Flecainide overdose – support using an intra-aortic balloon pump

Background

Flecainide is an antiarrhythmic agent which is being used increasingly for the management of super-ventricular arrhythmias. Overdose with flecainide is frequently fatal with mortality reported as high as 22% due to arrhythmias, myocardial depression and conduction defects leading to electro-mechanical dissociation and asytole. Supportive measures are often required during the case and previously have included inotropes, extracorporeal membrane oxygenation and cardiopulmonary bypass.

Case presentation

A 47 year old lady presented to the emergency department with a four hour history of severe central chest pain. Her ECG showed atrial fibrillation and broad QRS complexes with a sine wave appearance. She had a past history of paroxysmal atrial fibrillation and significant psychiatric history. Following thrombolysis for a presumed myocardial infarction she developed cardiogenic shock with severely impaired left ventricular function. An intra-aortic balloon pump was inserted and coronary angiography demonstrated normal coronary arteries. With inotropic support she improved over 48 hours, with both her QRS duration and left ventricular function returning to normal. Biochemical testing following her discharge demonstrated significantly elevated levels of flecainide.

Conclusion

The use of an intra-aortic balloon pump is a useful supportive measure during the acute phase of flecainide overdose associated with severe myocardial depression.     

DDD-Pacemaker Pseudomalfunction During Supraventricular Tachycardia

Asynchronous pacing during the presence of electromagnetic interference or other sources of "noise" is a protective mechanism available to prevent pacemaker output inhibition. We describe a patient with a DDD pacemaker who had asynchronous dual chamber or noise reversion pacing as a consequence of repetitive signals (QRS complexes) falling into the noise sampling period (NSP) of the pacemaker ventricular refractory period. During supraventricular tachycardia at a rate of 215 bpm, noise reversion mode pacing occurred when QRS complexes were well detected immediately after the termination of a normal pacemaker ventricular refractory period and treated as a premature ventricular depolarization, resulting in automatic refractory period extension. Recycling of this extended refractory period occurred when consecutive QRS complexes were detected during the NSP and forced asynchronous dual chamber pacing at the programmed lower rate. The mechanism is presented and was supported by subthreshold esophageal pacing simulating the tachycadia and initiating the noise reversion response.     

Late Sensing Due to Extremely Delayed Right Ventricular Activation in Arrhythmogenic Right Ventricular Cardiomyopathy

A patient with arrhythmogenic right ventricular cardiomyopathy/dysplasia, implanted with a dual-chamber implantable cardioverter-defibrillator programmed in DDD mode, showed an unexpected ventricular sensing dysfunction: despite a very long (320 ms) programmed atrioventricular (AV) interval, ventricular stimuli were delivered in the ST segment after each spontaneous conducted QRS complex. This suggested the presence of ventricular undersensing. When, however, the system was programmed in VVI mode, spontaneous QRS complexes were normally sensed, although electrogram (ECM) analysis revealed that ventricular sensing occurred 160 ms after the beginning of QRS complex. A new ventricular lead was then implanted in the outflow tract of the right ventricle, resulting in normal ventricular sensing function. At the time of intervention, the amplitude of the spontaneous ventricular signal recorded from the old ventricular lead was 2.8 mV. In this patient, no true undersensing occurred although ventricular stimuli were delivered 140 ms after the beginning of spontaneous QRS complexes when the system was in DDD mode: the cause of the apparent pacemaker malfunction was the extremely prolonged ventricular depolarization. Due to fibrofatty muscle replacement, the depolarization wavefront reached the ventricular muscle surrounding the pacemaker lead with such a delay that at the end of the programmed sensed AV interval (320 ms) the ventricular EGM had not yet attained the sensing threshold. This apparent undersensing should, thus, be defined as "late sensing."     

