title: Olmesartan reduces inflammatory biomarkers in patients with stable coronary artery disease undergoing percutaneous coronary intervention: results from the OLIVUS trial.
abstract: The OLmesartan on the progression of coronary atherosclerosis: evaluation by IntraVascular UltraSound (OLIVUS) trial demonstrated that an angiotensin II receptor blocker, olmesartan, reduces the rate of coronary atheroma progression as evaluated by intravascular ultrasound in patients with stable angina pectoris undergoing percutaneous coronary intervention. This substudy examined the impact of olmesartan on serum biomarkers and the relationship between biomarker changes and atheroma progression. Patients in the OLIVUS trial (n = 247) were randomly assigned to a control group or the olmesartan group. A subgroup of these patients (n = 135, 55 %) was analyzed at baseline and at 14 months. Patients' characteristics and blood-pressure control were identical between the control group (n = 65) and the olmesartan group (n = 70), and also between the subpopulation and total population. The change in the level of high-sensitivity C-reactive protein (hs-CRP) (mg/l) and adiponectin (μg/ml) was significantly greater in the olmesartan group than in the control group (between-group differences: 0.5 and -0.7; 95 % confidence interval: 0.2-0.8 and -1.3 to -0.1; P = 0.001 and 0.02, respectively). Multiple regression analysis revealed that the nominal changes in total atheroma volume and percent atheroma volume were significantly associated with the nominal change in hs-CRP in the olmesartan group but not in the control group. Olmesartan reduced hs-CRP in patients with stable angina, and this correlated with the change in coronary atheroma.
authors.affiliation: Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama, 700-8558, Japan, torumiyoshi@hotmail.com.
authors.forename: Toru
authors.initials: T
authors.lastname: Miyoshi
authors.forename: Atsushi
authors.initials: A
authors.lastname: Hirohata
authors.forename: Shinichi
authors.initials: S
authors.lastname: Usui
authors.forename: Keizo
authors.initials: K
authors.lastname: Yamamoto
authors.forename: Takashi
authors.initials: T
authors.lastname: Murakami
authors.forename: Issei
authors.initials: I
authors.lastname: Komatsubara
authors.forename: Shozo
authors.initials: S
authors.lastname: Kusachi
authors.forename: Tohru
authors.initials: T
authors.lastname: Ohe
authors.forename: Kazufumi
authors.initials: K
authors.lastname: Nakamura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ito
mesh_terms: D052242:Adiponectin / Q000097:blood; D000368:Aged; D060050:Angina, Stable / Q000097:blood / Q000175:diagnosis / Q000628:therapy*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D003324:Coronary Artery Disease / Q000097:blood / Q000175:diagnosis / Q000628:therapy*; D003331:Coronary Vessels / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D018450:Disease Progression; D015536:Down-Regulation; D005260:Female; D006801:Humans; D007093:Imidazoles / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000097:blood*; D007564:Japan; D008297:Male; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention; D058226:Plaque, Atherosclerotic; D011446:Prospective Studies; D013777:Tetrazoles / Q000627:therapeutic use*; D013997:Time Factors; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D047228:Angiotensin II Type 1 Receptor Blockers; D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D007093:Imidazoles; D018836:Inflammation Mediators; D013777:Tetrazoles; C437965:olmesartan; D002097:C-Reactive Protein
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