Psychological stress and ventricular arrhythmias during myocardial infarction in the conscious dog

The influence of psychological stress on cardiac rhythm was studied in eight conscious dogs before and after coronary arterial occlusion. The behavioral and cardiac responses of the animals were compared in stressful and nonstressful environments. Before coronary arterial obstruction, psychological stress lowered the vulnerable period threshold for repetitive ventricular responses by 82 percent. After myocardial infarction, presentation of stressful stimull provoked diverse ventricular arrhythmias including ventricular tachycardia and early extrasystoles with T wave interruption. Our study provides an experimental model for the systematic investigation of the role of psychological factors in the development of cardiac arrhythmias.     

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.     

The Duration of Induced Ventricular Tachycardia as Related to Clinically Sustained Ventricular Tachycardia

Programmed electrical stimulation has been extremely useful in the management of patients with sustained ventricular tachycardia or cardiac arrest. However, the definition of sustained ventricular tachycardia is controversial, and the relationship between the duration of induced ventricular tachycardia and the risk for spontaneous ventricular tachycardia has not been adequately defined. Thus, we examined the records of 64 patients with at least three beats of induced ventricular tachycardia during EP studies using single and double premature stimuli in sinus rhythm and during ventricular paced rhythm (two sites, up to three drive cycle lengths) and using ventricular burst pacing to correlate maximum length of induced ventricular tachycardia with the nature of their spontaneous arrhythmias. Forty-nine patients (77%) had ventricular tachycardia requiring intervention to terminate it, which we called sustained. Nine patients (14%) had ten or fewer beats of ventricular tachycardia; four patients (6%) had 11 to 20 beats of ventricular tachycardia; and two patients (3%) had more than 20 beats of ventricular tachycardia which did not require intervention for termination. Inducible sustained ventricular tachycardia had a sensitivity of 88% and a specificity of 92% for identifying patients with clinical sustained ventricular tachycardia or fibrillation. More than 20 beats of inducible ventricular tachycardia had a sensitivity of 92% and a specificity of 92%. More than 10 beats of inducible ventricular tachycardia achieved a sensitivity of 98% and a specificity of 91% for identifying patients with sustained ventricular tachycardia or fibrillation. The criteria used for the duration of inducible ventricular tachycardia are arbitrary and the interpretation of inducible nonsustained ventricular tachycardia must depend on the purpose of the test and the prior probability of each result.     

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.     

Ventricular tachycardia: prediction of response to oral aprindine with intravenous aprindine

Aprindine was administered both intravenously and orally to 25 patients with ventricular tachycardia refractory to conventional antiarrhythmic agents to test the hypothesis that the response to intravenous aprindine predicts the response to oral aprindine. Ten patients had incessant ventricular tachycardia and 15 had paroxysmal sustained inducible ventricular tachycardia. Eleven patients (43 percent) had conversion to sinus rhythm with intravenous aprindine (nine with incessant and two with paroxysmal sustained ventricular tachycardia). Thirteen patients (all with paroxysmal sustained ventricular tachycardia) manifested slowing of the tachycardia without conversion, whereas in one patient with incessant ventricular tachycardia, the tachycardia became less frequent and nonsustained after intravenous aprindine. All 11 patients who had conversion to sinus rhythm with intravenous aprindine remained free of ventricular tachycardia during oral treatment with aprindine (at 2 weeks) and for a follow-up period of 2 to 38 months (mean 16 +/- 13). Of the 14 patients who did not have conversion to sinus rhythm with intravenous aprindine, 12 had spontaneous or inducible ventricular tachycardia, or both, at evaluation 1 to 2 weeks after initiation of oral aprindine. In conclusion, administration of intravenous aprindine to patients with ventricular tachycardia is helpful in predicting the subsequent response to oral aprindine. In addition, the pattern of ventricular tachycardia predicted the response to aprindine; patients with incessant ventricular tachycardia tended to respond, and those with paroxysmal sustained ventricular tachycardia tended not to respond.     

