THe PeRIOPeRaTIve use OF ß-BlOCkeRs

Perioperative myocardial infarction is a leading cause of postoperative morbidity and mortality (1). The etiology of postoperative MI is the subject of some debate but is thought to include prolonged ischemia resulting from tachycardia (2). Perıoperatıve blockade could prevent perioperative cardiac damage and improve long-term cardiac outcome in noncardiac surgical patients. The beneficial effects of ß-blockers on myocardial function have been widely described (3). Beta-blockers reduce myocardial oxygen consumption by decreasing heart rate and extending the time of diastole, allowing better coronary perfusion. Furthermore, they attenuate the excitotoxic effects of catecholamines (4). The American College of Cardiology and American Heart Association guidelines on perioperative assessment recommend perioperative blockers for noncardiac surgery. The most marked effects are observed in high-risk patients undergoing vascular surgery In cardiac surgery, the efficacy of ß-blockers is limited to the prevention of postoperative atrial fibrillation in coronary artery bypass graft (CABG) surgery, and only one observational analysis suggested a small but consistent survival benefit for patients receiving ß-blocker therapy and undergoing CABG surgery (5). Beta-adrenergic antagonists bind selectively to the b-adrenoceptors producing a competitive and reversible antagonism of the effects of ß-adrenergic stimuli on various organs (Table 1). Their pharmacological effects can be explained from the knowledge of the responses elicited by these receptors in the various tissues and the activity of the sympathetic tone. Thus, ß-blockers