BACKGROUND: There are no studies yet on the usefulness of myeloperoxidase (MPO) as a prognostic tool in patients with stable coronary artery disease (CAD). METHODS: The study included 382 patients with clinical and angiographic confirmation of stable CAD. Blood samples for MPO measurement were taken before angiography. Myeloperoxidase was determined using an enzyme immunoassay. The primary end point of the study was all-cause mortality. RESULTS: Patients were categorized into 2 groups: the high-MPO group included patients in the third tertile of MPO levels (>75.0 microg/L; 127 patients), and the low-MPO group included patients in the first (<52.6 microg/L) and second tertiles (52.6-75.0 microg/L) of MPO levels (255 patients). The median follow-up was 3.5 [3.3-4.8] years. There were 35 deaths (9.2%) during the follow-up. The MPO concentration was 60.1 [47.0; 83.8] microg/L in survivors and 72.7 [54.8; 105.1] microg/L in nonsurvivors (P = .06). There were 17 deaths in the high-MPO level and 18 deaths in the low-MPO group: Kaplan-Meier estimates of mortality were 18.3% and 10.5% with an odds ratio of 1.96 (95% confidence interval [1.02-3.76], P = .04). The Cox proportional hazards model adjusting for correlates of mortality showed that plasma MPO was not an independent correlate of mortality (hazard ratio 1.06, 95% confidence interval [0.71-1.59], P = .77 for 1 SD increase in the log variable). CONCLUSION: Although elevated plasma MPO concentration is associated with a more advanced cardiovascular risk profile, plasma MPO does not predict mortality independent of other cardiovascular risk factors in patients with stable CAD.
BACKGROUND: There are no studies yet on the usefulness of myeloperoxidase (MPO) as a prognostic tool in patients with stable coronary artery disease (CAD). METHODS: The study included 382 patients with clinical and angiographic confirmation of stable CAD. Blood samples for MPO measurement were taken before angiography. Myeloperoxidase was determined using an enzyme immunoassay. The primary end point of the study was all-cause mortality. RESULTS:Patients were categorized into 2 groups: the high-MPO group included patients in the third tertile of MPO levels (>75.0 microg/L; 127 patients), and the low-MPO group included patients in the first (<52.6 microg/L) and second tertiles (52.6-75.0 microg/L) of MPO levels (255 patients). The median follow-up was 3.5 [3.3-4.8] years. There were 35 deaths (9.2%) during the follow-up. The MPO concentration was 60.1 [47.0; 83.8] microg/L in survivors and 72.7 [54.8; 105.1] microg/L in nonsurvivors (P = .06). There were 17 deaths in the high-MPO level and 18 deaths in the low-MPO group: Kaplan-Meier estimates of mortality were 18.3% and 10.5% with an odds ratio of 1.96 (95% confidence interval [1.02-3.76], P = .04). The Cox proportional hazards model adjusting for correlates of mortality showed that plasma MPO was not an independent correlate of mortality (hazard ratio 1.06, 95% confidence interval [0.71-1.59], P = .77 for 1 SD increase in the log variable). CONCLUSION: Although elevated plasma MPO concentration is associated with a more advanced cardiovascular risk profile, plasma MPO does not predict mortality independent of other cardiovascular risk factors in patients with stable CAD.
Authors: Htet W Khine; John F Teiber; Robert W Haley; Amit Khera; Colby R Ayers; Anand Rohatgi Journal: Atherosclerosis Date: 2017-06-03 Impact factor: 5.162
Authors: Hubert Scharnagl; Marcus E Kleber; Bernd Genser; Sandra Kickmaier; Wilfried Renner; Gisela Weihrauch; Tanja Grammer; Christine Rossmann; Bernhard R Winkelmann; Bernhard O Boehm; Wolfgang Sattler; Winfried März; Ernst Malle Journal: Int J Cardiol Date: 2014-04-03 Impact factor: 4.164