To the Editor:—
We read with interest the recent article by Dr. Lange et al. ,1who reported that β-blockade with esmolol abolished the cardioprotective effect of anesthetic preconditioning with 1 minimum alveolar concentration sevoflurane or desflurane but not that elicited by ischemic preconditioning in a rabbit in vivo cardiac ischemia–reperfusion model. As interesting and important as these findings may be for the further elucidation of the signaling process involved in these powerful cardioprotective mechanisms, they certainly also add to the debate of whether anesthetic preconditioning will ever become a clinically applicable cardioprotective strategy. After all, the patients who would benefit the most from perioperative cardioprotection by volatile anesthetics are the ones who have coronary artery disease and are undergoing noncardiac or cardiac surgery, and these patients are typically on a β-blocker for perioperative cardioprotection. Together with numerous other clinical constraints, such as, age, comorbidities, timing, and dosing of the anesthetic,2the results from this study may help to explain the unfortunate discrepancy found so far between the impressive degree of cardioprotection by volatile anesthetics in basic science research3and the much milder results in recent clinical studies.4,5As such, we would be interested in how the authors interpret the relevance of their findings to the clinical practice of anesthesia.
*Medical College of Wisconsin, Milwaukee, Wisconsin. email@example.com