Lura Harrison

Cryosurgical ablation of the A-V node-His bundle: a new method for producing A-V block.

A cryosurgical instrument was used to ablate atrioventricular conduction. The procedure was carried out in 20 dogs and subsequently in three patients with drug resistant, life-threatening supraventricular tachycardias. In patients, the cryosurgical unit lowered the temperature of the His bundle area to 0°C, effecting complete but reversible heart block. Rewarming resulted in resumption of normal atrioventricular conduction. The His bundle region then was cooled to −60°C; complete heart block was produced with two or more 90–120 second freezes. Postoperative evaluations revealed persistent atrioventricular conduction block. The lesion showed no tendency to rupture, form aneurysm, or interfere with valvular function. In the clinical cases, postoperative studies demonstrated a stable pacemaker arising proximal to the branching portion of the His bundle. A potential application of the cryosurgical technique might be ablation of sites of dysrhythmia (i.e., ectopic foci, re-entry circuits, accessory pathways).

The transition to ventricular fibrillation induced by reperfusion after acute ischemia in the dog: a period of organized epicardial activation.

Ventricular fibrillation was induced in eight of 10 open-chest dogs by reperfusion after a 15-minute occlusion of the proximal circumflex coronary artery. Simultaneous recordings were made from 27 epicardial electrodes spaced over both ventricles. Analysis of the initial 1.5–2.5 seconds of the transition from sinus rhythm or ventricular tachycardia to fibrillation revealed that ventricular activation occurred in an orderly, rapidly repeating sequence in all hearts. Each activation front arose near the border of the ischemicreperfused region and passed across the nonischemic portion of the ventricles to the opposite side of the heart as a single, organized wavefront. As the arrhythmia progressed, the time between the appearance of successive activation fronts on the epicardium decreased. Concurrently, the time for each activation front to traverse the ventricles increased. The simultaneous increase in rate of appearance and decrease in conduction velocity for each successive cycle resulted in overlapping cycles in which a new activation front arose from the ischemicreperfused region before the previous front terminated over the right ventricle. The overlap between successive activation fronts increased as the arrhythmia continued. Thus, ventricular activation during the transition to ventricular fibrillation arose near the border of the ischemic-reperfused region and was organized as it passed across the nonischemic tissue, but the body surface ECG appeared disorganized because of variable spacing between successive, coexistent activation fronts.

Cryosurgical ablation of the atrioventricular node-His bundle: long-term follow-up and properties of the junctional pacemaker.

We used a cryosurgical technique to ablate the atrioventricular (AV) node-His bundle in twenty-two selected patients with disabling supraventricular tachyarrhythmias unresponsive to medical management. Successful AV block was achieved in seventeen. There was no intraoperative mortality and significant surgical complications were not encountered. Electrophysiologic studies performed 7-10 days after surgery revealed that the subsidiary pacemaker had a narrow QRS complex morphology and a mean cycle length of 1244 msec. Isoproterenol (1-4 microgram/min i.v.) significantly increased (p less than 0.01) the rate of the subsidiary pacemaker (mean maximum response 1008.3 msec); atropine (2 mg i.v.) had no effect on its rate. The cycle length of the subsidiary pacemaker during long-term follow-up (mean 14.8 months) showed a small but significant (p = 0.024) increase (mean cycle length 1430 msec). Treadmill exercise in seven patients did not result in the subsidiary pacemaker exceeding the rate of the implanted demand pacemaker set at 70 beats/min. The properties of the subsidiary pacemaker suggest an intra-Hisian site of impulse formation.

A computerized method for the rapid display of ventricular activation during the intraoperative study of arrhythmias.

