Mechanism of ventricular fibrillation in man. Observations based on electrode catheter recordings.
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Biomedical subjects
Publications and source records attributed to L N Horowitz.
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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.
Two or more morphologically distinct ventricular tachycardias were observed during electrophysiologic study in 14 patients with chronic sustained ventricular tachycardia. Nine of these patients had clinical ventricular tachycardia with multiple morphologies. During the study 13 patients manifested both right bundle branch block (RBBB) and left bundle branch block (LBBB) morphologies. The remaining patient had RBBB with both right and left axis deviation. Changing morphologies were observed spontaneously in four patients and could be produced in all 14 by ventricular stimulation. In 12 patients both RBBB and LBBB originated in the left ventricle, and in 11 of these patients, from within a left ventricular aneurysm. Diastolic fragmented activity representing reentry was unchanged during both morphologies in four patients and during one morphology in five patients. Epicardial mapping confirmed the aneurysm as the site of origin of multiform ventricular tachycardias in two patients. Our data suggest that 1) ventricular tachycardia is frequently pleomorphic; 2) multiple morphologies usually represent variable exit sites and/or ventricular activation during the same tachycardia; and 3) there is a frequent association of pleomorphic ventricular tachycardia with left ventricle aneurysm.
The electrocardiographic pattern of right bundle branch block (RBBB) is routinely observed after transatrial repair of tetralogy of Fallot even though no ventriculotomy has been performed. The mechanism of this conduction disturbance was studied in 16 patients with tetralogy of Fallot and one patient with infundibular pulmonic stenosis. Preoperative ECGs and vectorcardiograms showed right ventricular hypertrophy and no RBBB. Epicardial activation maps were obtained before and after total surgical repair in all patients and after infundibular resection but before closure of ventricular septal defect (VSD) in four of these patients. After infundibular resection, RBBB appeared and activation was markedly delayed (greater than 30 msec) over the pulmonary outflow tract, but was unchanged over the body of the right ventricle. No further changes in ventricular activation occurred after closure of the VSD. This study shows that RBBB after transatrial repair of tetralogy of Fallot is usually produced by infundibular resection, but not by VSD closure, and is associated with delayed activation of the pulmonary outflow tract and base of the right ventricle which results from damage to portions of the right ventricular conduction system.
The ventricular fibrillation threshold (VFT) was measured in 28 patients at the time of cardiac surgery. The VFT was measured with a 100 Hz train of 24 rectangular pulses positioned across the ST segment and T wave. Current was applied to the epicardial surface of either ventricle with a bipolar electrode probe. In six patients, the normal right VFT was 24.3 +/- 5.2 mA, and in 10 patients the normal left VFT was 33.6 +/- mA (p less than 0.05). In 12 patients with greater than or equal to 75% obstruction of the left anterior descending coronary artery, the left VFT was 18.6 +/- 6.9 mA. This value was significantly less than the left VFT in patients without coronary artery disease (p less than 0.001). This study shows that the VFT can be measured in man and that coronary artery disease reduces this parameter.
Twelve patients with medically refractory ventricular tachycardia secondary to ischemic heart disease underwent surgery for cure of their arrhythmia. Preoperatively, the tachycardia could be reproducibly initiated and terminated in each patient by programmed stimulation. In all instances, intraoperative mapping localized the tachycardia to the border of the aneurysm, a site not routinely resected during aneurysmectomy. In nine instances, the area of origin involved the septum. During bypass the tachycardia could still be induced after standard aneurysmectomy or ventriculotomy in 11 of 12 patients. On the basis of intraoperative mapping, resection of endocardium in the area of origin (25--40% the circumference of the aneurysmectomy) up to normal muscle was performed. In one patient without a discrete aneurysm, endocardial excision alone through a ventriculotomy was performed. There was one operative death due to cardiogenic shock (preoperative ejection fraction 5%) and one late death due to rupture of a mycotic aneurysm in the pulmonary artery. Before discharge, all patients underwent a repeat relectrophysiologic study off antiarrhythmic agents and in none could ventricular tachycardia be initiated. Hemodynamic and angiographic catheterization showed improved hemodynamics and ejection fractions in all. The 10 survivors remained free of sustained ventricular tachycardia for 9--20 months, with one late nonarrhythmic death.
