Electrophysiologic studies in nonsustained ventricular tachycardia: Relation to underlying heart disease

Electrophysiologic studies were performed in 83 patients with spontaneous episodes of nonsustained ventricular tachycardia (VT). The clinical arrhythmia was reproduced in 63% (in 42 patients by programmed stimulation and in 10 by isoproterenol infusion). In 15 patients sustained VT could be reproducibly induced by programmed stimulation. Inducibility was related to the associated heart diseases: programmed stimulation induced VT in 25 of 33 patients (75%) with coronary disease, 6 of 18 patients (33%) with cardiomyopathy (dilated in 16, hypertrophic nonobstructive in 2), in 4 of 8 patients (50%) with mitral valve prolapse and in 7 of 24 patients (29%) without structural heart disease. Isoproterenol infusion induced VT in no other patient with coronary artery disease, 1 other patient with mitral valve prolapse, 3 patients with cardiomyopathy, and in 6 of 24 patients without structural heart disease. Sustained VT was induced only in patients with structural heart disease, and correlated with the presence of left ventricular aneurysms: Sustained VT was induced in 9 of 13 patients with left ventricular aneurysms. The study demonstrates that electrophysiologic techniques can reproduce episodes of nonsustained VT in most patients with spontaneous arrhythmias. Some patients who demonstrate only nonsustained VT spontaneously have inducible, sustained VT, most often in the setting of coronary artery disease and left ventricular aneurysms.     

Electropharmacology of nonsustained ventricular tachycardia: effects of class I antiarrhythmic agents, verapamil and propranolol

Forty-seven patients with spontaneous and inducible nonsustained ventricular tachycardia (VT) underwent serial electrophysiologic studies to evaluate the effects of antiarrhythmic agents on inducible arrhythmias, the role of electrophysiologic testing in the evaluation of pharmacologic therapy for these arrhythmias, and potential mechanisms underlying these arrhythmias. Type I antiarrhythmic agents prevented induction of VT by programmed stimulation in 18 of 37 patients and by isoproterenol in 9 of 11 patients. Verapamil and propranolol did not prevent or alter the mode of induction of VT by programmed stimulation, nor did they slow the induced tachycardias. Propranolol prevented induction of VT by isoproterenol in all 14 patients tested. Type I antiarrhythmic agents converted nonsustained into sustained VT in 2 of 37 patients. Inducible VT was prevented in 88% of patients without underlying heart disease, in contrast to only 38% of patients with associated cardiac disease (p less than 0.02). This study demonstrates that electrophysiologic studies may be used to identify antiarrhythmic agents with both beneficial and potentially harmful effects in patients with nonsustained VT. The responses of inducible tachycardias to antiarrhythmic agents in this group of patients with spontaneous nonsustained VT are similar to those previously observed in patients with sustained VT. Finally, the results suggest that VT induced by isoproterenol may frequently respond to type I antiarrhythmic agents in addition to beta blockers.     

Prognostic factors in nonsustained ventricular tachycardia

Electrophysiologic studies were performed in 83 consecutive patients with spontaneous nonsustained ventricular tachycardia (VT). VT was inducible in 52 patients (nonsustained VT only in 37 patients, nonsustained and sustained VT in 13 and sustained VT only in 2). During a follow-up of 3 to 111 months (mean 33), 10 patients died suddenly, 5 with coronary artery disease (CAD) and 5 with dilated cardiomyopathy. All patients with sudden death had an ejection fraction ≤0.40. Sudden death occurred in 4 of 15 patients with inducible sustained VT, 2 of 37 patients with only nonsustained VT and 4 of 31 patients without inducible VT. One patient with dilated cardiomyopathy and VT inducible only by isoproterenol died suddenly. Three of 5 patients with CAD who had sudden death had had inducible sustained VT, but 3 of 5 patients with cardiomyopathy who had sudden death had no inducible VT. Multivariate analysis revealed that patients with inducible sustained VT or an ejection fraction ≤0.40 had a 3-fold increased risk of sudden death, and patients with both factors had a 7-fold increased risk of sudden death. This study demonstrates that patients with nonsustained VT with an ejection fraction > 0.40 have an uncomplicated course; however, noninducibility does not predict such a course, particularly in patients with cardiomyopathy. The most powerful predictor of risk for sudden cardiac death is a left ventricular ejection fraction ?0.40, but the presence of inducible sustained VT is an independent risk factor for sudden death.     

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.     

