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Ann Thorac Surg 2007;83:2073
© 2007 The Society of Thoracic Surgeons
Division of Cardiothoracic Surgery, State University of New York—Stony Brook, T19,080 Health Sciences Center, Stony Brook, NY 11794-8191
(Email: ibkmd{at}hotmail.com).
One hallmark of interesting science is that more questions are raised than answered. This article by Jin and colleagues [1] certainly fulfills that criterion. Decades of scientific investigations have convincingly proven the existence of the intrinsic myoprotective response termed "preconditioning," yet few reports have suggested true clinical efficacy, particularly in the cardiothoracic surgical population undergoing cardioplegic arrest and reperfusion. Now Jin and colleagues [1] seem to demonstrate in their clinical series that "postconditioning" may be biologically feasible and relevant to clinical outcomes in this patient population.
Despite these provocative data, one must consider that the clinical operative environment provides many triggers for classical "preconditioning," some of which include administration of narcotics, inhalational anesthetics, alpha agonists, and simply the institution of cardiopulmonary bypass with its attendant catecholamine release. It is not clear that these triggers and their effects can be cleanly dissected away from the "postconditioning" outcomes in this clinical series.
Adenosine infusion right after aortic unclamping was associated with significant hypotension (BP < 30 mm Hg) for more than 3 minutes. This begs the question of whether adenosine was the conditioning trigger or instead the hypotension with its associated physiologic responses (eg, catecholamine release), or perhaps that the combination of both adenosine and hypotension exceeded the threshold to stimulate the myocardial protective response termed "postconditioning."
The immediate postischemic period prior to weaning from bypass was too short for one to postulate a purely metabolic effect from the adenosine. Instead it is more likely that the drug administration was a trigger. It is especially intriguing to consider that notwithstanding the multitude of "preconditioning" triggers that pertain prior to the ischemic interval, the "postconditioning" activation of intrinsic myoprotection during reperfusion after cardioplegic arrest is even feasible. The biological mechanisms that underlie this clinical observation in the cardiothoracic surgical arena remain to be elucidated.
These authors are to be congratulated for this creative clinical series. Many more questions are raised than answered, which should send us all back to the research laboratory and the operating room to rethink our myocardial protective paradigms.
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