Arrhythmias which last for only a few cycles or exhibit activation sequences that change from cycle to cycle may occur during the intraoperative study of ventricular tachyarrhythmias. To map these transient, varying arrhythmias requires recording from numerous sites simultaneously, which cannot be done with a single, hand-held electrode probe. Therefore, a computerized method was developed to record potentials simultaneously from up to 27 electrodes and to display epicardial and transmural activation sequences rapidly.Three arrays of electrodes are used. The electrodes of the first array are distributed over the epicardium of both ventricles and fixed within a flexible nylon mesh sock. The electrodes of the second array form a 3-cmsquare grid and are used to obtain a more detailed activation map of a small region of epicardium. The electrodes of the third array are spaced along the shafts of needles that are inserted through the myocardium to record transmural activation. The potentials recorded from an array of electrodes and the computer-selected activation times at the electrodes are displayed for visual inspection after which a map of activation is drawn. The activation sequence of a single cycle can be displayed 10 minutes after recording the potentials. The activation map obtained from the sock array determines the placement of the grid array; the map resulting from the grid array determines the placement of the needle array. Thus, the region responsible for initiating an arrhythmia can be determined if the arrhythmia can be induced three or more times.

Epicardial mapping of the onset of ventricular tachycardia initiated by programmed stimulation in the canine heart with chronic infarction.

The initial beats of ventricular tachycardia (VT) induced by programmed stimulation (PS) of the heart have frequently been observed to differ in QRS configuration from the subsequent uniform QRS complexes of tachycardia. The transient nature of these initial beats has made their study difficult during epicardial mapping with conventional, hand-held recording electrodes. Twenty-four dogs were studied with PS 1-10 months after coronary ligation. Twenty-six epicardial electrograms were recorded simultaneously during PS. The data were digitized for computer generation of isochronic maps for any desired beat. Three patterns of initiation were observed in episodes of tachycardia in which the initial beats differed from the subsequent beats of VT (11 of 18 runs of VT). Most frequently, the initial beats of VT originated near the pacing electrode before moving to a stable infarction zone location. Less frequently, the initial beats were due to transient reentry in the bundle branches or a transient shifting of early breakthrough sites in the infarction zone.

Electrophysiological effects of lidocaine on distal Purkinje fibers of canine heart

Abstract These studies were designed to examine the electrophysiological effects of lidocaine on distal Purkinje fibers of the canine heart. Standard microelectrode techniques were used to record transmembrane action potentials from the right bundle branch, free running strands of Purkinje tissue, and ventricular muscle. The duration of action potentials was maximal in the distal Purkinje fibers. The long duration of action potentials in these distal fibers determined the functional refractory period of the Purkinje-muscle junction. Early premature beats initiated on either side of the distal Purkinje fibers propagated with decrement or were blocked. Lidocaine shortened the action potential of Purkinje fibers but had little effect on muscle. The effect of lidocaine on action potential duration was dose dependent and was maximal in these distal Purkinje fibers. As a consequence of its ability to shorten action potential duration, lidocaine reduced the degree of nonuniformity of recovery of excitability. Lidocaine shortened the functional refractory period of distal Purkinje fibers and abolished decremental conduction of early premature beats. These effects may contribute to the antiarrhythmic actions of lidocaine.

The sock electrode array: a tool for determining global epicardial activation during unstable arrhythmias.

The conventional technique for mapping the sequence of epicardial activation uses a hand‐held electrode moved over the heart to record from a number of epicardial sites one at a time, and requires 5–15 minutes to record from 50 or more sites distributed over the entire ventricular epicardium. This method is inadequate for arrhythmias that are transient or vary from beat to beat. To overcome these limitations the “sock electrode array,” a contour‐fitting sock containing 26 or 52 electrodes, has been developed. The nylon mesh sock is pulled over the heart and permits simultaneous recording of potentials from electrodes distributed over the entire ventricular epicardium. The electro‐grams are recorded and converted to digital form for computer generation of isochronous maps. Maps of the epicardial activation sequence derived from the sock electrode were compared to those obtained by the hand‐held electrode in six normal dogs during sinus rhythm and ventricular pacing. The sequence of local activation times acquired by both methods showed similar areas of early and late activation and comparable isochronous maps. The hand‐held electrode technique required 10–15 minutes for data acquisition and another 15–30 minutes for analysis. The sock electrode array allowed electrograms from 26 epicardial electrodes to be recorded simultaneously during one cardiac cycle and computer generated isochronous maps could be displayed within 10 minutes. This method allows rapid recording and analysis of epicardial electrical phenomena and should meet the time constraints imposed during the intraoperative study of ventricular tachyarrhythmias in patients.

