UNLABELLED: ATP-sensitive potassium channels are opened during the course of ischemic preconditioning (IP). As experimental data suggest that opening of sarcolemmal ATP-sensitive potassium channels underlie ST elevation during myocardial ischemia, one would expect to observe increased ST elevation during ischemia following IP. However, clinical studies have reported IP to attenuate ST elevation during repeated brief coronary occlusions. The objective of this study was to characterize the temporal course of ST elevation during coronary occlusion following IP. Twenty-eight closed-chest pigs were subject to catheter-based left anterior descending coronary artery occlusion/ reperfusion for 45/120 minutes. Thirteen animals were preconditioned by two occlusion/reperfusion cycles of 10/30 minutes. Fifteen pigs served as controls. The electrocardiographic ST vector magnitude was continuously monitored. IP reduced the infarct size normalized for area at risk (IP 9.6 +/- 15.8%; control 71.2 +/- 14.7%; p < 0.001). IP increased the time between coronary artery occlusion and appearance of significant rise in ST vector magnitude from 51 +/- 17 to 94 +/- 33 seconds (p < 0.01). IP reduced the rise in ST vector magnitude after 120 seconds of occlusion from 202 +/- 85 microV to 68 +/- 28 microV (p < 0.001) and increased the rise in ST vector magnitude after 600 seconds from 265 +/- 106 microV to 427 +/- 232 microV (p < 0.001). CONCLUSION: Ischemic preconditioning reduced and delayed early ST elevation during subsequent coronary artery occlusion, but increased late ST elevation. Thus, ischemic preconditioning causes a dynamic and critically time-dependent biphasic pattern of ST elevation during repeated coronary occlusions.
UNLABELLED: ATP-sensitive potassium channels are opened during the course of ischemic preconditioning (IP). As experimental data suggest that opening of sarcolemmal ATP-sensitive potassium channels underlie ST elevation during myocardial ischemia, one would expect to observe increased ST elevation during ischemia following IP. However, clinical studies have reported IP to attenuate ST elevation during repeated brief coronary occlusions. The objective of this study was to characterize the temporal course of ST elevation during coronary occlusion following IP. Twenty-eight closed-chest pigs were subject to catheter-based left anterior descending coronary artery occlusion/ reperfusion for 45/120 minutes. Thirteen animals were preconditioned by two occlusion/reperfusion cycles of 10/30 minutes. Fifteen pigs served as controls. The electrocardiographic ST vector magnitude was continuously monitored. IP reduced the infarct size normalized for area at risk (IP 9.6 +/- 15.8%; control 71.2 +/- 14.7%; p < 0.001). IP increased the time between coronary artery occlusion and appearance of significant rise in ST vector magnitude from 51 +/- 17 to 94 +/- 33 seconds (p < 0.01). IP reduced the rise in ST vector magnitude after 120 seconds of occlusion from 202 +/- 85 microV to 68 +/- 28 microV (p < 0.001) and increased the rise in ST vector magnitude after 600 seconds from 265 +/- 106 microV to 427 +/- 232 microV (p < 0.001). CONCLUSION:Ischemic preconditioning reduced and delayed early ST elevation during subsequent coronary artery occlusion, but increased late ST elevation. Thus, ischemic preconditioning causes a dynamic and critically time-dependent biphasic pattern of ST elevation during repeated coronary occlusions.