Eighty patients (69 with documented or suspected recurrent ventricular tachycardia or fibrillation, ten with left bundle-branch block, and one with the Wolff-Parkinson-White syndrome) underwent both right ventricular and left ventricular programmed electrical stimulation, including ventricular pacing and the introduction of one or two ventricular extrastimuli or electrode catheter mapping of the left ventricle (or both). Left ventricular catheters were introduced precutaneously via the femoral artery (of 61 patients, one required secondary repair) or via brachial arteriotomy (of 19 patients, two required secondary repair). All patients received an intravenously administered bolus of hep arin (5,000 units) following the insertion of the left ventricular catheter and then 1,000 units/hr after the first hour of study. No patients had cerebrovascular, systemic thromboembolic, or cardiac sequelae. In four (12 percent) of 34 patients with inductible ventricular tachycardia, programmed electrical stimulation of the left ventricle was required for initiation. Extensive left ventricular endocardial mapping was performed in 45 patients. Our experience suggests that (1) electrophysiologic study of the left ventricle can be performed safely, (2) programmed electrical stimulation of the left ventricle is indicated when a suspected ventricular tachyarrhythmia cannot be induced from the right ventricle, and (3) endocardial mapping of the left ventricle is indicated when surgery is being considered to abolish recurrent sustained ventricular tachycardia.
Twelve of 60 consecutively studied patients undergoing electrophysiologic study for paroxysmal supraventricular tachycardia had atrioventricular (A-V) bypass tracts functioning as the retrograde limb of the reentrant circuit. None had evidence of preexcitation in the surface electrocardiogram, but in two patients anterograde preexcitation could be produced by pacing from the coronary sinus. In all 12 patients with concealed bypass tracts the retrograde atrial activation sequence or effect of left bundle branch block aberration during the tachycardia, or both, confirmed the left-sided bypass tract. A negative P wave in lead I during the tachycardia was also diagnostic of a left-sided bypass tract. Dual A-V nodal pathways were found in five patients with concealed bypass tracts but were unrelated to the development of the tachycardia. When compared with supraventricular tachycardia due to A-V nodal reentry, clinical findings suggestive of a concealed bypass tract included: (1) P wave following the QRS complex (12 of 12 versus 12 of 40), (2) negative P wave in lead I during the tachycardia, and (3) bundle branch block aberration during the tachycardia (8 of 12 versus 3 of 40). Other characteristics of patients with concealed bypass tracts that were of less value in individual cases were shorter cycle lengths of tachycardia, younger patient age and lesser incidence of organic heart disease.
Two hundred patients underogoing coronary bypass graft surgery were studied to determine the frequency and significance fo new fascicular conduction distrubances. The follow-up period ranged from 13 to 39 months. New disturbances developed in 39 patients (20 percent). Isolated right bundle branch block (6 percent) and left anterior hemiblock (6 percent) were the most common disturbances. Righ bundle branch block was usually transient and was not associated with further complications in the follow-up period. However, patients with either transient or persistent left bundle branch block or left anterior hemiblock, or both, had (1) increased later mortality compared with patients without new fascicular conduction disturbances (5 of 26 versus 11 of 161; P less than 0.02), and (2) increased late myocardial infarction (2 of 26 versus 2 of 161; P less than 0.05). New left fascicular conduction disturbances after coronary surgery identified a subset of patients with more extensive ischemic heart disease, suggesting that these patients require close follow-up care.
Ventricular fibrillation occurred in 10 (3.3 percent) of 300 patients consecutively studied with programmed ventricular stimulation. One hundred twenty-five of these patients were studied with double ventricular extrastimuli including 68 patients with and 57 patients without documented or suspected ventricular tachycardia or fibrillation, or both. Ventricular fibrillation did not develop in response to a single ventricular extrastimulus delivered during sinus rhythm, ventricular pacing or ventricular tachycardia or in response to ventricular pacing at cycle lengths of 300 msec or greater and occurred only in response to double ventricular extrastimuli. All 10 patients who manifested ventricular fibrillation during programmed stimulation were in the group of patients with suspected or documented ventricular tachycardia or fibrillation. Ventricular fibrillation was initiated in seven patients with double ventricular extrastimuli delivered during sinus rhythm or ventricular pacing and in three patients with double ventricular extrastimuli delivered during ventricular tachycardia. Four patients had spontaneous conversion to sinus rhythm and the remainder underwent defibrillation without sequelae. Recurrent ventricular fibrillation occurred clinically in 7 of the 10 patients. This study suggests that ventricular fibrillation occurs uncommonly during programmed ventricular stimulation and only in response to double ventricular extrastimuli in patients in whom spontaneous episodes are likely to occur.