Role of electrophysiologic testing in managing patients who have ventricular tachycardia unrelated to coronary artery disease

This study examined the usefulness of programmed electrical stimulation in managing 83 patients who had ventricular tachycardia not due to coronary artery disease. Among 39 patients with a history of sustained ventricular tachycardia, programmed stimulation induced ventricular tachycardia in 14 of 14 patients with mitral valve prolapse or primary electrical disease (arrhythmias without evidence of structural heart disease) and in 13 of 25 with cardiomyopathy (total 27 of 39, 69 percent). Programmed stimulation induced nonsustained ventricular tachycardia in 15 (34 percent) of 44 patients with a history of nonsustained tachycardia (5 of 13 with mitral valve prolapse, 6 of 19 with primary electrical disease and 4 of 12 with cardiomyopathy). Seventy-three of the 83 patients were treated with antiarrhythmic drugs and then followed up for 14.4 ± 11.4 months (mean ± standard deviation). Drug therapy was determined with serial electrophysiologic testing in 31 patients. Twenty-four of these 31 patients had a history of sustained ventricular tachycardia, and drugs prevented induction of ventricular tachycardia in 9 (none of whom manifested symptomatic events) but did not prevent it in 15 (6 of whom had symptomatic events). Among seven patients with a history of nonsustained ventricular tachycardia, drugs prevented induction of ventricular tachycardia in five (none of whom had symptomatic events) and did not prevent it in two (none of whom had symptomatic events). Forty-two patients were treated using the results of noninvasive testing. Drugs suppressed spontaneous ventricular tachycardia in 15 of 15 patients with a history of sustained tachycardia (7 of whom had symptomatic events including one sudden death), and in 26 of 27 with a history of nonsustained tachycardia (6 of whom had symptomatic events including one sudden death).Thus, in patients with ventricular tachycardia unrelated to coronary artery disease: (1) programmed electrical stimulation induced ventricular tachycardia less often than in patients whose tachycardia was due to coronary artery disease; (2) programmed stimulation induced ventricular tachycardia less often in patients with a history of nonsustained versus sustained tachycardia; and (3) suppression of inducible ventricular tachycardia appeared to predict effective drug therapy but drug therapy predicted with noninvasive testing appeared to be unreliable.     

Radiofrequency ablation of ventricular tachycardia in patients with ischemic cardiopathy

PURPOSE: We analyze the efficacy of radiofrequency catheter ablation and the clinical significance of inducible ventricular tachycardia that had never been documented before (non clinical ventricular tachycardia) in patients with ventricular tachycardia and coronary artery disease. METHODS: Thirty-four patients (30 men, aged 61 +/- 10 years, left ventricular ejection fraction 31 +/- 10%) with coronary artery disease and documented clinical ventricular tachycardia underwent radiofrequency ablation. Thirty-four clinical ventricular tachycardia and 11 non clinical ventricular tachycardia were treated with radiofrequency. Initial therapeutic success was considered when none of the ventricular tachycardia treated with radiofrequency could no longer be induced at the last stimulation protocol before discharge. RESULTS: Clinical ventricular tachycardia was successfully ablated in 23 patients (68%). Initial therapeutic success was obtained in 21 patients (62%). In 6 of them, 7 non clinical ventricular tachycardia poor tolerated were also induced. During a mean follow-up of 26 +/- 15 months ventricular tachycardia recurred in 6 patients (29%). Five of the 6 patients who recurred were discharged with no inducible non clinical ventricular tachycardia. Three patients died during the follow-up. Two of them from heart failure (one with previous recurrence) and the other suddenly with documented asystole after loss of consciousness without previous recurrence. CONCLUSIONS: In our series of patients with ventricular tachycardia and coronary artery disease selected for radiofrequency ablation, acute success was obtained in 62%. After a mean follow-up of 2 years, 44% of all the patients were free from ventricular tachycardia. Although the possibility of ventricular tachycardia recurrence is high (29%), the recurrence rate is not increased by the inducibility of non clinical ventricular tachycardia.     