Perioperative coronary arterial spasm: Long-term follow-up

Six patients who survived episodes of coronary arterial spasm occurring immediately after coronary bypass grafting were followed up for 15 to 30 (mean 20) months after operation. In all patients coronary spasm occurred in an unobstructed dominant right coronary artery and caused inferior transmural ischemia. Sudden circulatory collapse occurred in five of the six patients as a consequence of acute coronary spasm. All patients were treated with nitroglycerin followed by nifedipine. No patient has had recurrent angina or other evidence of spontaneous coronary spasm since surgery. Cardiac catheterization studies, including ergonovine maleate testing, were repeated 3 to 12 months after surgery in five of the six patients. The right coronary artery and all bypass grafts were patent in all five. Four patients had new inferior wall motion abnormalities. Ergonovine provoked focal right coronary arterial spasm in one patient.It is concluded that manifestations of coronary spasm after myocardial revascularization range from asymptomatic S-T segment elevation to severe hypotension. These episodes of perioperative spasm may cause myocardial necrosis. Coronary spasm has not recurred in patients who survived perioperative spasm, but some patients may have a continued predisposition to development of coronary spasm late after surgery.     

Electrocardiographic left atrial enlargement electrophysiologic, echocardiographic and hemodynamic correlates

The mechanism of the electrocardiographic pattern termed left atrial enlargement was evaluated in 21 patients. Left atrial size and pressure as well as interatrial conduction were correlated with electrocardiographic left atrial enlargement using echocardiography, mean pulmonary capillary wedge pressure and activation time from the P wave to the coronary sinus. In the group as a whole only prolongation of interatrial conduction time was consistently related to the electrocardiographic pattern of left atrial enlargement; left atrial size or pressure was not predictably abnormal in patients with this pattern. Five patients had neither elevation of pulmonary capillary wedge pressure nor echocardiographic evidence of an enlarged left atrium. When the etiologic type of heart disease was analyzed, an enlarged left atrium correlated with electrocardiographic left atrial enlargement only in patients with rheumatic mitral valve disease (eight of nine patients). Elevated pulmonary capillary wedge pressure correlated with electrocardiographic left atrial enlargement in all four patients with cardiomyopathy. In patients with coronary artery disease the electrocardiographic pattern was unrelated to either left atrial pressure or volume overload. Thus, the electrocardiographic pattern termed left atrial enlargement appears to represent an interatrial conduction defect that can be produced by a variety of factors.     

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)     

Amiodarone for control of sustained ventricular tachyarrhythmia: clinical and electrophysiologic effects in 51 patients

We evaluated the electrophysiologic effects of amiodarone and its ability to control ventricular arrhythmia in a selected group of 51 patients with refractory sustained ventricular arrhythmia. Amiodarone in doses of 400 to 800 mg/day prolonged refractoriness in the atria, atrioventricular (AV) node, and ventricle as well as conduction through the AV node and His-Purkinje system. Although it had no effect on measurements of sinus nodal function (sinus nodal recovery time and sinoatrial conduction time), it prolonged the sinus cycle length and 2 patients required a permanent pacemaker for symptomatic sinus bradycardia. Amiodarone did not alter the ease of inducibility in any consistent manner, and only 5 of 43 patients (12%) who had inducible ventricular tachycardia before amiodarone therapy had none induced during amiodarone treatment. The clinical effectiveness of amiodarone could be evaluated in 46 patients followed up for 8.6 +/- 6 months (range 0.5 to 22). It provided effective therapy in 23 patients (50%), partly effective therapy in 13 (28%), and was ineffective in 10 (22%). Adverse effects were noted in 28 of 51 patients (55%), and in 11 of these (22%) the drug had to be discontinued because of adverse effects. We conclude that amiodarone is a useful agent for the treatment of refractory sustained ventricular arrhythmia. Its use should be reserved for patients with life-threatening sustained arrhythmia because of the significant incidence of adverse effects. Furthermore, good clinical response can be observed in patients receiving amiodarone in spite of continued inducibility.     

Identifying patients at risk of sudden death after myocardial infarction: Value of the response to programmed stimulation, degree of ventricular ectopic activity and severity of left ventricular dysfunction

The ability of programmed ventricular stimulation to identify risk of sudden death after acute myocardial infarction (MI) was compared with 24-hour electrocardiographic assessment of ventricular ectopic activity and determination of left ventricular (LV) dysfunction. Forty-six patients underwent programmed stimulation 8 to 60 days (mean 22) after documented MI. Programmed stimulation consisted of single and double extrastimuli from the right ventricular apex at 2 times diastolic threshold during ventricular pacing and normal sinus rhythm. Of the 46 patients, 44 underwent electrocardiographic monitoring at least 6 days after MI. In 43 of the 46 patients, LV ejection fraction (EF) and the presence of LV aneurysm were determined. In response to programmed ventricular stimulation, 5 patients had sustained ventricular tachycardia (VT), 5 had nonsustained VT (≥4 beats), 13 had intraventricular reentrant repetitive responses, and 23 had either bundle branch reentrant repetitive responses or no extra responses to programmed ventricular stimulation (negative study).