Broad QRS tachycardia: Electrocardiographic diagnosis and management

The diagnostic difficulties between supraventricular tachyarrhythmias with intraventricular conduction delay and ventricular tachycardia have challenged the physician since the first recording of a ventricular tachycardia by Lewis in 1909. The examples selected emphasize some of the diagnostic and therapeutic dilemmas of "broad QRS tachycardias" and their major differential features from abberrancy. Multiple simultaneous surface ECG leads are valuable in showing the direction of the initial activation forces of the QRS complexes, the frontal QRS axis and the configuration of the QRS in lead V1. Vagal maneuvers and intra-atrial or esophageal leads are very useful in demonstrating the underlying atrial rhythm and atrioventricular dissociation when present. In life-threatening situations, urgent therapy or D.C. cardioversion may be required before a definitive diagnosis has been established. In recent years electrode catheter techniques for the diagnosis, for arrhythmia induction and for the selection and assessment of the effectiveness of the antiarrhythmic drug therapy have been carried out in the management of recurrent broad QRS tachycardia. In view of the inherent risks with the use of this invasive technique, it should be restricted to a carefully selected number of patients with recurrent life-threatening dysrhythmias as suggested by Scheinman.     

Ventricular Tachycardia and Ventricular Fibrillation in Patients with Short P-R Intervals and Narrow QRS Complexes

Eleven patients with short P-R Intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an expression of the “enhanced A-V conduction” that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamicaliy unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies     

"Invisible" Pseudo-Pseudofusion Beats

Three simultaneous leads (I, II and VI) were recorded in a patient with a normally functioning bipolar AV sequential (DVI) pacemaker. Superimposition of the ineffectual atrial spikes upon the early part of the QRS complexes resulted in pseudo-pseudofusion beats, clearly identified in lead II, However, the small spikes were hardly seen in lead I and not seen at all in lead VI. Therefore, the pseudo-pseudofusion beats were "almost invisible" and "invisible," respectively, in these leads. Delivery of atrial spikes within the beginning of the QRS complexes was possible because sensing of the ventricular electrogram occurred after the onset of ventricular depolarization in the surface leads. (PACE, Vol. 5. March-April, 1982)     

MCL1 and MCL6 Compared to V1 and V6 in Distinguishing Aberrant Supraventricular from Ventricular Ectopic Beats

Use of V1 and V6 has been suggested for distinguishing aberrant supraventricular from ventricular ectopy. For two decades, "modified" leads MCL1 and MCL6 have been widely used as V1 and V6 substitutes for bedside monitoring, but their use has never been validated. To determine the value of MCL1 and MCL6, 81 morphologically distinct wide QRS ectopic beats were recorded from 46 patients during cardiac electrophysiological study. As determined by the His-bundle electrogram, 31 of the ectopics were aberrant supraventricular, 50 were ventricular. A new criterion, measurement of QRS onset to the predominant peak or nadir of the complex, was valuable in diagnosing wide complexes in MCL6 and V6. An interval of 50 msec or less predicted aberrant supraventricular ectopy; an interval of 70 msec or more predicted ventricular ectopy. There was agreement between the modified and conventional precordial leads regarding which QRS patterns were useful in distinguishing aberrant supraventricular from ventricular ectopy. A greater proportion of wide complexes in MCL1 and V1 exhibited patterns useful in making the diagnosis compared to MCL6 and V6. Using well-established criteria, the proportion of correct diagnoses that was made from individual leads was: MCL1 = 86%, V1 = 85%, MCL6 = 72%, V6 = 67%. The bedside leads (MCL1 and MCL6) were not statistically different in diagnostic accuracy from their conventional lead counterparts (V1 and V6); however, MCL1 and V1 were superior to MCL6 and V6. When the new criterion was added to make the diagnosis from MCL6 and V6, no difference in diagnostic accuracy was present between the four leads.     

Analysis of the electrocardiographic waveforms produced by right ventricular pacing: relation to the nonpaced patterns

