-blocker therapy was associated with an improved car- diac outcome, overall mortality was increased in the metoprolol-treated group. This was partially related to the increased incidence of postoperative stroke occur- ring early after surgery. These findings might have im- portant implications on perioperative -blocker use, not only for initiation of therapy before surgery in -blocker naive patients but also whether or not to continue ther- apy throughout surgery. This commentary reviews the incidence and pathophysiology of perioperative stroke and the relation of -blockers and perioperative stroke, focusing on noncardiac surgery. The risk of clinically apparent perioperative brain in- jury such as stroke varies widely among different types of surgery. Whereas patients undergoing general surgery appear to be at low risk (0.08 - 0.7%), those undergoing heart valve surgery and aortic arch repair have a high incidence of perioperative stroke (8 -10%). 2 In Europe, 40 million general surgical procedures are performed annually. Therefore, it is estimated that 32,000 -280,000 patients suffer from postoperative stroke. However, the true incidence of cerebral complications is probably underestimated because subtle forms of brain injury are commonly classified as delirium that may only be de- tected by rigorous neuropsychological testing. The knowledge of the pathophysiology of postopera- tive cerebral complications is predominantly based on cardiothoracic surgery patients. It is estimated that 62% of strokes in this population have an embolic origin, 10% are related to hypoperfusion, and 10% have multiple causes. 2 Importantly, only 1% of strokes are caused by intracerebral hemorrhage. However, it should be ac- knowledged that the true pathophysiological basis of perioperative stroke is not as straightforward as it might seem. Embolic and hypoperfusion cerebral infarction most likely do not occur in isolation. 3 Impaired clear- ance of emboli (washout) seems to be the link between hypoperfusion, embolism, and ischemic stroke. 4 Intra- operative microemboli and low middle cerebral artery blood flow velocity are additive in predicting develop- ment of cerebral ischemic events after carotid endarter- ectomy. 5 Second, newer data wherein sensitive diffusion weighted magnetic resonance imaging (MRI) was per- formed suggest that as many as two-thirds of postcardiac surgery strokes have watershed or hypoperfusion pat- tern. 6 Finally, what appears to be occurring in cardiac surgery patients is that there is a rising prevalence of mostly unrecognized cerebral vascular disease concur- rent with the rising age of our population. In fact, one study (that interestingly excluded patients with known cerebral vascular disease) found that as many as 75% of patients had evidence of impaired cerebral perfusion based on single photon emission computed tomography (SPECT) imaging before coronary artery bypass grafting (CABG) surgery. 7 Approximately 45% of perioperative strokes are iden- tified within the first day after surgery. The remaining 55% occur after uneventful recovery from anesthesia, from the second postoperative day onward. Early embo- lism results especially from manipulations of the heart and aorta or release of particulate matter from the car- diopulmonary-bypass pump. Delayed embolism is often attributed to postoperative atrial fibrillation, myocardial infarction resulting from an imbalance between myocar- dial oxygen supply and demand, and coagulopathy. Compared to stroke after cardiac surgery, the pathophys- iology of stroke after noncardiac surgery is ill defined. Perioperative hemodynamic instability and cardiac events, such as myocardial infarction and arrhythmias, likely play a major role. Recently, the POISE study identified a new risk factor for perioperative ischemic strokes: high-dose meto- prolol succinate initiated for cardiac protection in patients undergoing noncardiac surgery.