Antiarrhythmic Efficacy of Oral Sotalol in Patients with Sustained Ventricular Tachycardia or Ventricular Fibrillation Postmyocardial Infarction

In order to assess the antiarrhythmic efficacy of oral sotalol we studied 46 patients with sustained monomorphic ventricular tachycardia (n = 40) or ventricular fibrillation (n = 6) by programmed ventricular stimulation. All patients had coronary artery disease with a history of myocardial infarction. Prior to sotalol, patients were treated with a mean of 3.4 ± 1.4 antiarrhythmic Class I drugs. None of these drugs prevented sustained monomorphic ventricular tachycardia or ventricular fibrillation. During control programmed ventricular stimulation (PVS 1) ventricular fibrillation was induced in 7 patients (15%), sustained monomorphic ventricular tachycardia in 30 patients (65%), and nonsustained ventricular tachycardia in 9 patients (20%). After loading with oral sotalol (320 mg/day) programmed ventricular stimulation (PVS 2) was repeated 4.2 ± 3.3 weeks after PVS 1. Ventricular fibrillation was not inducible in any of the patients; in 10 patients (22%) sustained monomorphic ventricular tachycardia was induced, and nonsustained ventricular tachycardia was induced in 10 patients (22%). In 26 patients (57%) either no response or a short ventricular response was inducible. Our data show that oral sotalol is an effective antiarrhythmic agent in patients with sustained monomorphic ventricular tachycardia or ventricular fibrillation following myocardial infarction.     

Day to day reproducibility of electrically inducible ventricular arrhythmias in survivors of acute myocardial infarction

Day to day reproducibility of the response to programmed ventricular stimulation has not been evaluated in survivors of acute myocardial infarction. Programmed ventricular stimulation was performed prospectively on 2 consecutive days in 56 patients on an average of 12 +/- 5 days (range 7 to 29) after an acute myocardial infarction. No patient had a history of documented or suspected sustained ventricular tachycardia or fibrillation occurring greater than 48 h after infarction. During initial programmed ventricular stimulation, 21 patients had induction of sustained ventricular tachycardia or fibrillation (Group I), and 35 patients had induction of either nonsustained ventricular tachycardia or no ventricular tachycardia (Group II). Repeat programmed ventricular stimulation in Group I patients induced sustained ventricular tachycardia or fibrillation in 16 of 21 patients (reproducibility 76%); the maximal induced response in the other 5 patients was nonsustained ventricular tachycardia in 2 patients and fewer than six repetitive ventricular responses in 3 patients. The day to day reproducibility was significantly higher for inducible sustained ventricular tachycardia of cycle length greater than or equal to 240 ms compared with rapid sustained ventricular tachycardia of cycle length less than 240 ms (100% versus 44%, p less than 0.009) or ventricular fibrillation (100% versus 43%, p less than 0.009). Repeat programmed ventricular stimulation in Group II patients did not induce sustained ventricular arrhythmias in 31 of 35 patients (reproducibility 89%). Thus, in survivors of acute myocardial infarction, inducible slow sustained ventricular tachycardia was a highly reproducible finding, whereas inducibility of rapid sustained ventricular tachycardia and ventricular fibrillation showed a significant day to day variability.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognosis in Patients with Left Ventricular Dysfunction and Ventricular Tachycardia Following Programmed Ventricular Stimulation