Background: Ventricular aberrant conduction has a confounding effect on the known relationships between the electrocardiogram (ECG) and left ventricular (LV) mass. By relating the ECG of right ventricular pacing to LV mass and to nonpaced recordings, clarification of these effects might emerge.
Methods and Results: In 30 patients (age, 81 ± 7 years; 13 women) who had right ventricular paced ECGs and echocardiograms, 24 of who also had nonpaced ECGs, comparative analyses were performed. Although the nonpaced ECGs had strong correlations with various echocardiographic measurements, for paced ECGs, only QRS complex voltage and interventricular septal thickness (IVS) were significantly related. However, paced QRS complex voltage relationships correlated with those of nonpaced QRS complexes, ranging from an r = 0.54, P < 0.006, for the sum of the R in aVL and the S in V-3 to r = 0.78, P < 0.001, for the sum of the R in I and the S in III. Paced ECGs had a QRS complex with a greater spatial amplitude, a longer duration, and a more superior position, and had more deeply inverted T waves than nonpaced ECGs. The differences between the voltages of paced and nonpaced QRS complexes, moreover, diminished as LV mass and/or IVS increased. When compared with nonpaced ECGs, paced ECGs showed the most similarity to nonpaced ECGs having a left bundle branch block (LBBB) pattern. Except for the presence of more superiorly directed QRS complexes, paced impulses were not significantly different (P < 0.008) from nonpaced impulses having a LBBB pattern. Also, the nonpaced ECG pattern had no discernable effect on ECG produced by right ventricular (RV) pacing.
Conclusions: Despite having weak relations with echocardiographic measurements, the QRS complex voltage of the paced ECG correlated with those of nonpaced ECGs, and the voltage differences between them were smaller as LV mass increased.     

Far-field QRS complex sensing: prevalence and timing with bipolar atrial leads

Sensing of far-field QRS complex through the atrial pacemaker lead may cause a number of pacemaker function disturbances, most of which are rarely seen with modern pulse generators. However, certain pulse generator algorithms will still be jeopardized by far-field QRS complex sensing. Intracardiac electrograms with markers were obtained by telemetry in 30 patients following implantation of a permanent bipolar atrial lead and a DDDR pulse generator. The occurrence and timing of far-field QRS complex sensing was studied at different atrial amplifier sensitivity settings. With paced ventricular complexes, QRS sensing was documented in all 30 cases at the maximum atrial sensitivity (0.1 mV). The median QRS complex sensing threshold was 0.3 mV, and the sensing window at high atrial sensitivities was 67-202 ms following the ventricular pacing impulse. In one case, QRS complex sensing was seen up to an atrial sensitivity of 1.5 mV. In 12 of 13 patients with 1:1 AV conduction, atrial sensing of spontaneously conducted ventricular complexes was seen (median sensing threshold 0.2 mV; the sensing window was -23 to 114 ms relative to the ventricular amplifier sensing event). Far-field QRS complex sensing was also found in all 12 patients in whom ventricular fusion complexes were obtained (median sensing threshold 0.2 mV; the window of sensing was 64-187 ms after the ventricular pacing impulse). Constant or intermittent QRS complex sensing via the atrial bipolar lead was thus universally demonstrable. It occurred in only a minority (20%) of patients at a sensitivity of 0.5 mV or less. Knowledge regarding the timing of the oversensing as related to the atrial sensitivity setting may aid in the design of algorithms of future pacemakers and cardioverter defibrillators.     

Changes in Morphology of the Paced QRS Complex Related to Atrial Contraction

A patient with 2:1 AV block underwent temporary ventricuJar pacing. AU the paced stimuli resuited in ventricular capture, but a marked variability in morphology of the paced QRS complexes occurred. Two different types of paced QRS complex (labeled A and B) were recognized. Type B complexes were manifest only when the pacing stimulus was preceded hy a sinus P wave within a time interval ranging from 0.15 to 0.52 sec. The P wave-induced changes in morphology of the paced QRS complexes were interpreted as due to displacement of the pacing ventricular lead caused by atrial systole.     

Left ventricular systolic and diastolic dyssynchrony in coronary artery disease with preserved ejection fraction

