Abstract
Purpose
The present study investigated whether therapy with statins, beta-blockers and angiotensin-converting enzyme (ACE) inhibitors on admission affects the plasma level of myeloperoxidase (MPO) in patients with coronary artery disease (CAD).
Methods
This study included a consecutive series of 680 patients with angiographically confirmed CAD: 382 patients with stable CAD, 107 patients with unstable angina and 191 patients with ST-segment elevation acute myocardial infarction. Blood samples for MPO measurement were taken before angiography prior to heparin administration.
Results
On admission, 316 patients were receiving statins, 432 patients were receiving beta-blockers and 354 patients were receiving ACE inhibitors. MPO level was: 65.5 [48.8–101.6] μg/L among patients on statin therapy versus 86.7 [56.0–159.9] μg/L among patients without statin therapy (P < 0.001); 68.1 [50.1–105.1] μg/L among patients on beta-blocker therapy versus 97.3 [56.0–181.9] μg/L among patients without beta-blocker therapy (P < 0.001) and 65.5 [49.2–102.0] μg/L among patients receiving ACE inhibitors versus 92.0 [56.1–171.1] μg/L among patients not receiving ACE inhibitors on admission (P < 0.001). The MPO-lowering effect of these drugs was observed only in patients with acute coronary syndrome but not in patients with stable CAD. The multivariable analysis, adjusting for cardiovascular risk factors, clinical variables and concomitant therapy identified beta-blockers on admission as an independent correlate of lower MPO levels (P = 0.016).
Conclusions
In patients with symptomatic CAD, beta-blocker therapy on admission was independently associated with lower levels of plasma MPO. Pre-admission therapy with statins, beta-blockers or ACE inhibitors reduced MPO levels in patients with acute coronary syndromes, but not in patients with stable CAD.
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Ndrepepa, G., Braun, S., Schömig, A. et al. Impact of therapy with statins, beta-blockers and angiotensin-converting enzyme inhibitors on plasma myeloperoxidase in patients with coronary artery disease. Clin Res Cardiol 100, 327–333 (2011). https://doi.org/10.1007/s00392-010-0247-2
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DOI: https://doi.org/10.1007/s00392-010-0247-2