We performed programmed ventricular stimulation on 69 patients with left ventricular ejection dysfunction (ejection fraction < 50%) and clinically recognized ventricular tachycardia including 28 patients with sustained ventricular tachycardia and 41 patients with nonsustained ventricular tachycardia. An inducible arrhythmia (> 6 beats ventricular tachycardia) was found in 74% of patients. Patients with clinically sustained arrhythmias were frequently inducible (89%) with a high incidence of inducible monomorphic ventricular tachycardia (82%). Patients with clinically nonsustained ventricular tachycardia had a lower rate of inducibility (63%) including a high incidence of inducible polymorphic ventricular tachycardia (27%). Inducible patients with left ventricular dysfunction and ventricular tachycardia had a low incidence of electrophysiologically demonstrated effective drug therapy (16%). However, if an effective drug was found, the prognosis was good. Empirical drug therapy was associated with a poor prognosis in inducible and noninducible patients. Finally, an unfavorable prognosis was associated with a clinically sustained arrhythmia, a lower ejection fraction, and the presence of a left ventricular aneurysm. An inducible arrhythmia did not predict an unfavorable course. Indeed, patients with noninducible ventricular tachycardia in this group of patients were still at risk for sudden cardiac death.     

Prevalence,characteristics and significance of ventricular tachycardia (three or more complexes) detected with ambulatory electrocardiographic recording in the late hospital phase of acute myocardial infarction

A 24 hour electrocardiographic recording was performed before hospital discharge in 430 patients who survived the cardiac care unit phase of acute myocardial infarction. Fifty patients (11.6 percent) had ventricular tachycardia, that is, three or more consecutive ventricular complexes. In 25 (50 percent) of these 50 patients, there was only one episode of ventricular tachycardia and, in 15 patients (30 percent), the longest run of ventricular tachycardia was only three consecutive ventricular premature depolarizations. The average rate of tachycardia was 119/min. Tachycardia rarely started with R on T ventricular premature complexes (4 of 1,370 episodes in 50 patients).There was no difference between the groups with and without ventricular tachycardia with respect to age and sex, but the patients with tachycardia had a significantly greater prevalence of previous myocardial infarction, left ventricular failure in the cardiac care unit, atrial fibrillation, ventricular tachycardia or ventricular fibrillation in the cardiac care unit and significantly more frequent use of digitalis and diuretic and antiarrhythmic drugs at the time of hospital discharge.The group with tachycardia had a 38.0 percent 1 year mortality rate compared with the rate of 11.6 percent in the group without tachycardia. Ventricular tachycardia had a strong association with 1 year mortality (odds ratio = 4.7). Although ventricular tachycardia had a significant association with many other postinfarction risk factors, it was still significantly associated with the 1 year mortality (p < 0.05) when other important risk variables were controlled statistically using a multiple logistic regression model. The 36 month cumulative mortality rate was 54.0 percent in the group with ventricular tachycardia compared with 19.4 percent in the group without tachycardia.     

The mechanisms of ventricular tachycardia in humans determined by intraoperative recording of the electrical activation sequence

We recorded ventricular activation sequence during ventricular tachycardia in 76 patients who underwent surgical therapy of refractory ventricular tachycardia. Ventricular tachycardia arose from a discrete site (focal origination) in 28 patients (37%) or resulted from reentry around scar (macroreentry) in 22 patients (29%). The mechanism responsible for ventricular tachycardia was not discernable in the remaining 26 patients (34%), usually because of inadequacy of activation data. We conclude: (1) although focal originating of ventricular tachycardia is common, more frequently the mechanism is either macroreentry or uncertain, as assessed by conventional recording techniques; thus, a search for the "site of earliest activation" during ventricular tachycardia frequently may fail to direct rationally the operative procedure; (2) conventional techniques for intraoperative study of electrical activation during ventricular tachycardia are inadequate.     

Mode of stimulation versus response: validation of a protocol for induction of ventricular tachycardia

