A Study on the Occurrence and Prevention of Perioperative Stroke after Coronary Artery Bypass Grafting

Abstract

Cerebral infarction after coronary artery bypass grafting (CABG) is a serious complication and a problem that remains unsolved. We will report the onset of cerebral infarction in CABG patients in our institution, and its cause, preventive method. The subjects of this research were 761 patients who underwent on-pump isolated CABG. Preoperative, intraoperative and postoperative factors, onset of cerebral infarction and atrial fibrillation were investigated. Postoperative cerebral infarction and postoperative atrial fibrillation were recognized in 1.4% and 24% of the patients, respectively. The risk factors for cerebral infarction were carotid artery stenosis,

The Role of β-Blockers in Cardiac Perioperative Management

“…8) In a study performed at our hospital, perioperative and postoperative β-blocker therapy had a strong influence on the occurrence of POAF, but preoperative administration of β-blockers showed no preventive effect. 6,9) The results of our two studies showed that preoperative oral administration of β-blocker could not prevent POAF probably because of a small number of patients treated with β-blocker preoperatively.…”

“…The results of our study performed in 761 patients undergoing isolated coronary artery bypass grafting (CABG) showed that the risk factors for POAF were an age of 75 or older, chronic kidney disease, emergency surgery, cardiopulmonary bypass time >180 min, intraoperative carperitide non-use, intraoperative landiolol hydrochloride non-use, preoperative ARB non-use, preoperative calcium antagonist use, preoperative statin use, postoperative β-blocker non-use, and postoperative aldosterone blocker non-use, preoperative, perioperative and postoperative drug therapy also has a strong influence on the occurrence of POAF. 6) The results of the above-mentioned study suggested that perioperative and postoperative β-blocker use was important, and emphasized the need for β-blocker therapy to suppress pathological sympathetic hyperactivity.…”