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Ann Thorac Surg 2005;80:1732-1737
© 2005 The Society of Thoracic Surgeons

Original article: Cardiovascular

Changing Incidence, Type, and Natural History of Conduction Defects After Coronary Artery Bypass Grafting

David J. Cook, MD * , Joseph M. Bailon, BSN, CRNA, Tonia T. Douglas, BSN, CRNA, Kathleen D. Henke, BSN, CRNA, John R. Westberg, BScN, CRNA, Mary E. Shirk-Marienau, MS, CRNA, Thoralf M. Sundt, MD

Mayo Clinic College of Medicine, Rochester, Minnesota

Accepted for publication April 22, 2005.

* Address correspondence to Dr Cook, Mayo Clinic, 200 1st Street SW, Rochester, MN 55905 (Email: cook.david{at}mayo.edu).

BACKGROUND: Cardiac conduction defects occur after cardiac surgery. We hypothesized that population aging and increased use of ß-blockers would increase the incidence of new conduction defects after coronary surgery.

METHODS: We examined the medical records of 800 coronary artery bypass grafting (CABG) patients (400 from 1991 and 400 from 2001). Exclusion criteria included the following: preexisting conduction defect, permanent pacemaker, and perioperative atrial fibrillation, leaving 303 and 269 patients, respectively, included in the two study years. The incidence, type, and persistence of new conduction defects were determined from the preoperative, postoperative, and the predischarge electrocardiogram. Multivariate analysis identified predictors of new defects.

RESULTS: Study populations were well-matched. There was a marked decrease in the incidence of new postoperative conduction defects from 1991 (19%) to 2001 (6%). There was also a change in the most frequently occurring block, from a right-bundle-branch-block in 1991 (10%) to first-degree atrioventricular block (3%) in 2001. Finally, conduction defects in 1991 were more transient. While 19% of 1991 patients showed a conduction defect early postoperatively, only 9% were persistent. In 2001, the incidence of conduction defects at discharge (7%), was equivalent to that early postoperatively (6%). Predictors of new conduction defects included year of operation, age, intraaortic balloon counterpulsation, number of vessels bypassed, and crystalloid cardioplegia.

CONCLUSIONS: Our results were the opposite of those predicted. Our report identifies a changing incidence, type, and natural history of conduction defects after CABG. Our comparison demonstrated a decrease in the incidence of new conduction defects, as well as a qualitative change in the defects identified. Multivariate analysis provided predictors of new conduction defects after CABG.






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