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Neutrophil‐Derived Oxidative Stress After Myocardial Ischemia Induced by Incremental Atrial Pacing
Author(s) -
GIANNITSIS EVANGELOS,
TETTENBORN IVO,
WIEGAND UWE,
POTRATZ JUERGEN,
SHEIKHZADEH ABDOLHAMID,
STIERLE ULRICH
Publication year - 1998
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1998.tb01080.x
Subject(s) - medicine , cardiology , ischemia , coronary artery disease , coronary sinus , oxidative stress , myocardial infarction , pathogenesis , lactate dehydrogenase , chemistry , enzyme , biochemistry
We studied the effect of atrial pacing‐induced myocardial ischemia on the generation of oxygen free radicals (OFR) in 8 patients with verified coronary artery disease (CAD) and in a control group of 4 patients without coronary atherosclerosis. Myocardial ischemia was measured metabolically by simultaneous lactate sampling from coronary sinus (CS) and arterial blood. Generation of OFR from purified viable polymorphonuclear neutrophils (PMN) was assessed by means of the chemiluminescence (CL) method. At peak pacing, 7 of 8 patients with CAD exhibited transient myocardial ischemia (mean lactate extraction ratio at rest: 23.6 ± 7.7 vs 5.21 ± 5.1 % at peak pacing, p= 0.012). In these patients, unstimulated PMN harvested from the CS depicted a significant increase of luminol‐enhanced CL (from 1.06 ± 0.54 to 2.15 ± 1.28 cpm x 10 5 , p= 0.012) after atrial pacing. There was no additional effect from further ex vivo stimulation with phorbol myristate acetate. This finding underscores the role of myocardial ischemia as a potent endogenous activator of PMN function and may have implications in the pathogenesis and progression of atherosclerosis.