SUMMARY We studied the electrophysiologic characteristics of ventricular muscle and Purkinje fibers from the hearts of five patients undergoing cardiac transplantation. All five patients had congestive failure and coronary artery disease before surgery and were receiving digitalis therapy. Ventricular DURING the last 2 years we have obtained ventricles from patients undergoing cardiac transplantation. These cardiac tissues were well preserved and not subjected to local trauma at cardiac surgery. In this paper, we report the cellular electrophysiologic properties of myocardial and Purkinje fibers from these hearts and the response of these fibers to certain cardioactive drugs. Methods Hearts were obtained from five patients at cardiac transplantation. Informed consent was obtained from each patient.Patient I was a 49-year-old female who had acute rheumatic fever at 19 years of age and an acute myocardial infarction at 45 years of age, followed by coronary artery bypass surgery. Congestive heart failure developed and was treated with digoxin, but her health continued to deteriorate; during the 6 months before From her cardiac transplantation she had two episodes of ventricular fibrillation. Before transplantation, severe biventricular failure with poor contractility of both ventricles was demonstrated. Her medications included digoxin, quinidine and, just before surgery, lidocaine. Patient 2 was a 15-year-old female in whom tetralogy of Fallot was diagnosed at 3 months of age. At 4 months of age she underwent a shunt procedure to increase pulmonary blood flow. Approximately 2 years before cardiac transplantation she began having episodes of hemoptysis. Cardiac catheterization revealed an occluded shunt and she underwent open heart repair of tetralogy of Fallot, during which she had a large anterolateral myocardial infarction. Subsequently, cardiac catheterization revealed severe right and left ventricular dysfunction and a large anteroapical aneurysm. Because of persistent severe congestive failure, cardiac transplantation was performed. Her medications before transplantation were digoxin and furosemide.Patient 3 was a 48-year-old male who had an acute myocardial infarction at 41 years of age. One year later, he had left ventricular failure that required digitalis and diuretics. Five months before transplantation, coronary angiography showed complete occlusion of the right coronary artery and a 60% proximal occlusion of the left anterior descending artery. Because of severe coronary artery disease deemed not remediable by bypass techniques, and severe cardiomyopathy, cardiac transplantation was performed.Patient 4 was a 48-year-old male who had his first myocardial infarction at the age of 43 years. This was

The HP diagnostic index relies less heavily on symptoms, subjective evaluations, and invasive tests than the Kenosha criteria, but both identified similar subsets of the 61 patients as having HP. The HP diagnostic index could provide a useful tool in future HP outbreaks, which are increasingly being recognized in metalworking facilities.

Both abnormal automaticity and triggered activity induced by delayed afterdepolarizations have been proposed as the primary mechanism for ventricular tachycardia (VT) occurring in dogs 24 hr after ligation of the left anterior descending coronary artery. Because of this controversy, we studied the effects of ventricular pacing and therapeutic concentrations of lidocaine and ethmozin on sustained rhythmic activity of isolated subendocardial preparations excised from the infarct, and on VT in conscious dogs. There were differences in the sustained rhythmic activity cycle length of isolated preparations and the VT cycle length that were attributable to the absence of sympathetic input in the former and its presence in the latter. In isolated tissues, pacing for 1 or 10 beats reset the sustained rhythmic activity and pacing for 1 min induced overdrive suppression. Lidocaine (5 gtg/ml) had no effect on sustained rhythmic activity but ethmozin (2 g.g/ml) suppressed it. Delayed afterdepolarizations occurred but appeared to be induced by pacing or by the hyperpolarization associated with recovery. Although delayed afterdepolarizations were infrequent at 24 hr, their frequency increased with the hyperpolarization of the membrane that occurred at 48 to 96 hr after infarction. Delayed afterdepolarizations also occurred more readily when superfusate temperature was lowered. In conscious dogs, pacing the VT for 1 or 10 beats or 1 min had no effect. Lidocaine (2 to 10 ,Lg/ml) did not affect the VT but ethmozin (2 to 5 gg/ml) increased VT cycle length significantly. Pacing for 1 min in the presence of ethmozin, but not lidocaine, converted VT to sinus rhythm. Our results suggest that although delayed afterdepolarizations occur at 24 hr after infarction in the standard Harris preparation, they are most readily seen as an accompaniment of hyperpolarization, pacing, or lowering of bath temperature. The predominant rhythm at 24 hr appears to be automatic. Circulation 71, No. 6, 1224-1236, 1985 PREVIOUS STUDIES 14have shown that the origin of the ventricular tachycardia (VT) that occurs 24 hr after ligation of the left anterior descending coronary artery in the dog is in the subendocardial zone of the infarct. These studies attributed the VT to automaticity of depressed subendocardial Purkinje fibers that survived the infarct, although the possibility of reentry was considered.2' 3 Triggered activity resulting from delayed afterdepolarizations has also been noted in the 24 hr infarct, and From the

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The effects of overdrive stimulation were studied on preparations of isolated canine cardiac Purkinje fibers using standard microelectrode techniques. Preparations were made from false tendons, the subendocardial right bundle branch and 24 hour infarct zone Purkinje fibers. Three types of automaticity were recognized: high potential automaticity occurred in fibers with maximal diastolic potentials greater than -70 mV, intermediate potential automaticity occurred in fibers with maximal diastolic potentials between -61 and -70 mV and low potential automaticity occurred in fibers with maximal diastolic potentials less than -60 mV. Short periods of overdrive (15 seconds or 30 beats) resulted in marked suppression of high potential automaticity, slight suppression of intermediate potential automaticity and little or no suppression of low potential automaticity. The extent of postoverdrive suppression of intermediate potential automaticity was related to the rate and duration of the overdrive train and the amount of hyperpolarization that occurred in the pacemaker fiber. Finally, in three experiments on Purkinje fibers from 24 hour infarct zones, delayed afterdepolarizations occurred. In two of these preparations, overdrive stimulation resulted in biphasic responses (postoverdrive enhancement followed by postoverdrive suppression). The results of this study suggest that it may be possible to design simple electrophysiologic tests to determine whether an automatic arrhythmia is being caused by normal or partially depolarized ectopic pacemakers.