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Ann Thorac Surg 1986;41:622-629
© 1986 The Society of Thoracic Surgeons
Department of Surgery, Duke University Medical Center, Durham, NC, and the Department of Surgery, Division of Cardiothoracic Surgery, Washington University School of Medicine, St. Louis, MO
Accepted for publication September 9, 1985.
* Address reprint requests to Dr. Cox, 3108 Queeny Tower, 4989 Barnes Hospital Plaza, St. Louis, MO 63110
The addition of calcium channel-blocking agents to a standard hyperkalemic hypothermic cardioplegic solution has been examined both experimentally and clinically. None of these studies, however, have investigated the effect of calcium blockade during cardioplegic arrest on the specialized cardiac conduction tissues and on the subsequent development of arrhythmias after arrest. The present study examined the effect of adding nifedipine to standard cardioplegic solution administered in a canine experimental preparation modeled on routine clinical techniques. The time to and duration of electrical arrest following the administration of cardioplegia and the functional electrophysiological variables before and after arrest were measured using a 32-channel data acquisition system. The addition of nifedipine shortened the time to electrical arrest and prolonged the duration of arrest compared with standard potassium cardioplegic solution alone, without a deleterious effect on conduction function immediately after arrest. The occurrence of low-amplitude electrical activity (LEA) in both atria and ventricles during arrest was significantly reduced by the addition of nifedipine, thereby suggesting a possible correlation between LEA and calcium-mediated conduction occurring under conditions of standard cardioplegic arrest.
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T. B. Ferguson Jr., L. S. Smith, P. K. Smith, R. J. Damiano, and J. L. Cox Electrical Activity in the Heart during Hyperkalemic Hypothermic Cardioplegic Arrest: Site of Origin and Relationship to Specialized Conduction Tissue Ann. Thorac. Surg., April 1, 1987; 43(4): 373 - 379. [Abstract] [PDF] |
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