During a mean follow-up of 18 months, 10 patients died, 6 suddenly. One of the 10 patients with sustained or nonsustained VT died suddenly, compared with 3 of 13 patients with intraventricular reentrant responses and 2 of 23 patients with a negative study (difference not significant). Of 25 patients with Grade 0 to 2 ventricular ectopic activity, 3 died suddenly after MI, compared with 3 of 19 patients with Grade 3 or 4 activity (difference not significant). By comparison, the frequency of sudden death was greater in patients with an LVEF of <40% (5 of 16 versus 1 of 27 patients) or an LV aneurysm (5 of 13 versus 1 of 30 patients).

Thus, using the described protocol, the response to programmed ventricular stimulation is not helpful in identifying patients at risk for sudden death after MI. The presence of an LV aneurysm or EF of <40% appears to provide the greatest prognostic information with respect to risk for sudden cardiac death.     

Mexiletine for control of drug-resistant ventricular tachycardia: Clinical and electrophysiologic results in 44 patients

The antiarrhythmic efficacy of mexiletine was evaluated in 44 patients with drug-resistant ventricular tachyarrhythmias. In 33 of these patients, the efficacy of mexiletine was assessed on the basis of the results of programmed ventricular stimulation. Mexiletine did not alter the ventricular effective refractory period, the Q-Tc interval, or the methods of tachyarrhythmia induction and termination during programmed stimulation. The mean cycle length of ventricular tachycardia (VT) increased from 270 ± 49 to 313 ± 80 ms in 21 patients in whom VT remained inducible on mexiletine alone (p < 0.002). Overall, VT remained inducible with methods similar to control (no drugs) inductions in 25 patients receiving mexiletine alone or in combination with a type I agent. VT induction was prevented in only 8 patients, 3 on mexiletine alone and 5 receiving mexiletine combined with another drug. Mexiletine alone (in 2 patients) or with another agent (in 3) suppressed clinical recurrence of VT in an additional 5 of 11 patients who did not undergo electrophysiologic study. These 13 patients were discharged on mexiletine alone (5 patients) or in combination with other drugs (8 patients), and remained arrhythmia-free over a mean follow-up period of 7.7 ± 4.1 months. Adverse effects occurred in 27 of 44 patients (61%) and were gastrointestinal in 17 and/or neurologic in 22. The drug was discontinued because of adverse effects in 6 patients (14%). Thus, mexiletine has limited efficacy when used alone, but when combined with other drugs it may be useful in up to 30% of patients with drug-resistant ventricular arrhythmias. Adverse effects are relatively common.     

Human ventricular refractoriness: Effects of increasing current

The ventricular effective refractory period is commonly employed as a measurement of ventricular excitability. Because the current strength used to make this determination varies among laboratories, the relation of refractoriness and current was examined over a range of current strengths from 0.1 to 10 mA. Sixty determinations of refractoriness at variable current strengths were made in 40 patients using the extrastimulus technique with a rectangular pulse of 1 ms duration. These data were obtained by measuring the effective refractory period at threshold current and at 0.25 to 0.50 mA increments from threshold up to 10 mA. In these studies the drive stimulus (S₁) and extrastimulus (S₂) were kept at the same amplitude. In all patients the ventricular effective refractory period decreased as the current increased. The total decrease ranged from 8 to 100 ms (mean ± standard deyiation 36.9 ± 17.1). The current strength at which the ventricular effective refractory period became fixed (that is, less than 2 ms change in ventricular effective refractory period with further increase in current strength) varied among the patients, but in all instances equaled or exceeded 1.8 mA, which in all but three patients was greater than three times threshold. The curves relating current strength and refractoriness were shifted to the left at shorter cycle lengths with no change in threshold.These data suggest that (1) current strength-effective refractory period curves more completely characterize ventricular excitability than does a ventricular effective refractory period at single current strength; and (2) studies of drug effects, alterations of autonomic tone, or reentrant arrhythmias, which may affect or are affected by ventricular refractoriness, may be enhanced by more complete measurements of refractoriness afforded by the current strength-effective refractoriness curves.     

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.     

