TY - JOUR
T1 - Time course of lysophosphatidylcholine release from ischemic human myocardium parallels the time course of early ischemic ventricular arrhythmia
AU - Sedlis, Steven R.
AU - Hom, Mae
AU - Sequeira, Jeffrey M.
AU - Tritel, Marc
AU - Gindea, Aaron
AU - Ladenson, Jack H.
AU - Jaffe, Allan S.
AU - Esposito, Rick
PY - 1997
Y1 - 1997
N2 - Background: We determined the kinetics of the release of lysophosphatidylcholine (LPC) into the coronary sinus of patients undergoing stress tests after coronary artery bypass grafting. The kinetics were consistent with a role for this amphiphile in the pathogenesis of ischemic ventricular arrhythmia, a major cause of sudden death. Methods: Stress testing was initiated in the operating suite by pacing at a rate of 160 beats/min for 2 min. Ischemia was then induced by clamping the bypass grafts to the anterior wall for a maximal time of 4 min. Results: The pacing procedure induced a prompt but reversible increase in coronary sinus LPC concentration from a baseline of 60.9 ± 2.5 to 83.8 ± 5.0 μmol/l via pacing alone, and a further increase to 101.8 ± 6.7 μmol/I when the grafts were clamped for 2 min (P< 0.01). Six minutes after the cessation of pacing, LPC concentration returned to 67.5 ± 4.4 μmol/I. Conclusions: These results demonstrate that severe myocardial ischemia is an agonist for rapid release of LPC from the myocardium. Kinetics of this release paralleled the time- course of early onset of electrophysiologic changes in isolated myocytes and perfused heart preparations in vitro. These results indicate that LPC may have an important role in the pathogenesis of ischemic ventricular arrhythmia in patients.
AB - Background: We determined the kinetics of the release of lysophosphatidylcholine (LPC) into the coronary sinus of patients undergoing stress tests after coronary artery bypass grafting. The kinetics were consistent with a role for this amphiphile in the pathogenesis of ischemic ventricular arrhythmia, a major cause of sudden death. Methods: Stress testing was initiated in the operating suite by pacing at a rate of 160 beats/min for 2 min. Ischemia was then induced by clamping the bypass grafts to the anterior wall for a maximal time of 4 min. Results: The pacing procedure induced a prompt but reversible increase in coronary sinus LPC concentration from a baseline of 60.9 ± 2.5 to 83.8 ± 5.0 μmol/l via pacing alone, and a further increase to 101.8 ± 6.7 μmol/I when the grafts were clamped for 2 min (P< 0.01). Six minutes after the cessation of pacing, LPC concentration returned to 67.5 ± 4.4 μmol/I. Conclusions: These results demonstrate that severe myocardial ischemia is an agonist for rapid release of LPC from the myocardium. Kinetics of this release paralleled the time- course of early onset of electrophysiologic changes in isolated myocytes and perfused heart preparations in vitro. These results indicate that LPC may have an important role in the pathogenesis of ischemic ventricular arrhythmia in patients.
KW - coronary artery bypass grafting
KW - lysophostidylcholine
KW - myocardial ischemia
KW - stress testing
KW - ventricular arrythmia
UR - http://www.scopus.com/inward/record.url?scp=0030966109&partnerID=8YFLogxK
U2 - 10.1097/00019501-199701000-00003
DO - 10.1097/00019501-199701000-00003
M3 - Article
C2 - 9101118
AN - SCOPUS:0030966109
SN - 0954-6928
VL - 8
SP - 19
EP - 27
JO - Coronary Artery Disease
JF - Coronary Artery Disease
IS - 1
ER -