Endocardial ventricular mapping of 21 ventricular tachyardias (VT) in 17 patients was performed using electrode catheters. Activation at multiple left and right ventricular sites was utilized to determine the site of origin of the VT. Eleven VT had a left bundle branch block pattern (VT-LBBB) and 10 VT had right bundle branch block pattern (VT-RBBB). In all VT-RBBB the earliest site of activation was in the LV or septum. In VT-LBBB the earliest site was RV (4/11), LV (5/11) and septum (2/11). All ventricular tachycardias with QRS less than 140 msec arose in the septum. In patients with an aneurysm, the site of origin of ventricular tachycardia was always in the aneursm. All VT-LBBB arising from the left ventricle originated in an aneurysm involving the septum. QRS changes during ventricular tachycardia were associated with alterations in the patterm of ventricular activation without alteration of the site of origin. In three patients the site of origin predicted by endocardial ventricular mapping was confirmed intraoperatively by epi- and/or endocardial mapping. We conclude that endocardial ventricular mapping demonstrates the limitations of the surface electrocardiogram in localizing the site of origin of ventricular tachycardia. The method may provide important data upon which the surgical therapy of ventricular tachycardia is based.

We developed an isolated rabbit atrial preparation which responds consistently and reproducibly to brief, submaximal stimulation of the autonomic nerves contained in it. In 6 of 11 preparations in the presence of propranolol (1 mg/liter), the time course of changes in the atrial rate following 120 msec vagal stimulation was bimodal. The maximal slowing occurred at 0.64 +/- 0.16 second, and the peak secondary slowing occurred at 2.3 +/- 1.0 seconds. An acceleratory component occurred between the first and second peaks between 0.8 and 1.6 seconds. The total time course of vagal effect lasted for 5.0 +/- 2.0 seconds. These changes in rate could not be explained by shifts in the location of the primary pacemaker. The acceleratory component was due to a 4.7 +/- 2.0 (SD) mV depolarization of the maximum diastolic membrane potential of the primary pacemaker of the sinus node which lasted for 1.8 +/- 0.3 seconds. Following vagal stimulation, there was an increase of 0.2 mM in the activity of potassium in the extracellular space recorded with a potassium-sensitive electrode; this peaked between 1.4 and 2.5 seconds and cleared with an exponential time course. The halftimes for recovery ranged between 2.8 and 4.6 seconds. The initial peak slowing of the bimodal time course and the acceleratory component therefore appear to be direct effects of acetylcholine. The secondary slowing occurs after acetylcholine presumably has been inactivated and occurs coincidently with the accumulation of potassium in the extracellular space.

Standard microelectrode techniques were used to record transmembrane potentials and determine conduction characteristics in regions of mottled infarcts of canine epicardium, 3 to 5 days or 8 to 15 days after left anterior descending coronary artery occlusion and reperfusion. At 3 to 5 days, resting potential, action potential amplitude, maximal rate of depolarization and action potential duration at 30% repolarization were significantly reduced in the infarcted region. Cells on the epicardial surface showed improvement in resting potential, action potential amplitude and rate of depolarization between 3 to 5 days and 8 to 15 days after infarction. In normal noninfarcted tissues, conduction velocity parallel to fiber orientation was 0.54 +/- 0.06 m/s (mean +/- standard deviation). Slow conduction in infarcted regions ranged from 0.015 to 0.2 m/s. Action potentials recorded from slowly conducting regions tended to include cells with more depressed amplitude and rate of depolarization than other cells in infarcted regions; they also had inappropriately depressed overshoot relative to their resting potential. Action potentials in slowly conducting areas where local conduction block occurred were associated with prepotentials and notches on their depolarization and repolarization phases. The prepotentials and notches appeared to be caused by electrotonic interactions resulting from microcircuitous conduction around or across inexcitable areas. These findings demonstrate that areas of slow conduction are heterogenously distributed in the mottled infarct and suggest that disruptions in cell to cell electrical continuity and decreased excitability may contribute to this slow conduction.

The identification of afterdepolarizations and their relationship to arrhythmias in vivo is not available. Experiments were undertaken to determine whether afterdepolarizations could be detected in monophasic action potentials (MAPs) recorded in vivo and whether they were related to arrhythmias in an intact canine preparation of the long QT syndrome. Isolated cardiac tissues from six dogs were studied to validate the technique. In simultaneous MAP and transmembrane recordings, afterdepolarizations induced with barium (early) or acetylstrophanthidin (delayed) were detected in MAPs when present in microelectrode recordings. MAPs were then recorded in situ in eight dogs with cesium chloride-induced long QT syndrome associated with ventricular arrhythmias. Afterdepolarizations were identified in each of the dogs and were similar to early afterdepolarizations identified in vitro; they occurred during phase 3 and were attenuated during overdrive pacing. The afterdepolarizations were closely related to arrhythmias: (1) afterdepolarizations always preceded ventricular arrhythmias, (2) the coupling intervals (CI) of the afterdepolarizations (AD) and the ventricular premature beats (VPB) were nearly identical (VPB CI = 1.06 AD CI -10.24; r2 = .87), (3) the take-off potentials of the ventricular premature beats were nearly identical to the amplitude of the afterdepolarizations (take-off potential = 0.98 afterdepolarization amplitude +0.46, r2 = .87), and (4) afterdepolarizations and ventricular arrhythmias resolved concurrently during overdrive pacing and with time. Thus, a new catheter technique has been validated and has been used to directly identify afterdepolarizations and triggered activity in vivo.

The relationship between the functional refractory periods of the specialized cardiac conduction system and of the ventricular muscle is of major importance in the genesis of ventricular fibrillation by a single premature beat arising in the specialized conducting system. Wiggers and Wegria 1 demonstrated that premature ventricular excitation must occur in late systole during the inscription of the T wave in order for ventricular fibrillation to be initiated by a single premature stimulus, i.e., excitation must occur in the functional refractory period of ventricular fibers. If the functional refractory period of Purkinje tissue exceeds that of the ventricular muscle, an early premature discharge in the Purkinje system or an impulse transmitted from the A-V node could not excite the ventricles sufficiently early to cause ventricular fibrillation; excitation of ventricular muscle via the Purkinje system would by necessity occur after expiration of the ventricular vulnerable period. However, if the Purkinje tissue has a functional refractory period equal to or less than that of ventricular muscle, a premature systole conducted over