Relation of mode of induction and cycle length of ventricular tachycardia: Analysis of 104 patients

One hundred four consecutive patients with ventricular tachycardia (VT) were examined to correlate the cycle length with the mode of initiation of VT (single, double, and triple extrastimuli and rapid pacing). Tachycardias induced with a single extrastimulus were slower (342 ± 72 ms, mean cycle length) than those induced with double (295 ± 60 ms) or triple (282 ± 56 ms) extrastimuli or rapid pacing (293 ± 40 ms). There were no differences among the last 3 groups. In 38 patients who had endocardial catheter mapping to determine the site of origin of VT, distance from stimulation site to the site of origin was estimated and correlated with mode of initiation. There was no difference in mode of initiation when the stimulation site was close (< 3 cm), intermediate (3 to 5 cm), or distant (> 8 cm) from the site of origin. To address the issue of distance from stimulation site to the site of origin somewhat differently, mode of initiation was correlated with site of previous myocardial infarction in 69 patients with VT initiated from the right ventricular apex. Again, mode of initiation did not differ among patients with septal, inferior, lateral, or multiple myocardial infarctions. Thus, cycle length of VT initiated with a single extrastimulus was slower than that initiated with double or triple extrastimuli or rapid pacing and the mode of initiation of VT was unrelated to site of myocardial infarction or distance between stimulation site and site of origin of VT.     

Acute coronary vasoconstrictive effects of cigarette smoking in coronary heart disease

To investigate the effect of cigarette smoking on the coronary vasculature, coronary sinus flow and myocardial oxygen delivery were measured at rest and during incremental atrial pacing in 10 patients with coronary artery disease. Measurements were then repeated while the patients smoked 2 unfiltered, high-nicotine cigarettes. Although smoking significantly increased the heart rate at rest and double product, coronary sinus flow did not change significantly (141 +/- 32 vs 146 +/- 28 ml/min). At the lowest equivalent pacing rate before and during smoking, the double products were comparable. However, coronary sinus flow was reduced by smoking (146 +/- 28 vs 159 +/- 28 ml/min, p less than 0.01) and coronary vascular resistance was increased (0.96 +/- 0.15 vs 0.83 +/- 0.13 mm Hg ml-1 min, p less than 0.02). The double products were also comparable at the peak pacing rate before and during smoking. Nonetheless, the coronary sinus flow was again lower (167 +/- 23 vs 227 +/- 41 ml/min, p = 0.02) and the coronary vascular resistance was higher (0.77 +/- 0.10 vs 0.63 +/- 0.09 mm Hg ml-1 min, p less than 0.01) during smoking. The transmyocardial arteriovenous oxygen difference was unchanged by smoking; therefore, myocardial oxygen delivery was reduced in proportion to the reductions in coronary sinus flow. Thus, cigarette smoking appears to acutely alter the ability of the coronary vasculature to regulate flow in accordance with the oxygen requirements of the myocardium.     

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.     

Ventricular activation during ventricular endocardial pacing: I. Electrocardiographic patterns related to the site of pacing

The QRS configuration produced by pacing at multiple left ventricular endocardial sites was evaluated in eight patients with (group 1) and six patients without (group 2) left ventricular wall motion abnormalities. Pacing was performed at a total of 122 sites, 4 to 13 sites in each patient. The QRS configuration resulting from apical pacing locations was compared with that at basal, septal to lateral and inferior to superior locations. Significant differences in QRS configuration during pacing from apical and basal locations were observed in electrocardiographic leads I, V₁, V₂ and V₆ (probability [p] < 0.01). Specifically, a QS pattern in leads I, V₂ and V₆ was more characteristic of an apical pacing location (p < 0.001), and a monophasic R wave in leads V₁ and V₂ was more characteristic of a basal pacing location (p < 0.01). Significant differences in leads V₁ and V₂ were observed when septal and lateral pacing sites were compared (p < 0.001). A monophasic R wave in leads V₁ and V₂ was more characteristic of a lateral pacing location (p < 0.01); a QS complex in lead V₂ was more characteristic of a septal pacing location (p < 0.001). Pacing at superior sites usually produced an inferior axis and vice versa (p < 0.001). The electrocardiographic patterns produced by pacing at similar sites in patients in group 1 were less consistent than those in patients in group 2. The QRS complex during ventricular pacing was wider in patients in group 1 (159 ± 30 ms) than in patients in group 2 (132 ± 18 ms) (p < 0.001).It is concluded that the QRS configuration recorded with 12 lead electrocardiography during endocardial pacing can help locate the region of the pacing site in patients with and without organic heart disease, although precise localization is not possible.     

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.