Postconditioning During Percutaneous Coronary Intervention in Acute Myocardial Infarction
Author(s) -
Warren K. Laskey,
Alex Schevchuck
Publication year - 2013
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.113.005693
Subject(s) - medicine , myocardial infarction , percutaneous coronary intervention , cardiology , percutaneous
" Delaying the postconditioning intervention for even a few minutes while changing balloon catheters, or while allowing balloons to remain deflated beyond the period of time suggested by the algorithm, may abrogate the cardioprotective advantage of postconditioning " from Kim, H, et al 1 The ability of myocardium to protect itself under lethal ischemic conditions- so called ischemic conditioning- is a remarkably robust and reproducible experimental phenomenon demonstrable via direct measure of infarct size in virtually all animal models tested. 2 Despite inferences from the analysis of surrogate end-points in clinical studies, e.g., biomarker elevation, ST-segment shift, anginal discomfort (either preceding or accompanying ischemia), there are as yet no clinical studies directly assessing infarct size reduction consequent to pre-conditioning , as originally described by Murry, et al in a canine model. 3 Given the impossibility and implausibility of predicting exactly when an acute myocardial infarction (AMI) will occur in humans and the necessity for the pre-conditioning stimulus to be applied before the ischemic insult, it is clear that pre-conditioning human myocardium imminently facing infarction will likely not be achievable. However, this is a needlessly harsh refutation of the existence and other potential clinical benefits of ischemic pre-conditioning in humans during percutaneous coronary intervention 4 , open heart surgery 5 , ischemia-related arrhythmogenesis 6 - all reasonable models for the predictable and reproducible induction of myocardial ischemia in humans.
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