Biomedical subjects
Publications and source records attributed to R F Kehoe.
The history of surgical attempts to control ventricular arrhythmia is reviewed and current methodology is presented in detail. The results of the various surgical approaches and future trends in the management of this troublesome condition are discussed.
Pre- and postoperative electrophysiologic study (EPS), intraoperative cardiac mapping, and extended endocardial resection of scar (EER) has enabled us to identify subgroups among 94 patients who have had operation to control or prevent malignant ventricular arrhythmia. Operative mortality was 8.5% and cure or prevention of ventricular arrhythmia was accomplished in 92% of survivors. Group 1: 13 patients were resuscitated from "sudden death" due to ventricular fibrillation (VF). All had exercise-induced VF and/or ventricular tachycardia (VT). Preoperative EPS revealed no inducible VT/VF. All had coronary artery disease, without evidence of myocardial infarction (MI) or ventricular wall motion abnormality; all were cured with conventional myocardial revascularization. Group 2: 65 patients had MI with residual left ventricular wall motion abnormality, usually aneurysm. The malignant arrhythmia, either sustained VT (38 patients) or VF (27 patients), was inducible by EPS but not usually by exercise, and all were refractory to medical therapy. Treatment was operative mapping, aneurysmectomy, EER, and coronary revascularization. Operative mortality was 11.9%; 90% of survivors are arrhythmia free, off drugs; 10% are now drug responsive. Group 3: 3 patients without coronary disease had VT or VF caused by endocardial sarcoidosis or operative scar from a previous congenital heart operation. Treatment was EPS, operative mapping, and excision of abnormal endocardial scar with no operative mortality. Group 4: 13 patients underwent aneurysmectomy for indication other than arrhythmia, but had preoperative ventricular irritability which was not life-threatening. Operation was aneurysmectomy, prophylactic EER, and revascularization with no mortality and no postoperative arrhythmic events. After many years of unpredictable and unsatisfactory results from various empirical surgical approaches, the operative treatment of malignant ventricular arrhythmia is now based on sound electrophysiologic principles.
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A total of 40 patients with drug-refractory, life-threatening cardiac rhythm disturbances--ventricular tachycardia in 23 patients and ventricular fibrillation in 17 patients--underwent extended endocardial resection (EER) of scar tissue. Scarring was due to myocardial infarction in 38 patients, to previous congenital heart operation in 1 patient, and to sarcoidosis of the heart in 1. The EER procedure was directed by epicardial and endocardial mapping data whenever possible, and was usually combined with revascularization, aneurysmectomy, or, in 5 patients, mitral valve replacement. Operative mortality was 10%, incident to poor preoperative ventricular function and hemorrhage secondary to previous cardiac surgical procedures. Thirty-three of the 36 survivors (92%) are free of arrhythmia at follow-up periods ranging from 3 to 36 months (mean, 12.5 months); the arrhythmia in the remaining 3 patients is now drug controlled. Thirty-three patients had postoperative electrophysiological studies, and in 30 (91%), the arrhythmia was no longer inducible. The results of surgical treatment for ventricular tachycardia and ventricular fibrillation were similar. The results also proved satisfactory whether the EER procedure was directed by visual observation or mapping.
The clinical electrophysiologic findings in four patients with biopsy-proven polymyositis and bifascicular block are described. Atrioventricular (AV) block developed in two of these four patients, and intracardiac electrophysiologic studies documented the site of spontaneous block to be distal to the His bundle in one, whereas in the second marked His-ventricular prolongation was found, and distal block developed at low paced atrial rates. Sinus node and AV nodal function were normal in all four. These electrophysiologic data provide the first documentation of the site of AV block in patients with polymyositis and correlate well with findings of previous pathologic studies that have shown extensive fibrosis of the distal His bundle and bundle branches.
Oral administration of a 1.5-gm dose of N-acetylprocainamide (NAPA) to 9 patients with premature ventricular contractions (PVCs) confirmed previous indirect evidence that this metabolite of procainamide has antiarrhythmic efficacy and potency comparable to those of procainamide. Although the mechanism by which NAPA acts as an antiarrhythmic drug is not known, it was found that the 6 patients with coupled PVCs responded to NAPA therapy and that the 3 patients without coupled PVCs failed to respond. Coupling interval prolongation also occurred during NAPA therapy in 4 of the 6 responding patients. These observations suggest that NAPA may terminate coupled PVCs by slowing and then interrupting conduction of re-entrant impulses, as has been proposed for procainamide. NAPA plasma concentrations of 7.4-17.2 mug/ml were well tolerated by the patients and produced an average fall of 3 mm Hg in mean arterial pressure and a 7.6% mean increase in corrected QT interval.
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