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J Am Coll Cardiol, 2001; 38:1662-1667
© 2001 by the American College of Cardiology Foundation
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Irbesartan, an angiotensin type 1 receptor inhibitor, regulates the vascular oxidative state in patients with coronary artery disease

Bobby V. Khan, MD, PhD*,* {dagger} {ddagger}, Sushant Navalkar, MD* {dagger} {ddagger}, Qamar A. Khan, MD, FACC* {ddagger}, Syed T. Rahman, MD* {ddagger} and Sampath Parthasarathy, PhD{dagger} {ddagger}

* Emory University School of Medicine, Division of Cardiology, Atlanta Center for Vascular Research, Atlanta, Georgia, USA
{dagger} Emory University School of Medicine, Division of Gynecology/Obstetrics and, Atlanta Center for Vascular Research, Atlanta, Georgia, USA
{ddagger} Emory University School of Medicine, Division of Atlanta Center for Vascular Research, Atlanta, Georgia, USA



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Figure 1 Irbesartan decreases susceptibility to low-density lipoprotein (LDL) oxidation in patients with coronary artery disease (CAD). Patients with CAD were placed on placebo or irbesartan (150 mg/day) for a 12-week period. Serum samples were collected at the start of the study (0 weeks) and at 4 and 12 weeks of treatment. The LDL was isolated by centrifugation, and rate of oxidation was measured by spectrophotometric analysis as described in the Methods section. The p value, as determined by analysis of variance, was 0.027 for time, <0.0001 for group and 0.014 for the group-time interaction. Black diamond = placebo; black square = irbesartan; *p < 0.05 = difference between 0 weeks and 4 or 12 weeks within each group; #p < 0.05 = difference between placebo and irbesartan groups.

 


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Figure 2 Irbesartan decreases monocyte binding the CD11b monoclonal antibody in patients with coronary artery disease (CAD). Patients with CAD were placed on placebo or irbesartan (150 mg/day) for a 12-week period. Serum samples were collected and red blood cells were lysed. Using flow cytometry analysis, whole-blood monocyte CD11b expression was performed. The values expressed are a percentage of expression of CD11b by circulating monocytes. The p value, as determined by analysis of variance, was <0.0001 for time, for group and for the group-time interaction. Black square = placebo; white square = irbesartan; *p < 0.05 = difference between 0 weeks and 4 or 12 weeks within each group; #p < 0.05 = difference between placebo and irbesartan groups.

 


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Figure 3 Irbesartan decreases production of superoxide in the neutrophils of patients with coronary artery disease. Serum samples were collected from the patients who were placed on placebo or irbesartan (150 mg/day) for a 12-week period. Samples were collected at the start of the study (0 weeks) and at 4 and 12 weeks of treatment. The neutrophils were isolated and the peak levels of superoxide production after neutrophil respiratory burst were performed. The p value was <0.0001, as determined by analysis of variance, for time, for group and for the group-time interaction. Black diamond = placebo; black square = irbesartan; *p < 0.05 = difference between 0 and 4 or 12 weeks within each group; #p < 0.05 = difference between placebo and irbesartan groups.

 


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Figure 4 Irbesartan decreases lipid peroxidation in the serum of patients with coronary artery disease. Serum samples were collected during the 12-week period of treatment at the start of the study (0 weeks) and at 4 and 12 weeks of treatment. The thiobarbituric acid reactive substances (TBARS) assay was performed, as described in the Methods section, using spectrophotometric analysis at 568 nm. The p value, as determined by analysis of variance, was 0.027 for time, 0.012 for the group and 0.004 for the group-time interaction. Black square = placebo; white square = irbesartan; *p < 0.05 = difference between 0 weeks and 4 or 12 weeks within each group; #p < 0.05 = difference between placebo and irbesartan groups.

 




 
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