Anatomic and electrophysiologic correlates of ventricular tachycardia requiring left ventricular stimulation

In 108 patients with reproducible initiation of ventricular tachycardia by programmed ventricular stimulation, the ventricular tachycardia was initiated only by left ventricular stimulation in 12 (11 percent). Programmed ventricular stimulation included single and double extrastimuli at three cycle lengths and bursts of rapid pacing to cycle lengths of 250 ms. Clinical, electrocardiographic, angiographic, hemodynamic and electrophysiologic data were available in 74 of 96 patients with ventricular tachycardia initiated by right ventricular stimulation (Group A) and in all 12 patients with ventricular tachycardia initiated only by left ventricular stimulation (Group B). There were no significant differences between Groups A and B in clinical characteristics, hemodynamics or presence and site of infarction or aneurysm. Comparison of electrophysiologic variables revealed no significant differences between Groups A and B in mean A-H interval (92 ± 22 versus 89 ± 15 ms, respectively), H-V interval (59 ± 15 versus 59 ± 15 ms) or right ventricular (241 ± 38 versus 260 ± 40 ms) or left ventricular (232 ± 28 versus 251 ± 42 ms) effective refractory period. Ventricular tachycardia with right bundle branch block and superior axis was more prevalent in Group B (92 percent versus 31 percent, p <0.001) but was observed in 32 patients in Group A.It is concluded that 11 percent of patients with clinically documented sustained ventricular tachycardia will require left ventricular programmed stimulation to reproducibly initiate the tachycardia. No clinical, anatomic, electrocardiographic or electrophysiologic features can predict whether left ventricular programmed stimulation will be required. Because initiation of ventricular tachycardia by programmed ventricular stimulation has important prognostic and therapeutic implications in such patients, stimulation should be performed from the left ventricle when the tachycardia is not initiated by stimulation from the right ventricle.     

Electrophysiologic and hemodynamic studies in patients resuscitated from cardiac arrest

Fifty-two patients resuscitated from cardiac arrest underwent electrophysiologic studies. The earliest documented arrhythmia at the time of initial or recurrent (18 patients) cardiac arrest was ventricular fibrillation (30 patients) or ventricular tachycardia (20 patients); in 2 patients no arrhythmia was documented before defibrillation. Programmed ventricular stimulation revealed inducible arrhythmias in 33 patients (63 percent). Of the 30 patients with ventricular fibrillation as the initial arrhythmia, 13 had inducible arrhythmias—ventricular fibrillation (4 patients), sustained ventricular tachycardia (6 patients) and nonsustained ventricular tachycardia (3 patients). In the 20 patients with ventricular tachycardia as the initial arrhythmia, sustained ventricular tachycardia was initiated in 17 patients and torsade de pointes in 1. Patients with inducible arrhythmias had longer mean A-H and H-V intervals than those without inducible arrhythmias (91.1 versus 76.6 ms and 62.5 versus 50.3 ms, respectively). Prolonged H-V intervals (17 of 33) and intraventricular conduction defects (18 of 33) were more common in patients with than in those without inducible arrhythmias (4 of 19 and 7 of 19, respectively). Mean cardiac index was lower (2.4 versus 3.9 liters/min per m²), left ventricular end-diastolic pressure higher (17.0 versus 9.4 mm Hg), and ejection fraction lower (36.1 versus 57.2 percent) in the group with inducible arrhythmias than in those in whom no arrhythmia could be induced. These data suggest that (1) ventricular tachycardia often precipitates cardiac arrest; and (2) electrophysiologic testing may provide data on which to base therapy in patients resuscitated from cardiac arrest.     

Electrophysiologic characteristics of concealed bypass tracts: clinical and electrocardiographic correlates.

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.     

Ventricular fibrillation during programmed ventricular stimulation: Incidence and clinical implications

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.     