The present study aims to evaluate LV (left ventricular) mechanical dyssynchrony in CAD (coronary artery disease) with preserved and depressed EF (ejection fraction). Echocardiography with TDI (tissue Doppler imaging) was performed in 311 consecutive CAD patients (94 had preserved EF > or =50% and 217 had depressed EF <50%) and 117 healthy subjects to determine LV systolic and diastolic dyssynchrony by measuring Ts-SD (S.D. of time to peak myocardial systolic velocity during the ejection period) and Te-SD (S.D. of time to peak myocardial early diastolic velocity during the filling period) respectively, using a six-basal/six-mid-segmental model. In CAD patients with preserved EF, both Ts-SD (32.2+/-17.3 compared with 17.7+/-8.6 ms; P<0.05) and Te-SD (26.2+/-13.6 compared with 20.3+/-8.1 ms; P<0.05) were significantly prolonged when compared with controls, although they were less prolonged than CAD patients with depressed EF (Ts-SD, 37.8+/-16.5 ms; and Te-SD, 36.0+/-23.9 ms; both P<0.005). Patients with preserved EF who had no prior MI (myocardial infarction) had Ts-SD (32.9+/-17.5 ms) and Te-SD (28.6+/-14.8 ms) prolonged to a similar extent (P=not significant) to those with prior MI (Ts-SD, 28.4+/-16.8 ms; and Te-SD, 25.5+/-15.0 ms). Patients with class III/IV angina or multi-vessel disease were associated with more severe mechanical dyssynchrony (P<0.05). Furthermore, the majority of patients with mechanical dyssynchrony had narrow QRS complexes in those with preserved EF. This is in contrast with patients with depressed EF in whom systolic and diastolic dyssynchrony were more commonly associated with wide QRS complexes. In conclusion, LV mechanical dyssynchrony is evident in CAD patients with preserved EF, although it was less prevalent than those with depressed EF. In addition, mechanical dyssynchrony occurred in CAD patients without prior MI and narrow QRS complexes.     

QRS分数与QRS记分系统估测AMI患者左室射血分数的比较

对QRS分数及QRS记分系统估测急性心肌梗死（AMI）患者左空射血分数的价值进行了比较。结果表明，在急性前壁心梗患者，QRS分数与QRS记分均与左室射血分数显著相关，二者与左空射血分数的相关系数无显著差异。但在下／后壁心梗患者，二者与左空射血分数均无显著相关。结果表明，在前壁AMI，以QRS分数估测左空射血分数较QRS记分系统更为简便实用。     

Undersensing of the Tiny QRS Complexes That Emerged After the Isolation of the Right Ventricle in a Patient with Ventricular Tachycardia

This article describes a patient who underwent right ventricular disconnection for medically refractory ventricular tachycardia associated with arrhythmogenic right ventricular dysplasia. After the operation there was no ventricular tachycardia recurrence. Two years after the operation, he received a permanent VVI pacemaker for the symptomatic second-degree AV block. Sensing function of the pacemaker was normal for the normal QRS complexes, but the tiny QRS complexes that appeared after the arrhythmia surgery were not sensed by the pacemaker and therefore caused no problem.     

Effect of Propranolol on Ventricular Rate During Atrial Fibrillation in the Wolff-Parkinson-White Syndrome

Atrial fibrillation was induced during an electrophysiology study in 10 patients with the Wolff-Parkinson-White (WPW) syndrome, after determination of baseline properties of the accessory atrioventricular (AV) connection; intravenous propranolol (0.2 mg/kg) was then administered. Atrial fibrillation terminated during the drug infusion in three patients, allowing determination of propranolol's effects on conduction and refractoriness during sinus rhythm, before atrial fibrillation was reinduced. In these three patients propranolol had no effect on refractoriness or conduction properties of the accessory AV connection during sinus rhythm. The mean ventricular rate during atrial fibrillation was slowed by 15–56 beats/min in six patients, had no effect on the mean rate in three patients, and markedly increased the ventricular rate (203 to 267 beats/min) in one patient. In this patient, 54% of QRS complexes during atrial fibrillation were narrow, compared to 0–25% in the other patients. Propranolol reduced the percentage of QRS complexes that were narrow from 13 ± 16% to 1 ± 2% (mean ± standard deviation, p < 0.05). We conclude that propranolol may slow the ventricular rate during atrial fibrillation in some patients with the WPW syndrome, probably by blockcing the effects of adrenergic activation. However, propranolol should not be used in patients with the WPW syndrome who have atrial fibrillation, if most QRS complexes during atrial fibrillation are preexcited. When a large percentage of QHS complexes are narrow, propranolol may increase the ventricular rate, probably by eliminating concealed retrograde conduction in the accessory AV connection.     