A computer system for the intraoperative mapping of ventricular arrhythmias.

Abstract A computer system has been developed to measure the electrical activation sequence of the heart during ventricular tachyarrhythmias. The system incorporates 32 channels of parallel analog-to-digital conversion, rapid generation of results, a high degree of user interaction, and ability to capture events occurring at essentially random times. The system has been used extensively in the animal laboratory as a prototype for a system to be used in the surgical treatment of ventricular tachycardia. It has been shown to be an effective and practical tool in the location of the site of early activation during cardiac arrhythmias.

Mechanisms of bradycardia-induced ventricular arrhythmias in myocardial ischemia and infarction.

Experimental and clinical cases have been described in which bradycardia, i.e., heart rates below 60 beats/min or slowing of the heart rate, resulted in lethal ventricular arrhythmias during various stages of myocardial ischemia and infarction. The present study was designed to determine the relationship of lethal ventricular arrhythmias and slow heart rates. In 18 dogs anesthetized with sodium pentobarbital, the left anterior descending (LAD) coronary artery was ligated. Standard ECGs, His bundle electrograms and composite electrograms from intramural and epicardial areas in ischemic and normal zones were recorded during the first 3 hours of ischemia. Vagosympathetic trunk stimulation caused varying degrees of slowing and bradycardia. Of the 18 dogs, slowing of the heart rate or marked bradycardia induced ventricular ectopic beats coupled to the sinus beats in two, sustained ventricular tachycardia in two, and ventricular fibrillation in two. In another group of six dogs studied 17-25 days after LAD ligation, one dog showed sustained ventricular tachycardia in response to vagal-induced bradycardia. In all acute or chronic cases of arrhythmias after LAD ligation, continuous electrical activity was recorded on one or more of the electrograms within or overlying the ischemic or infarcted zones. This bridging electrical activation, which is indicative of slow conduction, provided strong presumptive evidence for reentry as the mechanism of lethal or potentially lethal ventricular arrhythmias triggered by bradycardia in the setting of myocardial infarction.

Analysis of interectopic activation patterns during sustained ventricular tachycardia.

We analyzed the patterns of interectopic continuous electrical activity recorded within interectopic intervals of sustained ventricular tachycardias. These arrhythmias were induced in dogs that were studied 4 days after left anterior descending coronary artery occlusion. Standard ECG leads and electrograms from the His bundle and left ventricular epicardium, both infarct and normal zone, were recorded. In 19 of 24 dogs with transmural myocardial infarction, one to three ventricular paced beats induced sustained ventricular tachycardia, characterized by continuous electrical activity between the initiating and spontaneous ectopic beat and between successive ectopic beats recorded from the epicardium over the infarct zone but not from the normal epicardium. Continuous activity consisted of discrete potentials that were reproduced in each cardiac cycle, suggesting slow conduction within a reentrant circuit. The interectopic activity was divided into three distinct temporal periods, delineated by potentials occurring at the initial portion, the mid-interectopic portion and terminal portion or exit of the slow conduction segment of the presumed reentrant circuit. In some cases, sustained ventricular tachycardia was induced only if an appropriate initial potential was engaged. Spontaneous termination of the sustained ventricular tachycardia was associated with Wenckebach-like block of conduction, in the initial or exit potential. Ventricular pacing caused alteration of the interectopic patterns and resulted in cessation of the arrhythmia. Procainamide produced dose-dependent slowing of the ectopic rate due to depression of conduction in the mid-interectopic portion of the continuous electric activity. Inducibility of the sustained ventricular tachycardia was inhibited by decremental conduction in this compartment of the presumed reentry circuit.The present study uses a preparation showing sustained ventricular tachycardia that is stable and regular. Functional analysis of the various portions of the continuous electrical activity during sustained tachycardias allows further insight into the mechanisms of initiation and termination of sustained ventricular tachycardias. The ability to localize the effect of antiarrhythmic drugs on specific portions of a possible reentrant circuit may provide important correlative data for the analysis and interpretation of detailed epicardial mapping studies.