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REPLY
On the basis of our echocardiographic data, which analyzed the amplitude of motion and thickening of the interventricular septum, we delineated two possible mechanisms for abnormal septal movement after coronary artery bypass graft surgery. The first, augmented anterior movement of the entire heart during systole because of pericardial disruption, is probably least important in coronary bypass surgery but explains why paradoxical septal motion can be seen with normal septal thickening as has been observed after pericardiectomy.’ Why only one of Lengyel’s five patients demonstrated abnormal septal movement after aneurysmectomy is not clear, especially since reversed septal motion is common after valve replacement surgery.2 Perhaps aneurysmectomy distorts the geometric relation of the septum to the left ventricle. The second and more important mechanism is reduced septal myocardial performance in the early postoperative period. The exact cause of this depressed function is unknown. We did not claim that the septum was infarcted in all of our patients with abnormal septal motion after coronary bypass surgery; in fact, we could confirm septal infarction in only one patient. Lengyel postulates that high blood flow velocity at the site of graft insertion in the mid left anterior descending coronary artery causes reduced flow in the more proximal septal perforating branches, which leads to early postoperative septal abnormalities. However, this theory does not explain why the septal abnormalities decrease late after operation in the majority of patients. Also, abnormal septal motion developed in two of our four patients with grafts to be proximal left anterior descending coronary artery. We do not know why we had such a small incidence of abnormal septal movement preoperatively compared with the incidence in other series. However, Gordon and Kerber3 recently found only a 46 percent incidence rate of septal abnormalities in a group of 26 patients with disease of the left anterior descending coronary artery. One possible explanation is that in almost all of our 37 patients with significant occlusion of this artery, the occlusion was located distal to the origin of the first septal perforating branch. Therefore, upper septal performance may have been fortuitously preserved in a larger number of our patients. Albert0 Righetti, MD Michael Ii. Crawford, MD, FACC Robert A. O’Rourke, MD, FACC Heinz Schelbert, MD Pat 0. Daily, MD, FACC John Ross, Jr., MD, FACC Division of Cardiology Department of Medicine University of California, San Diego La Jolla, California References
descending coronary artery and indicate that this difference is statistically significant (P
REPLY
On the basis of our echocardiographic data, which analyzed the amplitude of motion and thickening of the interventricular septum, we delineated two possible mechanisms for abnormal septal movement after coronary artery bypass graft surgery. The first, augmented anterior movement of the entire heart during systole because of pericardial disruption, is probably least important in coronary bypass surgery but explains why paradoxical septal motion can be seen with normal septal thickening as has been observed after pericardiectomy.’ Why only one of Lengyel’s five patients demonstrated abnormal septal movement after aneurysmectomy is not clear, especially since reversed septal motion is common after valve replacement surgery.2 Perhaps aneurysmectomy distorts the geometric relation of the septum to the left ventricle. The second and more important mechanism is reduced septal myocardial performance in the early postoperative period. The exact cause of this depressed function is unknown. We did not claim that the septum was infarcted in all of our patients with abnormal septal motion after coronary bypass surgery; in fact, we could confirm septal infarction in only one patient. Lengyel postulates that high blood flow velocity at the site of graft insertion in the mid left anterior descending coronary artery causes reduced flow in the more proximal septal perforating branches, which leads to early postoperative septal abnormalities. However, this theory does not explain why the septal abnormalities decrease late after operation in the majority of patients. Also, abnormal septal motion developed in two of our four patients with grafts to be proximal left anterior descending coronary artery. We do not know why we had such a small incidence of abnormal septal movement preoperatively compared with the incidence in other series. However, Gordon and Kerber3 recently found only a 46 percent incidence rate of septal abnormalities in a group of 26 patients with disease of the left anterior descending coronary artery. One possible explanation is that in almost all of our 37 patients with significant occlusion of this artery, the occlusion was located distal to the origin of the first septal perforating branch. Therefore, upper septal performance may have been fortuitously preserved in a larger number of our patients. Albert0 Righetti, MD Michael Ii. Crawford, MD, FACC Robert A. O’Rourke, MD, FACC Heinz Schelbert, MD Pat 0. Daily, MD, FACC John Ross, Jr., MD, FACC Division of Cardiology Department of Medicine University of California, San Diego La Jolla, California References
descending coronary artery and indicate that this difference is statistically significant (P