Electrophysiologic studies were prospectively performed in 91 consecutive patients referred for evaluation of sustained ventricular tachycardia or sudden cardiac death. Fifty-two patients had a history of sustained ventricular tachycardia and 39 patients had a history of sudden cardiac death. The identical stimulation protocol was used in all patients. The stepwise protocol involved atrial pacing, burst ventricular pacing, single, double, and triple extrastimuli during ventricular pacing. Stimulation was performed at the right ventricular apex at two and five times diastolic threshold. Using this protocol, ventricular tachycardia was inducible in 48 (92%) of the 52 patients with a history of sustained ventricular tachycardia and in 28 (72%) of 39 patients with a history of sudden cardiac death (p less than 0.02). The use of a third extrastimulus increased the yield of inducible ventricular tachycardia by 37% in patients with a history of sustained ventricular tachycardia and by 25% in patients with a history of sudden cardiac death. Stimulation at five times diastolic threshold and stimulation from the right ventricular outflow tract added a 15% increment in overall yield of inducible ventricular tachycardia in patients with a history of sustained ventricular tachycardia, and a 26% increment in yield in patients with a history of sudden cardiac death. Forty-four (92%) of the 48 inducible patients in the sustained ventricular tachycardia group had inducible monomorphic ventricular tachycardia as compared to 19 (68%) of 28 patients in the sudden cardiac death group (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in spontaneous sinus node rate as an estimate of cardiac autonomic tone during stable and unstable ventricular tachycardia

Changes in sinus node rate were measured as an estimate of reflex control of cardiac autonomic tone during 32 episodes of stable ventricular tachycardia (without loss of consciousness) and 21 episodes of unstable ventricular tachycardia (loss of consciousness requiring electrical cardioversion) in 32 patients without retrograde ventriculoatrial conduction. Sinus node rate was measured before induction of ventricular tachycardia (at 5 s intervals during tachycardia) and 5 s after termination of ventricular tachycardia. It increased from 85 +/- 12 beats/min to a maximum of 109 +/- 25 beats/min during stable ventricular tachycardia (p less than 0.001) and from 82 +/- 15 beats/min to a maximum of 105 +/- 34 beats/min during unstable ventricular tachycardia (p less than 0.001). During unstable ventricular tachycardia, the increase in sinus rate was more abrupt and was followed by a sharp decrease beginning before termination of the tachycardia and resulting in a slower rate after termination (56 +/- 15 beats/min) than before tachycardia (p less than 0.001). Stable ventricular tachycardia resulted in a continuous increase of sinus node rate, which remained higher after termination (102 +/- 15 beats/min) than before tachycardia (p less than 0.001). Autonomic mechanisms responsible for changes in sinus rate were evaluated by reinducing the ventricular tachycardia after beta-adrenergic blockade by propranolol in 10 patients. Intravenous propranolol (mean dose 11 +/- 4 mg) had no effect on the magnitude of increase in sinus rate (+18 +/- 6 beats/min before and +17 +/- 7 beats/min after propranolol).(ABSTRACT TRUNCATED AT 250 WORDS)     

Differences between patients with ventricular tachycardia and ventricular fibrillation as assessed by signal-averaged electrocardiogram, radionuclide ventriculography and cardiac mapping

This study examined 65 patients with ventricular tachycardia or fibrillation late after myocardial infarction to determine whether they differed with respect to duration of ventricular activation in sinus rhythm and left ventricular ejection fraction. Patients with spontaneous ventricular tachycardia had a longer ventricular activation time in sinus rhythm than did patients with spontaneous ventricular fibrillation. This difference was detected with the signal-averaged electrocardiogram (ECG) (tachycardia 181 +/- 33 ms, fibrillation 152 +/- 23 ms, p less than 0.001) and at epicardial mapping (tachycardia 210 +/- 17 ms, fibrillation 192 +/- 17 ms, p less than 0.02). Left ventricular ejection fraction was lower in patients with spontaneous ventricular tachycardia (0.22 +/- 0.09) than in patients with spontaneous ventricular fibrillation (0.27 +/- 0.09) (p less than 0.05). The patients with both spontaneous and inducible ventricular fibrillation had a shorter ventricular activation time on the signal-averaged ECG (129 +/- 17 ms) and a higher ejection fraction (0.36 +/- 0.05) than did either patients with spontaneous ventricular fibrillation and inducible ventricular tachycardia (158 +/- 21 ms and 0.25 +/- 0.08, respectively, each p less than 0.01) or patients with both spontaneous and inducible ventricular tachycardia (181 +/- 33 ms and 0.22 +/- 0.09, respectively, each p less than 0.001). Of the patients with inducible ventricular tachycardia, presentation with tachycardia rather than fibrillation was associated with a longer ventricular activation time on the signal-averaged ECG (181 +/- 33 versus 158 +/- 21 ms, p less than 0.02) and a longer cycle length of inducible ventricular tachycardia (290 +/- 61 versus 259 +/- 44 ms, p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Value of induction of pleomorphic ventricular tachycardia during programmed stimulation

