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Pacemaker Inhibition
473 Correspondence
Pacemaker Inhibition To the Editor: In "Pacemaker Inhibition in Cardiac Surgery," Hakki, Goel, and Mundth (Ann Thorac Surg 33:295, 1982) present an innovative means of inhibiting the function of permanent pacemakers during cardiac operations. While this method is simple and effective, we believe it is unnecessary in most cardiac procedures performed with the aid of hypothermic potassiuminduced cardioplegia. We recently operated on 5 patients who had previously implanted permanent pacemakers. With the use of cold potassium-induced cardioplegia, all ventricular myocardial activity stopped completely within one minute of the administration of cardioplegia, and the hearts remained quiet and flaccid with no response to the pacemaker until the aortic cross-clamp had been removed. Each of these patients resumed a regular paced rhythm soon after removal of the cross-clamp and without the need for electrical defibrillation. We know of no evidence to suggest that major injury occurs as a result of continued electrical stimulation of a heart that is rendered unresponsive by the use of adequate hypothermic potassium-induced cardioplegia. Therefore, the method described by Hakki and his associates, while certainly effective, may be unnecessary.
John M . Kratz, M . D . Fred A . Crawford, Jr., M . D . Robert M . Sade, M . D . Division of Cardiothoracic Surgery Medical University of South Carolina 171 Ashley Ave Charleston, SC 29425
Reply To the Editor: We agree with Dr. Kratz and his associates that with moderate to profound hypothermia the use of a pacemaker inhibition technique is limited to a short period. However, cardiac inhibition remains functional not only until the cardioplegic solution takes effect, but also during the rewarming period. We realize that giving more cardioplegia could negate the effect of possible activity during rewarming; however, we believe it is safer to use this fairly simple technique in all pacemaker patients undergoing cardiac operations. We are also aware of other groups of surgeons who use mild or moderate systemic hypothermia with no aortic cross-clamping or potassium cardioplegia in open-heart operations, including coronary artery bypass surgery (with a perioperative myocardial infarction rate of less than
2%).The use of our pacemaker inhibition technique would be of particular benefit to this group of patients.
A-Hadi Hakki, M . D . lnder P . Goel, M . D . Eldred 0. Mundth, M . D . Hahnemann University Hospital, Suite 6328 230 N Broad St Philadelphia, P A 191 02
Coronary Stenosis following Aortic Valve Replacement To the Editor: I believe a few points are worth mentioning regarding a recent article by D. Glenn Pennington, M.D., and his associates entitled "Coronary Artery Stenosis following Aortic Valve Replacement and Intermittent Intracoronary Cardioplegia" (Ann Thorac Surg 33:576, 1982). This article brings to our attention the frequent complications of coronary artery damage, which is caused by cannulation of the orifices or of the vessels themselves for injection of blood or clear cardioplegia. Since the authors clearly recognize that these complications are avoidable and result directly from the placement of tight-fitting cannulas in the coronary ostia, I wonder how they plan to avoid such problems in the future. It does not appear that any of the three methods of cannulating the coronary ostia that they have described is safe. The common pattern, however, is to introduce the entire dilated tip of the Spencer-Mallette cannula into the coronary ostia beyond the level of the aortic wall. There are no diagrams in the article showing how these cannulas are positioned, so we must assume that they are introduced in this fashion. The problem of coronary ostial damage, as was commonly seen in the 60s, practically disappeared as topical hypothermia and cardioplegic methods became popular. However, with the revival of blood cardioplegia and continuous infusion, we undoubtedly will see a return of this problem as well. The basic principle being violated is the acute distention by the ballooned portion of the cannula itself, and it would not matter whether this is a Mayo or a Spencer-Mallettecannula. The longer the catheter or cannula remains in the vessel, the more likely that it will produce stenosis in the same manner as endotracheal cuff tubes cause stenosis of the subglottic area of the trachea. The method that the authors describe of "holding the cannulas in place by hand with removal and reinsertion for each injection" (p 577) will not prevent or avoid the problem if the cannula itself, with a dilated portion, is advanced into the coronary artery beyond the ostia. I believe the
Pacemaker Inhibition To the Editor: In "Pacemaker Inhibition in Cardiac Surgery," Hakki, Goel, and Mundth (Ann Thorac Surg 33:295, 1982) present an innovative means of inhibiting the function of permanent pacemakers during cardiac operations. While this method is simple and effective, we believe it is unnecessary in most cardiac procedures performed with the aid of hypothermic potassiuminduced cardioplegia. We recently operated on 5 patients who had previously implanted permanent pacemakers. With the use of cold potassium-induced cardioplegia, all ventricular myocardial activity stopped completely within one minute of the administration of cardioplegia, and the hearts remained quiet and flaccid with no response to the pacemaker until the aortic cross-clamp had been removed. Each of these patients resumed a regular paced rhythm soon after removal of the cross-clamp and without the need for electrical defibrillation. We know of no evidence to suggest that major injury occurs as a result of continued electrical stimulation of a heart that is rendered unresponsive by the use of adequate hypothermic potassium-induced cardioplegia. Therefore, the method described by Hakki and his associates, while certainly effective, may be unnecessary.
