PURPOSE: C-reactive protein is an important risk factor for coronary artery disease, and plasma concentrations are lowered by treatment with pravastatin and aspirin. We examined whether other cardiovascular drugs that are used in the treatment of ischemic heart disease affect C-reactive protein concentrations. SUBJECTS AND METHODS: Plasma C-reactive protein concentration was measured by high sensitivity immunonephelometric assay in 333 consecutive patients with stable angina and confirmed coronary artery disease who underwent diagnostic angiography. RESULTS: Patients prescribed beta-blockers had significantly lower mean C-reactive protein concentrations than did patients in whom these were not prescribed (by 1.2 mg/L, or 40% difference in geometric mean concentration; P <0.001). This association remained significant (P = 0.03) after excluding patients with contraindications to the use of beta-blockers, and adjusting for the probability of beta-blocker therapy (propensity score) and other clinical predictors of C-reactive protein concentration, including body mass index, high-density lipoprotein cholesterol level, family history of coronary artery disease, and angiographic severity. No differences among types or dosages of beta-blockers were evident. CONCLUSION: Beta-blockers may affect C-reactive protein concentrations. Randomized studies are required to confirm these findings.
PURPOSE:C-reactive protein is an important risk factor for coronary artery disease, and plasma concentrations are lowered by treatment with pravastatin and aspirin. We examined whether other cardiovascular drugs that are used in the treatment of ischemic heart disease affect C-reactive protein concentrations. SUBJECTS AND METHODS: Plasma C-reactive protein concentration was measured by high sensitivity immunonephelometric assay in 333 consecutive patients with stable angina and confirmed coronary artery disease who underwent diagnostic angiography. RESULTS:Patients prescribed beta-blockers had significantly lower mean C-reactive protein concentrations than did patients in whom these were not prescribed (by 1.2 mg/L, or 40% difference in geometric mean concentration; P <0.001). This association remained significant (P = 0.03) after excluding patients with contraindications to the use of beta-blockers, and adjusting for the probability of beta-blocker therapy (propensity score) and other clinical predictors of C-reactive protein concentration, including body mass index, high-density lipoprotein cholesterol level, family history of coronary artery disease, and angiographic severity. No differences among types or dosages of beta-blockers were evident. CONCLUSION: Beta-blockers may affect C-reactive protein concentrations. Randomized studies are required to confirm these findings.
Authors: David E Chiriboga; Yunsheng Ma; Wenjun Li; Edward J Stanek; James R Hébert; Philip A Merriam; Eric S Rawson; Ira S Ockene Journal: Clin Chem Date: 2009-02 Impact factor: 8.327
Authors: Tim J McDonald; Beverley M Shields; Jane Lawry; Katharine R Owen; Anna L Gloyn; Sian Ellard; Andrew T Hattersley Journal: Diabetes Care Date: 2011-06-23 Impact factor: 19.112