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Published on: September 24, 2021
Neutrophil-derived oxidative stress after myocardial ischemia induced by incremental atrial pacing
E Giannitsis1, I Tettenborn, U Wiegand
1Department of Cardiology (Internal Medicine II), University of Lübeck, Germany.
Insights
Atrial pacing induced myocardial ischemia in coronary artery disease patients activates polymorphonuclear neutrophils (PMN). This activation, measured by chemiluminescence, suggests ischemia potentiates PMN function, potentially impacting atherosclerosis progression.
Area of Science:
- Cardiology
- Immunology
- Biochemistry
Background:
- Coronary artery disease (CAD) is a significant health concern.
- Oxygen free radicals (OFR) play a role in cardiovascular pathology.
- Polymorphonuclear neutrophils (PMN) are implicated in inflammatory processes.
Purpose of the Study:
- To investigate the effect of induced myocardial ischemia on oxygen free radical generation.
- To assess PMN activation in patients with CAD during ischemia.
- To explore the link between myocardial ischemia and PMN function.
Main Methods:
- Studied 8 CAD patients and 4 controls undergoing atrial pacing.
- Measured myocardial ischemia using lactate sampling from coronary sinus and arterial blood.
- Assessed OFR generation from PMN using luminol-enhanced chemiluminescence (CL).
Main Results:
- 7 of 8 CAD patients developed transient myocardial ischemia during pacing.
- Unstimulated PMN from the coronary sinus showed increased CL in ischemic patients (p=0.012).
- No additional PMN activation was observed with ex vivo phorbol myristate acetate stimulation.
Conclusions:
- Myocardial ischemia is a potent endogenous activator of PMN function.
- Activated PMN may contribute to the pathogenesis and progression of atherosclerosis.
- Findings highlight the interplay between ischemic heart disease and inflammatory cell activation.
Abstract:
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.
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