL) on apolipoprotein B-100 (apoB) particles detected by antibody E06 (OxPL/apoB), lipoprotein(a), IgG and IgM autoantibodies to malondialdehyde–low-density lipoprotein and apoB-immune complexes were measured at baseline and after 12 months of treatment. CAC progression was defined as an annual increase in CAC >15%. Vascular dysfunction was defined according to the tertiles of temperature-rebound at 1 year of follow-up. From baseline to 12 months, a strong inverse correlation was noted between an increase in CAC scores and increases in temperature-rebound (r² = −0.90), OxPL/apoB (r² = −0.85), and lipoprotein(a) (r² = −0.81) levels (p <0.0001 for all). The improvement in temperature-rebound correlated positively with the increases in OxPL/apoB (r² = 0.81, p = 0.0008) and lipoprotein(a) (r² = 0.79, p = 0.0001) but inversely with autoantibodies to malondialdehyde–low-density lipoprotein and apoB-immune complexes. The greatest CAC progression was noted with the lowest tertiles of increases in temperature-rebound, OxPL/apoB and lipoprotein(a) and the highest tertiles of increases in IgG and IgM malondialdehyde–low-density lipoprotein. In conclusion, the present results have documented a strong relation among markers of oxidative stress, vascular dysfunction, and progression of coronary atherosclerosis. Increases in OxPL/apoB and lipoprotein(a) correlated strongly with increases in vascular function and predicted a lack of progression of CAC.