SPEAK, JOSEPH F., AND E. NEIL MOORE. A comparison of alternation in myocardial action potentials and contractility. Am. J. Physiol. 220(6): 1708-1716. 197 1 .-The transmembrane potentials and isometric force of contraction were simultaneously recorded from the isolated papillary muscles of the cat, rabbit, guinea pig, and rat right ventricles, and from frog ventricular trabeculae. The pattern of behavior of the mammalian myocardium in response to rate, rhythm, and temperature changes argues that the basis for mechanical alternation is not alternation in the action potential. Alternation in the action potential appears to occur secondarily to alternation in contractile force. It is suggested

SUMMARY Ventricular tissues were obtained at the time of operation from 12 patients who underwent aneurysmectomy or mitral valve replacement. The electrophysiologic characteristics of these tissues were determined in a tissue bath using microelectrodes. Normal-appearing action potentials were recorded from surviving Purkinje fibers and ventricular muscle cells within infarcted ventricular tissues. Normal muscle action potential recordings from infarcted tissues were similar to action potentials from noninfarcted papillary muscles, except that the duration of the action potential was significantly longer in the former. In other areas slow response potentials were recorded. These action potentials conducted slowly and were eliminated by verapamil. We observed verapamil-sensitive slow response automaticity, but this did not correlate with ventricular tachycardias, present in three patients. Variable amplitude responses arising from normal resting potentials and characterized by stimulus intensity-dependent changes in action potential amplitude were recorded in tissues from two patients. These potentials had many characteristics similar to the slow response, but were not eliminated by verapamil. We also saw inexcitable cells with both normal and abnormal resting potentials. The heterogeneous electrophysiologic characteristics of these tissues provide a likely substrate for arrhythmias and may be the source of the ectopic ventricular rhythms observed in these patients. cardium 1-60 months after acute myocardial infarction. The observations indicate that both Purkinje fibers and muscle cells survive. We also document persistent electrophysiologic abnormalities in surviving cells of tissues obtained as late as 60 months after infarction. MethodsSpecimens of human ventricular tissue were obtained from 12 patients at the time of cardiac surgery. The patients ranged in age from 37-68 years. Aneurysmectomy was performed for intractable heart failure or ventricular tachycardia. Mitral valve replacement was performed for severe mitral regurgitation. Before surgery, all patients had some degree of chronic congestive heart failure (table 1). Three of the 12 patients had chronic sustained ventricular tachycardia. No patients had evidence of digitalis toxicity. Cardioactive drugs were discontinued at least 24 hours before operation in nine of 12 patients without ventricular tachycardia, but were continued in the three patients with arrhythmia to the time of surgery. Morphine and halothane were used as anesthetics.The tissues were resected promptly at the initiation of cardiopulmonary bypass and were placed in continuously oxygenated, cooled (20-21°C) Tyrode

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Little information is available on how acute ischemia modifies the electrophysiologic substrate associated with long Q-T interval conditions. We studied the effects of low-flow ischemia (10 min at 5.0 ml/min followed by 10 min of 2.5 ml/min) in Langendorff perfused rabbit hearts during control and in hearts 20 min after the addition to the perfusate of 92 microM d-sotalol, which reliably produced triggered activity. Epicardial electrograms, a left ventricular endocardial monophasic action potential (MAP), and simulated X and Y lead electrocardiograms were used to characterize myocardial activation and recovery during ventricular pacing. In the control hearts, conduction velocity as indicated by the mean epicardial activation time accelerated for most of the period of ischemia (maximum decrease of -9.4 +/- 7.9%). The mean activation-recovery interval, MAP duration, and Q-T interval were moderately decreased (-4.9 +/- 8.6%, -7.5 +/- 4.4%, and -4.6 +/- 2.3%, respectively). The mean standard deviation of the activation-recovery interval (epicardial heterogeneity of recovery) was increased by 34.6 +/- 23.4%. d-Sotalol had no effect on conduction but prolonged myocardial recovery time, increased heterogeneity, and produced triggered arrhythmias in all hearts. Within 2 min of ischemia triggered activity was eliminated. With d-sotalol, ischemia slowed conduction and produced relatively larger decreases in the activation-recovery interval, MAP duration, and Q-T interval (-11.8 +/- 10.3%, -13.9 +/- 12.0%, and -15.8 +/- 11.2%). The increased epicardial heterogeneity seen with d-sotalol was attenuated by ischemia. Thus ischemia superimposed on long Q-T conditions had antiarrhythmic as well as arrhythmogenic effects.

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