Incidence and clinical significance of induced ventricular tachycardia

Five hundred twenty-nine patients were studied with programmed ventricular stimulation for evaluation of supraventricular and ventricular tachyarrhythmias. Eighty-six patients had clinical ventricular tachycardia. Sustained ventricular tachycardia was induced in 52 (91 percent) of the 57 patients with a sustained form of the arrhythmia clinically. Nonsustained ventricular tachycardia was induced in 18 (62 percent) of 29 patients with a symptomatic nonsustained form clinically, in 2 (4 percent) of 57 patients with a sustained form and in 3 (0.7 percent) of the 443 patients with no documented spontaneous ventricular tachycardia. Ventricular tachycardia (sustained or nonsustained) was induced by double right or left ventricular extrastimuli in 47 patients (63 percent) and by single right ventricular extrastimuli in 23 (31 percent); in 5 (7 percent), it was inducible only by rapid ventricular pacing and in 9 (12 percent) only by left ventricular stimulation.All 52 patients with induced sustained ventricular tachycardia had the sustained form clinically. Of the 23 patients with induced nonsustained ventricular tachycardia, 18 (78 percent) had the nonsustained form clinically. Four hundred fifty-four patients had no induced ventricular tachycardia; only 14 (3 percent) of these had the arrhythmia spontaneously. The morphologic features, axis and cycle length of 54 of 62 episodes of induced ventricular tachycardia in 43 patients were similar to those of the clinically observed arrhythmia. It is concluded that ventricular tachycardia resembling the clinical variety can be induced in the laboratory in almost all patients with sustained ventricular tachycardia clinically, in the majority of those with symptomatic nonsustained ventricular tachycardia clinically, and only rarely in patients with no previously documented ventricular tachycardia. Conversely, induction of ventricular tachycardia implies the likelihood of spontaneous episodes of this arrhythmia.     

Mechanism of ventricular fibrillation in man. Observations based on electrode catheter recordings.

Observations are reported on the initiation and spontaneous termination of ventricular fibrillation in man using endocardial electrode catheter recordings. The report is based on 16 patients in whom ventricular fibrillation developed during electrophysiologic study. In 11 patients ventricular fibrillation was initiated by programmed ventricular stimulation and in 5 patients ventricular fibrillation occurred spontaneously. In each patient two to five simultaneous ventricular electrograms were recorded at the onset or termination, or both, of ventricular fibrillation. In most patients ventricular fibrillation began as a rapid and accelerating ventricular rhythm in which local electrograms remained discrete and with progressively shortening coupling intervals. Degeneration of local electrograms into fibrillatory activity occurred at random and at varying times. In four patients ventricular fibrillation developed spontaneously during sustained ventricular tachycardia. In these cases there was acceleration of the ventricular tachycardia before degeneration to ventricular fibrillation. Fragmentation and disorganization in local ventricular electrograms did not appear to spread between contiguous areas, but occurred randomly in widely separated areas. In six patients ventricular fibrillation spontaneously converted to sinus rhythm. In four of these cases spontaneous conversion was preceded by sequential reorganization of the electrograms and a tendency toward increasing interelectrographic intervals. These observations are compatible with the multiple wavelet (reentrant) theory of ventricular fibrillation.     

Electrophysiologic approach to therapy of recurrent sustained ventricular tachycardia.

The refinement of the techniques of programmed stimulation and intracardiac recording has led to understanding of the mechanism of ventricular tachycardia and these techniques can be applied clinically to the development of therapeutic regimens. The efficacy of drug therapy can be assessed in sequential studies evaluating the ability of drugs to prevent initiation of the arrhythmia by electrical stimulation. The efficacy of pacemaker therapy can be evaluated by assessing the effects of stimulation during the tachycardia. The recent development of endocardial mapping provides the surgeon with a tool to guide therapeutic surgical ablation of the site of origin of the tachycardia. Such an electrophysiologic approach to recurrent ventricular tachycardia can lead to the rapid development of successful therapy under controlled conditions.     

