Beta-blockers and anesthetic preconditioning: friend or foe?

摘要

To the Editor: We read with interest the recently-published article by Yu and Beattie reporting a meta-analysis investigating the effects of volatile anesthetics on morbidity and mortality in patients undergoing coronary artery bypass graft surgery. It was reported that volatile anesthetics do not reduce mortality compared to iv anesthesia, but reduce postoperative levels of troponin I as a marker of myocardial ischemic damage. Strikingly, patients receiving iv anesthetics had a significantly higher incidence (28%) of beta-blocker utilization compared to patients receiving volatile anesthetics. This is an extraordinarily important finding. Yu and Beattie conclude that "some myocardial protective effects of the inhalation anesthetics may have been counteracted as beta-blocker utilization was unequally distributed...". We agree with this conclusion insofar as the disproportion of beta-blocker use may have influenced the results. However, we surmise that concurrent beta-blocker therapy inhibited the cardioprotective effects of volatile anesthetics and that the beneficial effects of the volatile anesthetics would have been even more pronounced, if no beta block-ers had been used at all. This contention is derived from the fact that volatile anesthetic preconditioning is mediated by beta-adrenergic signalling. Unspecific blockade of beta-adrenergic receptors abrogates des-flurane-induced preconditioning in isolated human atrial myocardium. Furthermore, volatile anesthetic preconditioning is abolished by concurrent blockade of beta_1-adrenergic receptors by esmolol and downstream protein kinase A by the selective blocker H-89 in the rabbit heart in vivo. This result can also be obtained using the beta_1 selective blocker metopro-lol.