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The electropharmacology of tocainide, an orally active congener of lidocaine, was evaluated in 10 patients with coronary artery disease. Electrophysiologic measurements including sinus nodal recovery time, sinoatrial conduction time, intraatrial conduction time, atrial, atrioventricular (A-V) nodal and ventricular refractory periods and intraventricular conduction time were obtained before and after intravenous infusion of tocainide. At blood levels shown to be effective against ventricular arrhythmias, tocainide produced no statistically significant changes in the electrophysiologic measurements, although occasional marked individual effects were observed. No side effects were observed during these studies. No adverse effects on A-V conduction were observed in patients with an intraventricular conduction disturbance or a prolonged control H-V interval. Thus, plasma tocainide concentrations effective in the therapy of ventricular arrhythmias exert no adverse effects on cardiac electrophysiologic properties in patients with coronary artery disease.
The components of the reentrant circuit were evaluated in 26 patients in whom sustained ventricular tachycardia could be reproducibly initiated or terminated, or both. Observations suggesting that the proximal His-Purkinje system was not a requisite component included (1) lack of requirement for retrograde His-Purkinje delay or bundle branck reentry, or both, for initiation of the tachycardia: (2) anterograde depolarization of the His bundle during ventricular tachycardial without alteration of the QRS configuration or cycle length; and (3) the presence of random retrograde His potentials during the tachycardia. Evidence that the reentrant circuit was localized to a small area of the ventricles included (1) the ability to capture large segments of the ventricles transiently or continuously with occurrence of intermittent or continuous supraventricular capture either spontaneously or with atrial pacing without effect on the tachycardia. These findings suggest that the reentrant circuit must be small, electrocardiographically silent and relatively protected.
Electrophysiologic studies in one patient with spontaneous 2:1 atrioventricular block and variable PR intervals revealed two sites of conduction block. Typical 4:3 A-V nodal Wenckebach was present in addition to Mobitz type II infra-His block. The HV of conducted complexes was 120 msec and the shortest recorded AH interval was 250 msec. When 2:1 A-V block with fixed PR interval was present, only 2:1 Mobitz type II infra His-block was present. The mechanism of this example of spontaneous multilevel A-V block is discussed and compared to other previously reported cases.
The mechanism of supraventricular tachycardia was evaluated in twelve patients with mitral valve prolapse utilizing standard intracardiac recording and stimulation techniques. Eight patients had normal electrocardiograms, three had a short PR interval and normal QRS (Lown-Ganong-Levine syndrome) and one had Wolff-Parkinson-White type A. Six of the eight patients with normal electrocardiograms were demonstrated to have atrioventricular bypass tracts. Five patients had A-V nodal re-entrant supraventricular tachycardia. In two patients the bypass tract could be demonstrated to conduct antegradely when the left atrium was paced via the coronary sinus, while in four the bypass tract only conducted retrogradely. In all seven patients with atrioventricular bypass tracts, the accessory pathway was left-sided. We conclude that a) supraventricular tachycardia in the mitral valve prolapse syndrome appears related to a high frequency of bypass tracts; b) electrophysiological studies are required to diagnose these bypass tracts; and c) the atrioventricular bypass tracts may be related to the mitral valve abnormality since they are always left-sided.
The mechanism of recurrent sustained ventricular tachycardia (VT) was evaluated in 21 patients. Re-entry as the mechanism for VT was suggested by a) the reproducible initiation (19) and termination (15) of the arrhythmia by programmed stimulation. The rate, ventricle of origin, and stimulation site determined the method of termination. One VPD was usually required with VT rates less than 175/min and/or ventricle of origin ipsilateral to the stimulation site, while two VPDs were usually required for VT with faster rates originating in a contralateral ventricle. The proximal His-Purkinje system (HPS) was not required for initiation or maintenance of VT. Evidence localizing the site of re-entry to a small portion of the ventricles included: a) ventricular capture by ventricular premature depolarizations (VPDs) or pacing (VP) without terminating VT (5), b) sinus capture following VPDs and/or supraventricular fusions without terminating VT (12), and c) atrial pacing normalizing the QRS and H-V intervals without terminating VT (5).