John M . Kratz, M . D . Fred A . Crawford, Jr., M . D . Robert M . Sade, M . D . Division of Cardiothoracic Surgery Medical University of South Carolina 171 Ashley Ave Charleston, SC 29425
Reply To the Editor: We agree with Dr. Kratz and his associates that with moderate to profound hypothermia the use of a pacemaker inhibition technique is limited to a short period. However, cardiac inhibition remains functional not only until the cardioplegic solution takes effect, but also during the rewarming period. We realize that giving more cardioplegia could negate the effect of possible activity during rewarming; however, we believe it is safer to use this fairly simple technique in all pacemaker patients undergoing cardiac operations. We are also aware of other groups of surgeons who use mild or moderate systemic hypothermia with no aortic cross-clamping or potassium cardioplegia in open-heart operations, including coronary artery bypass surgery (with a perioperative myocardial infarction rate of less than
2%).The use of our pacemaker inhibition technique would be of particular benefit to this group of patients.
A-Hadi Hakki, M . D . lnder P . Goel, M . D . Eldred 0. Mundth, M . D . Hahnemann University Hospital, Suite 6328 230 N Broad St Philadelphia, P A 191 02
Coronary Stenosis following Aortic Valve Replacement To the Editor: I believe a few points are worth mentioning regarding a recent article by D. Glenn Pennington, M.D., and his associates entitled "Coronary Artery Stenosis following Aortic Valve Replacement and Intermittent Intracoronary Cardioplegia" (Ann Thorac Surg 33:576, 1982). This article brings to our attention the frequent complications of coronary artery damage, which is caused by cannulation of the orifices or of the vessels themselves for injection of blood or clear cardioplegia. Since the authors clearly recognize that these complications are avoidable and result directly from the placement of tight-fitting cannulas in the coronary ostia, I wonder how they plan to avoid such problems in the future. It does not appear that any of the three methods of cannulating the coronary ostia that they have described is safe. The common pattern, however, is to introduce the entire dilated tip of the Spencer-Mallette cannula into the coronary ostia beyond the level of the aortic wall. There are no diagrams in the article showing how these cannulas are positioned, so we must assume that they are introduced in this fashion. The problem of coronary ostial damage, as was commonly seen in the 60s, practically disappeared as topical hypothermia and cardioplegic methods became popular. However, with the revival of blood cardioplegia and continuous infusion, we undoubtedly will see a return of this problem as well. The basic principle being violated is the acute distention by the ballooned portion of the cannula itself, and it would not matter whether this is a Mayo or a Spencer-Mallettecannula. The longer the catheter or cannula remains in the vessel, the more likely that it will produce stenosis in the same manner as endotracheal cuff tubes cause stenosis of the subglottic area of the trachea. The method that the authors describe of "holding the cannulas in place by hand with removal and reinsertion for each injection" (p 577) will not prevent or avoid the problem if the cannula itself, with a dilated portion, is advanced into the coronary artery beyond the ostia. I believe the