BACKGROUND: Myeloperoxidase (MPO) has emerged as a critical mediator in the physiopathology of atherosclerosis from plaque formation and growth until destabilization and rupture leading to acute coronary syndrome (ACS). Using coronary stenting as a model of plaque injury, we aimed to determine the evolution of systemic MPO levels following coronary stenting in stable angina patients and in patients with acute myocardial infarction (AMI). METHODS: Plasma levels of MPO, lactoferrin, interleukin (IL)-6, C-reactive protein and PMN counts were assessed in 13 patients with Non-ST-elevation myocardial infarction (NSTEMI) (Group A) and in 29 patients with stable angina pectoris (Group B), undergoing coronary stenting. Serial blood samples were taken before angioplasty (baseline) and at 1, 6 and 24 h following initial balloon inflation. RESULTS: Following angioplasty, the overall plasma MPO levels significantly increased at 1 h in group B (120.5+/-79.0 to 166+/-79.5, p=0.003) but not in group A (121+/-63.4 to 124.7+/-76.9, p=0.753). In Group B, the increase in MPO levels at 1 h were significantly higher in the presence of complex lesions compared to patients with simple lesions (p=0.023). Lactoferrin levels showed no change over time except for a significant decrease at 6 h in group B. CONCLUSIONS: In stable angina patients, coronary stenting is associated with an acute and transient increase in plasma MPO levels, but not in lactoferrin levels, with an enhanced response in the presence of complex lesions. In contrast, we observed no changes in plasma MPO and lactoferrin levels following stenting in patients with AMI. Given its pro-inflammatory properties, the potential implication of MPO release on clinical outcome in stable patients undergoing stenting needs further investigation. 2009 European Federation of Internal Medicine.
BACKGROUND:Myeloperoxidase (MPO) has emerged as a critical mediator in the physiopathology of atherosclerosis from plaque formation and growth until destabilization and rupture leading to acute coronary syndrome (ACS). Using coronary stenting as a model of plaque injury, we aimed to determine the evolution of systemic MPO levels following coronary stenting in stable anginapatients and in patients with acute myocardial infarction (AMI). METHODS: Plasma levels of MPO, lactoferrin, interleukin (IL)-6, C-reactive protein and PMN counts were assessed in 13 patients with Non-ST-elevation myocardial infarction (NSTEMI) (Group A) and in 29 patients with stable angina pectoris (Group B), undergoing coronary stenting. Serial blood samples were taken before angioplasty (baseline) and at 1, 6 and 24 h following initial balloon inflation. RESULTS: Following angioplasty, the overall plasma MPO levels significantly increased at 1 h in group B (120.5+/-79.0 to 166+/-79.5, p=0.003) but not in group A (121+/-63.4 to 124.7+/-76.9, p=0.753). In Group B, the increase in MPO levels at 1 h were significantly higher in the presence of complex lesions compared to patients with simple lesions (p=0.023). Lactoferrin levels showed no change over time except for a significant decrease at 6 h in group B. CONCLUSIONS: In stable anginapatients, coronary stenting is associated with an acute and transient increase in plasma MPO levels, but not in lactoferrin levels, with an enhanced response in the presence of complex lesions. In contrast, we observed no changes in plasma MPO and lactoferrin levels following stenting in patients with AMI. Given its pro-inflammatory properties, the potential implication of MPO release on clinical outcome in stable patients undergoing stenting needs further investigation. 2009 European Federation of Internal Medicine.
Authors: Tamás Horváth; Gyöngyi Serfőző; Ádám Györkei; Imre Földesi; Tamás Forster; Margit Keresztes Journal: PLoS One Date: 2019-04-11 Impact factor: 3.240