The morphology of the first documented, the recurrent and theinduced ventricular tachycardia were studied in 41 patientswith an old myocardial infarction and documented sustained ventriculartachycardia. During a mean follow-up of29 ± 11 monthsrecurrent ventricular tachycardia was present in 24 of 41 patientswith the same morphology as the first ventricular tachycardiain nine (37.5%) and a different morphology in 15 patients (62.5%).Ventricular tachycardia with the same morphology as the spontaneousventricular tachycardia were induced without significant differencesbetween patients with recurrent events and those without. However,multiple morphologies of ventricular tachycardia (pleomorphism)were induced more frequently in patients with subsequent recurrenceof ventricular tachycardia (off drugs: 9 of 13, 69%, on drugs:14 of 23, 61%) than in patients without (off drugs: 4 of 10,40%, on drugs: 2 of 11,18%) (P <0.05). Pleomorphism of ventricular tachycardia induced during programmedstimulation identifies patients at a higher risk of subsequentrecurrent events. Recurrent ventricular tachycardia has a differentmorphology than the first one in two thirds of patients.     

Ventricular tachycardia with QRS configuration similar to that in sinus rhythm and a myocardial origin: differential diagnosis with bundle branch reentry.

INTRODUCTION: Tachycardia with a QRS configuration which resembles that in sinus rhythm is usually thought to be supraventricular. Ventricular tachycardia, with a similar QRS configuration to that in sinus rhythm on the 12-lead ECG, can occur. The mechanisms of this form of ventricular tachycardia have not been previously reported. METHODS AND RESULTS: The mechanism of ventricular tachycardia was defined during electrophysiological study in five patients. During sinus rhythm, all patients had a wide QRS complex (>0.12 s) on the 12-lead ECG. The morphology remained grossly unchanged during spontaneous, symptomatic tachycardia. Four of the five patients had coronary artery disease and left ventricular dysfunction. The remaining patient had idiopathic dilated cardiomyopathy. The relationship between the His bundle, deflection, the right bundle branch and the QRS complex was evaluated during tachycardia. Atrial and ventricular pacing, and ventricular activation mapping were performed during tachycardia to define the tachycardia mechanism. The tachycardia induced at electrophysiological testing, which was similar to the clinical tachycardia, was proven to be ventricular tachycardia in each patient. The morphology of ventricular tachycardia was right bundle branch block in two patients and left bundle branch block in three patients. The median tachycardia cycle length was 300 ms (range: 260-480 ms). His bundle activation occurred in a 1:1 relationship with ventricular activation during tachycardia in all patients at least intermittently. The tachycardias were thought initially to be bundle branch reentry tachycardia. With further intervention and continued observation, it became clear that His bundle activation was passive and was not required for the tachycardia to sustain. During tachycardia, His bundle activation appeared to precede the local ventricular activation. Instead, the His bundle was activated slowly from the previous ventricular beat causing a long ventricular-His (VH) interval. This was shown by: (1) activation patterns, (2) response to pacing, (3) intermittent VH dissociation, and (4) termination of ventricular tachycardia. CONCLUSION: A unique form of ventricular tachycardia is described. The QRS complex morphology on the 12-lead ECG during tachycardia was grossly similar to that during sinus rhythm. The His bundle activation was passive and occurred with a long activation time from the ventricle to the His bundle. Although it mimics usual bundle branch reentry, this form of ventricular tachycardia appears to be due to a different mechanism in which the His bundle is not obligatory for the continuation of the reentrant phenomenon.     

