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Soluble L‐Selectin and Neutrophil Derived Oxidative Stress After Pacing Induced Myocardial Ischemia in Chronic Stable Coronary Artery Disease
Author(s) -
GIANNITSIS EVANGELOS,
TETTENBORN IVO,
WIEGAND UWE,
STIERLE ULRICH,
KATUS HUGO A.
Publication year - 2000
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.1540-8159.2000.tb06754.x
Subject(s) - medicine , coronary artery disease , cardiology , coronary sinus , ischemia , artery , blood sampling , oxidative stress
We studied the effect of atrial pacing induced myocardial ischemia on levels of soluble L‐selectin (sL‐selectin) and generation of neu‐trophil derived reactive oxygen species (ROS) in 10 patients with coronary artery disease (CAD) and sta‐ble angina and in six individuals without CAD. Myocardial ischemia was measured metabolically by lac‐tate sampling from the coronary sinus (CS) and arterial blood at each pacing step. Before each pacing step, at peak pacing and shortly after cessation, plasma concentrations of sL‐selectin and generation of ROS using the chemiluminescence method were measured in CS and femoral artery blood. Baseline sL‐selectin levels in CS samples were significantly lower in the CAD compared to the control group (547 ± 80 vs 836 ± 82 ng/mL, P = 0.03). At peak pacing, nine often patients with CAD developed myocardial ischemia (lac‐tate extraction ratio at rest 28%± 7%, at peak pacing ‐16%± 6%). In these patients, luminol‐enhanced chemiluminescence (CL, 0.88 ± 0.45 vs 3.9 ± 0.9 cpm × 10 5 , P = 0.09) and levels of sL‐selectin (547 ± 80 vs 764 ± 86 ng/mL, P ‐ 0.03) from naive neutrophils increased significantly in CS blood suggesting a po‐tent in vivo activation of neutrophils. In control patients, incremental pacing caused neither myocardial ischemia nor a significant change of chemiluminescence or of sL‐selectin levels. In conclusion, myocar‐dial ischemia induced by pacing tachycardia is able to activate neutrophils in patients with chronic sta‐ble coronary artery disease leading to increased generation of ROS and shedding of L‐selectin into the coronary circulation.