Clinical characteristics and long-term follow-up in 119 survivors of cardiac arrest: relation to inducibility at electrophysiologic testing

Electrophysiologic studies were performed in 119 survivors of cardiac arrest. Sustained ventricular arrhythmias were initiated by programmed ventricular stimulation in 72 patients (61%). Coronary artery disease patients with induced sustained ventricular arrhythmias had a higher incidence of prior myocardial infarction (95 versus 72%) and ventricular aneurysm (59 versus 28%) and a lower ejection fraction (37 versus 50%) than those with no inducible sustained ventricular arrhythmias. Of the 72 patients with inducible ventricular arrhythmias, 11 (15%) died suddenly during a mean follow-up of 18 months (range 15 days to 58 months). In this group, 6 of 41 patients (15%) discharged on a successful antiarrhythmic regimen and 5 of 27 patients (19%) discharged on an unsuccessful regimen or without a predischarge study have died suddenly. Of these 27 patients, 1 of 12 patients treated with amiodarone and 4 of 15 (27%) with conventional antiarrhythmic therapy died suddenly. The remaining 4 patients died of nonarrhythmic causes in the postoperative period. Of 47 patients without inducible sustained ventricular arrhythmias, 15 (32%) died suddenly at a mean follow-up of 20 months, 10 (34%) with and 15 (28%) without empiric therapy. It is concluded that sustained ventricular arrhythmias can be initiated in most patients resuscitated from cardiac arrest. Patients with inducible arrhythmias have greater left ventricular dysfunction than those without inducible arrhythmias. Medical or surgical therapy that prevented the induction of sustained ventricular arrhythmias was predictive of a successful outcome in 85% of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Atrial flutter. I. Electrophysiologic substrates and modes of initiation and termination

Forty-one of 525 consecutively studied patients had sustained (2 or more minutes) atrial flutter in response to programmed atrial simulation. Of these 41 patients, 31 had previously documented spontaneous atrial flutter or fibrillation, or both, and 10 had paroxysmal palpitations without documentation of the cause. Programmed atrial stimulation and atrial endocardial mapping were used to analyze the substrate of atrial conduction as well as the mode of initiation and termination of flutter. Atrial conduction defects were present in 36 of the 41 patients. Atrial flutter was induced by one or two atrial extrastimuli in 31 patients. In most of these patients the onset of flutter was characterized by a brief period of irregular atrial activity in one or more intracardial leads. Stimulation from the high right atrium was more successful (29 of 31 patients) than that from the coronary sinus (6 of 12 patients). Rapid atrial pacing at cycle lengths of 350 to 200 ms initiated flutter in 29 of 35 patients in whom it was attempted (in 27 of 35 from the high right atrium and in 10 of 18 from the coronary sinus). Termination of flutter was accomplished by rapid pacing in 34 patients at cycle lengths 20 to 55 ms less than the flutter cycle length. Failure to terminate flutter was associated with local areas of atrial fibrillation in one or more intracardiac leads.     

Strength-interval relation in the human ventricle: Effect of procainamide

The effects of procainamide on strength-interval relations were evaluated in 18 patients. At plasma concentrations of 4.3 to 13.6 μg/ml procainamide had minimal effects on threshold current in late diastole, but in early diastole it shifted the strength-interval curve to the right. The basic strength-interval relation (that is, decreasing refractory period as current is increased) was not altered. The control refractory period decreased by a mean of 44 ms as the current was increased from threshold to 10 mA, whereas a mean decrease of 42 ms was observed after procainamide. However, the steep portion of the strength-Interval curve (absolute refractory period) was shifted to longer coupling intervals by a mean value of 24 ms. These findings suggest that procainamide may primarily affect active membrane properties, but exert little net effect on passive membrane properties late in diastole.     

Sustained ventricular tachycardia: Evidence for protected localized reentry

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 branch reentry, or both, for initiation of the tachycardia; (2) anterograde depolarization of the His bundle during ventricular tachycardia 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 ventricular stimulation without affecting the tachycardia, and (2) the occurrence of intermittent or continuous supraventricular capture either spontaneously or with atrlal pacing without effect on the tachycardia. These findings suggest that the reentrant circuit must be small, electro-cardiographically silent and relatively protected.     