高浓度极化液联合曲美他嗪对急性心肌梗死面积及心功能的影响

目的：评价高浓度极化液（GIK）联合曲美他嗪经代谢途径治疗对急性心肌梗死（AMI）患者梗死面积及心功能的影响。方法：将46例急性前壁心肌梗死患者随机分为代谢药物治疗组（n=25）和对照组（n=21）,记录每例患者入院即刻和第1、3、7、14天12导联心电图。用Wagner的QRS记分预测梗死面积。于治疗14d后行核素心血池心室造影,判断心功能。结果：经代谢途径治疗后第7、14天,QRS记分较对照组显著降低,梗死面积的扩大、保护缺血心肌的损伤及改善心功能均有显著疗效。     

Intracardiac QRS Electrogram Width—An Arrhythmia Detection Feature for Implantable Cardioverter Defibrillators: Exercise Induced Variation as a Base for Device Programming

Delivery of inappropriate therapy of implantahle cardioverter defibrillators (ICD) due to inaccurate arrhythmia detection represents a major clinical problem. Different arrhythmia detection criteria such as the “stability” of the cycle length or the suddenness of “onset” of tachycardia have been implemented in ICD software to prevent inappropriate therapy. The new Medtronic model 7223Cx ICD offers an additional detection parameter (QHS width), which reflects changes in the duration of ventricular depolarization as a tool to distinguish supraventricular from ventricular tachycardias. Although this criterion can be programmed based on ECG parameters derived from resting ECGs, this may not be sufficient since QRS width is subject to considerable changes due to transient myocardial ischemia, changes in autonomic tone, or frequency dependent effects of antiarrhythmic drugs. The present study aimed to determine frequency dependent changes in QRS width in individual patients at rest and during symptom-limited exercise testing in 16 patients with documented ventricular tachycardia (N = 13) or ventricular fibrillation (N = 3). The optimal EGM slew threshold and the individual variation of QRS width were determined. Measurements obtained at the end of the implantation procedure were compared to those performed at hospital discharge. The majority of patients showed a wider variation in QRS duration as measured from 30 consecutive cycles during exercise as compared to rest. For example, the QRS range (i.e., the difference between the maximal and the minimal QRS width measured) averaged 7 ± 3 ms at rest and increased to 11 ±3 ms during exercise (P = 0.004) with an increase of ≥ 4 ms observed in 11 (69%) of 16 patients. In 13 (81%) of 16 patients a reprogramming of at least one QRS width parameter from its value at the time of implantation was necessary. Thus, the QRS width measured from the intracardiac EGM shows significant intra-individual variations in different physiological conditions. Eor optimal programming of the QRS width parameter, measurements obtained during exercise are important.     

Evolution of QRS duration after myocardial infarction: clinical consequences

The natural history of late potentials after acute myocardial infarction (AMI) has been studied in the first 2 years following myocardial infarction (MI). The purpose of the study was to assess the influence of some time delays since MI, including a time delay longer than 2 years on signal-averaged ECG (SAECG). SAECG was recorded at 40-Hz high pass filtering in 40 patients 10 days after acute MI (SAECG 1), then repeated 6-12 months later (mean 9 +/- 3 months) (SAECG 2), and then, 2-4 years later (mean 3 +/- 2 years) (SAECG 3). QRS duration, root mean square voltage of the last 40 ms of QRS (RMS 40), and low amplitude signal duration (LAS) were measured at the first (1), second (2), and third recording (3). Results: (***P < 0.001) [table: see text] The analysis of individual results showed a lengthening QRS duration at the third recording only in patients who had a decreased left ventricular ejection fraction (LVEF) at the third recording. In 12 patients with LVEF > 40%, QRS duration did not change at the first and third recording (104 +/- 15 vs 101 +/- 12 ms). In all 28 patients, but one with LVEF < 40%, QRS duration increased from 107 +/- 12 to 128 +/- 18 ms***. There was no correlation between QRS duration and LVEF at the second recording and no correlation between QRS duration increase at the third recording and the presence or not of late potentials at the first recording. QRS duration lengthening at the third recording was significantly correlated with a left ventricular (LV) dilatation occurrence at the two-dimensional echocardiogram. All arrhythmic events, but two, occurred in patients who developed a QRS duration prolongation and were significantly correlated (P < 0.01) to a mean longer QRS duration (132 +/- 20 ms) than in patients without arrhythmic events (113 +/- 17 ms). In conclusion, the patients with a LV impairment, and who developed a LV dilatation several months after AMI, presented a delayed lengthening of QRS duration noted only at least 2 years after infarction. These patients are at risk of arrhythmic events.     