Coincident atrioventricular nodal reentrant and idiopathic ventricular tachycardia

Double tachycardia appears to be relatively rare. Our single-center experience of coincident typical atrioventricular nodal reentrant and idiopathic ventricular tachycardia was reviewed. Between September 2003 and February 2005, 40 patients with idiopathic ventricular tachycardia underwent catheter ablation for right ventricular outflow tract tachycardia in 20, left ventricular outflow tract tachycardia in 2, and left ventricular septal tachycardia in 18. In 5 patients (2 men and 3 women, aged 27-49 years) there was a combination of typical atrioventricular nodal reentrant tachycardia and idiopathic ventricular tachycardia. They had no structural heart disease. The presenting arrhythmia was supraventricular in one and ventricular in 4. There was no case of inducibility of one arrhythmia by the other (tachycardia-induced tachycardia), but an interaction was observed in one tachycardia in which inducibility was seen only after ablation of the other arrhythmia. Radiofrequency ablation of either arrhythmia did not prevent induction of the other.     

Characteristics of non-sustained ventricular tachycardia found during dynamic ECG in patients with recent myocardial infarction

The characteristics of ventricular tachycardia found during Holter ECG monitoring before discharge in patients hospitalized because of acute myocardial infarction were analyzed. One or more ventricular tachycardia episodes were found in 29 of 251 patients (11.5%). On the whole, there were 233 episodes of ventricular tachycardia: 18 patients (62%) had only one episode of ventricular tachycardia, 9 (31%) 2-5 episodes and 2, respectively, 68 and 118 episodes. Episodes of ventricular tachycardia were more numerous in patients with frequent or polymorphic premature ventricular complexes than in patients with sporadic or monomorphic premature ventricular complexes. Fifty-seven ventricular tachycardia episodes were analyzed: 30 of 3 beats, 25 of 4-9 beats and 2 of 15 beats. Forty-seven episodes were monomorphic and 10 (17.5%) were polymorphic. The ventricular tachycardia rate was 136.4 +/- 25 b/m' (range 104-200). The RR'/QT ratio (where RR' = coupling interval of the first beat of ventricular tachycardia) was 1.67 +/- 0.42 and was not correlated either with the rate or the number of beats of ventricular tachycardia. Heart rate at the moment of ventricular tachycardia was 82 +/- 15 b/m' and QT interval 0.36 +/- 0.05 sec; there was no difference when compared to their values of 1 and 5 minutes before ventricular tachycardia. Furthermore, the heart rate showed no difference when compared to the mean value of the hours in which ventricular tachycardia episodes occurred. In addition, heart rate was not correlated with ventricular tachycardia rate, whereas a good correlation was found between the last RR interval preceding ventricular tachycardia and RR' interval (r = 0.61, P less than 0.01).     

Malignant premature ventricular beats in ambulatory patients.

The characteristics of premature ventricular beats predisposing to ventricular tachycardia or fibrillation were assessed by 24-h ambulatory monitoring and maximal treadmill exercise testing in 339 cardiac patients with premature ventricular beats. Premature ventricular beats were divided into early (Q-premature ventricular beat less than QT), late (within the last 20% of the cardiac cycle), and midcycle. Ventricular tachycardia was recorded in 45 patients and ventricular fibrillation, in three. The frequency of ventricular tachycardia or fibrillation was 32% in patients with late, 16% in patients with early, and 7% in patients with midcycle premature ventricular beats (P less than 0.05). Patients with frequent (less than 10/min) multiformed premature ventricular beats had a frequency of ventricular tachycardia or fibrillation of 44%, while only 13% of patients with frequent uniformed premature ventricular beats had ventricular tachycardia (P less than 0.05). Ambulatory patients with ventricular tachycardia or fibrillation have frequent multiformed premature ventricular beats, and the ventricular tachycardia or fibrillation is usually triggered by late premature ventricular beats.