Atrial conduction: effects of extrastimuli with and without atrial dysrhythmias

The effects of cycle length and stimulation site on intraatrial conduction and refractoriness were evaluated in patients with and without atrial flutter (AFI) or fibrillation (AF) using the extrastimulus technique. Nineteen patients with spontaneous sustained AFI or AF were compared with 19 control patients. Programmed stimulation was performed at the right atrium and coronary sinus at drive cycle lengths of 600 and 450 ms. The atrial effective refractory period was similar in the patients with atrial dysrhythmias and the control group. The right atrial effective refractory period at a drive cycle length of 600 ms was significantly shorter in patients with AF (211 ms) than in patients with AFI (235 ms, p = 0.05). The conduction time of late (coupling intervals more than 50% of the drive cycle length) premature impulses was similar in the patients with atrial dysrhythmias and the control group. However, early extrastimuli (coupling intervals less than 50% of the drive cycle length) at a drive cycle length of 600 ms produced significantly more intraatrial conduction delay in the patients with atrial dysrhythmias than in the control patients. At a drive cycle length of 450 ms, similar delays in intraatrial conduction occurred in the patients with and without atrial dysrhythmias because of an increase in the maximal-observed intraatrial conduction delay in the control patients. This study shows that delay in conduction of early premature atrial stimuli at a drive cycle length of 600 ms is a marker of patients with spontaneous AFI and AF.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular activation during ventricular endocardial pacing. II. Role of pace-mapping to localize origin of ventricular tachycardia

Intraoperative pace-mapping has been proposed as a method of identifying the origin of ventricular tachycardia; however, both epicardial activation and electrocardiographic configuration have limitations in localizing the origin of ventricular tachycardia. Because most ventricular tachycardias associated with ischemic heart disease appear to arise near the endocardium, this study evaluated the ability of bipolar catheter endocardial pacing at or near the endocardial site of origin of spontaneous ventricular tachycardia to mimic the QRS configuration of the spontaneous tachycardia. Twelve patients were studied who had ventricular tachycardia whose origin was determined with catheter endocardial mapping. Three patients had ventricular tachycardia with two distinct configurations. The electrocardiogram of ventricular tachycardia was compared with the electrocardiogram produced by pacing at the site of origin (10 patients) and at multiple (two to nine) additional sites in 8 patients. It was observed that (1) pacing at the known site of origin of ventricular tachycardia produced an electrocardiogram and activation sequence similar to those produced by the ventricular tachycardia; (2) pacing at sites in close proximity to the site of origin of ventricular tachycardia produced either a similar or a grossly different electrocardiographic pattern from that during ventricular tachycardia.It is concluded that catheter endocardial pace-mapping (1) is a corroborative method of identifying the origin of ventricular tachycardia; (2) may be useful in patients with noninducible ventricular tachycardia or rapid ventricular tachycardia who cannot undergo catheter or intraoperative mapping; and (3) is neither easier, more accurate nor quicker than direct localization by mapping during ventricular tachycardia.     

Role of catheter mapping in the preoperative evaluation of ventricular tachycardia

Although surgery is an accepted mode of therapy for refractory ventricular tachycardia, routine aneurysmectomy has yielded unpredictable results. This is believed to have occurred because there was no documentation that the arrhythmia actually arose from resected aneurysmal tissue. Catheter endocardial mapping has been used to localize preoperatively the area of origin of the arrhythmia. This technique has established that the arrhythmias arise near the endocardium at the borders of the aneurysm or infarction, or both. These regions, particularly when they occur in the interventricular septum, are not resected by standard aneurysmectomy. Intraoperative endocardial and epicardial mapping have validated the accuracy of this technique.We believe that catheter mapping should be performed before surgery for the following reasons: (1) In some patients ventricular tachycardia is not inducible in the operating room (for example, automatic ventricular tachycardia can be mapped in the catheterization laboratory); (2) in some patients not all morphologic forms of tachycardia can be induced or mapped intraoperatively because of failure of inducibility, time constraints or degeneration of the arrhythmia to ventricular fibrillation; and (3) intraoperative endocardial mapping occasionally cannot be performed because of lack of technical skills, physical factors such as mural thrombosis, or the inability to induce ventricular tachycardia after aneurysmectomy. Other methods currently being evaluated to localize the origin of ventricular tachycardia that do not require induction of arrhythmia are analysis of ventricular electrograms during sinus rhythm and pacemapping.