Localization of late potential sources in myocardial infarction

Introduction: Late potentials (LP) are markers of arrhythmogenic events after myocardial infarction (MI). The localization of LP sources would help to identify arrhythmogenic myocardium. The purpose of this study was to localize these LP sources from non-invasive body surface mapping data. Methods and Results: Six patients were investigated with cardiac MRI and signal averaged 62-lead magnetocardiography after MI. Three of them were suffering from sustained ventricular tachycardia (VT). Sophisticated computer algorithms were used in order to compute the current density on the surface of the left ventricle. We compared these current density distributions for the entire QRS complex and the high frequency LP signals. In the three patients which had premature ventricular complexes (PVCs) we localized the exit sites of these arrhythmias. We found a close matching of the low current density areas based on the QRS complexes and the high current density areas based on the LP signals. These areas predominantly corresponded to sites of the infarctions. Exit sites of PVCs were located close to these areas. Conclusions: By means of sophisticated computer algorithms we were able to localize LP sources. This would be useful in steering catheter ablation and coronary revascularization therapies. However, the method has to be proven with the help of invasive mapping in a larger number of patients.     

An Analysis of Post-Pacing R-R Intervals During Atrial Fibrillation

Bursts of ventricular pacing at cycle lengths of 350-260 ms were introduced during atrial fibrillation in nine patients, and the post-pacing R-R intervals were compared to the R-R intervals of spontaneous QRS complexes. In eight of nine patients, the mean post-pacing R-R interval was 126-199 ms longer than the mean spontaneous R-R interval (p less than 0.005). Spontaneous runs of aberrantly conducted supraventricular complexes were recorded during atrial fibrillation in one patient. The mean R-R interval following the runs of aberrantly conducted supraventricular complexes was significantly longer than the mean R-R interval of spontaneous narrow QRS complexes (p less than 0.001), but not significantly different than the mean post-pacing R-R interval. The findings of this study suggest that the R-R interval that follows a wide-complex tachycardia during atrial fibrillation is unlikely to be of value in differentiating ventricular tachycardia from aberrantly conducted supraventricular complexes. Analysis of R-R intervals that follow bursts of ventricular pacing suggests that there is likely to be considerable overlap between the R-R intervals that follow runs of ventricular tachycardia and the spontaneous R-R intervals during atrial fibrillation. Furthermore, even when the post-tachycardia R-R interval clearly exceeds the longest spontaneous R-R interval during atrial fibrillation, this is still of little diagnostic value, because a long pause may occur after either a run of ventricular tachycardia or a run of aberrantly conducted QRS complexes of supraventricular origin.     

Observations on the Initiation of Sustained Ventricular Tachycardia by Programmed Stimulation

We analyzed the initiation of sustained monomorphic ventricular tachycardia (VT) by programmed ventricular stimulation (PVS) in 50 consecutive patients who had clinical VT or aborted sudden cardiac death with remote myocardial infarction. In 25 of 50 patients, the first induced QRS complex of VT was morphologically identical to the succeeding QRS complexes of VT (type I). In 25 other patients, the first VT beat had a different morphology (type II). Type I had a significantly longer VT cycle length than type II (333 +/- 65 msec and 293 +/- 66 msec, P = 0.036). Type II VT initiation required more aggressive stimulation protocol than type I (type I: type II; number of extrastimulus required for induction 2.5 +/- 0.9 : 3.0 +/- 0.6, P = 0.026; shortest extrastimuli coupling interval 244 +/- 28 msec : 220 +/- 23 msec, P = 0.002). The interval between the last extrastimulus and the onset of the first VT beat was 408 +/- 88 msec in type I and 336 +/- 75 msec in type II (P = 0.004). Furthermore, there was good correlation between the VT cycle length and the interval from last extrastimulus to the onset of nonpaced beat in type I but not in type II.(ABSTRACT TRUNCATED AT 250 WORDS)