Ashman's phenomenon--a source of nonsustained wide-complex tachycardia: case report and discussion.

The refractory period of the right bundle branch is increased when the R-R interval between the prior two conducted impulses is long. Thus, an impulse that arrives soon after the second of two impulses separated by a long R-R interval may be aberrantly conducted with a right bundle branch block morphology on electrocardiogram. This aberrant conduction is termed "Ashman's phenomenon" and is often responsible for isolated wide QRS complexes in the presence of underlying atrial fibrillation. This process may also produce runs of wide QRS complexes that must be distinguished from nonsustained ventricular tachycardia. A case of such multibeat Ashman's phenomena is presented, and the characteristics used to identify this phenomenon are discussed. A brief review of several recent studies on the differentiation of sustained ventricular tachycardia from supraventricular tachycardia with aberrancy in the setting of a regular underlying rhythm is given as well.     

Triggered Activity Induced By Pacing During Digitalis Intoxication: Observations During Programmed Electrical Stimulation in the Conscious Dog With Chronic Complete Atrioventricular Block

In isolated Purkinje fibers, digitalis intoxication induces triggered activity, which is based upon delayed afterdepolarizations. The characteristics of delayed afterdepolarizations have been studied systematically by programmed electrical stimulation. The present investigations were done to study the role of triggered activity during digitalis intoxication in the intact heart. For this purpose, a pacing protocol, similar to that used in experiments of isolated Purkinje fibers, was used. The experiments were done on conscious dogs with chronic complete atrioventricular block. Ventricular tachycardia was induced with digoxin IV 0.1 mg/kg/1-1 1/2 hr. The effect of programmed electrical stimulation on the first post-pacing interval was determined during sustained ventricular tachycardia and, following its spontaneous termination during an episode when ectopic activity could only be induced by pacing. During sustained ventricular tachycardia there was a direct linear relation between the interstimulus interval of regular pacing and the first post-pacing interval. During the episode when ectopic activity could only be induced by pacing, shortening of the post-pacing interval resulted in biphasic behavior of the first post-pacing interval. Pacing with interstimulus intervals of more than 400 ms induced a first post-pacing interval equal to the interstimulus interval, whereas shorter interstimulus intervals induced a first post-pacing interval twice the interstimulus interval. When during regular pacing only the last pacing interval was changed, a similar biphasic response resulted. When toxicity had almost subsided, ectopic activity could only be induced following short pacing intervals (200-320 ms). Again, a direct linear relation was found between the pacing interval and the first post-pacing interval. Our findings strongly suggest that at different levels of digitalis intoxication triggered activity is the underlying mechanism for the first post-pacing QRS complex.     

Effects of Different Modes of Stimulation on the Morphology of the First QRS Complex Following Pacing During Digitalis-Induced Ventricular Tachycardia: Observations in the Conscious Dog With Chronic Complete Atrioventricular Block

During digitalis-induced, sustained, monomorphic ventricular tachycardia, programmed electrical stimulation was performed and the effect on the first post-pacing QRS morphology was determined. Ventricular tachycardia was induced in nine conscious dogs with chronic complete atrioventricular block by administering digoxin i.v. 0.1 mg/kg given in 1-½ hour. Spontaneous ventricular tachycardia most frequently had a right bundle branch block morphology and an extreme left axis suggesting an origin in the apex of the left ventricle. Less frequently, a left bundle branch block-like configuration with an intermediate axis was observed, compatible with an origin in the basal part of the right ventricle. Following pacing close to one of these predilection sites, the first post-pacing QRS morphology suggested an origin close to the site of stimulation. Pacing distant from these predilection sites resulted in fusion complexes between electrical activaion from these predilection sites and the stimulation site. The amount of fusion depended on interstimulus interval and the number of stimuli. Long interstimulus intervals and few stimuli induced a QRS complex similar to that of the spontaneous tachycardia. The faster and longer the stimulation train, the more the QRS complex became similar to the paced QRS complex. Similar findings were also observed on decreasing the last paced interval only. Our findings suggest that triggered activity is the underlying mechanism for the first post-pacing QRS complex. QRS configuration and the relation between the R-R interval and QRS configuration during tachycardia suggest that triggered activity is also the mechanism for the spontaneously occurring ventricular tachycardia during digitalis intoxication. These observations may have important clinical implications.     

Electrophysiological Significance of QRS Alternans in Narrow QRS Tachycardia

To investigate the electrophysiological significance of QRS alternans during narrow QRS tachycardia, transesophageal atrial pacing and recording was performed in 24 patients with a history of paroxysmal supraventricular tachycardia. Standard electrocardiograms showed ventricular preexcitation in 15 patients and normal QRS pattern in nine patients. The ventriculoatrial interval during tachycardia, as defined by means of transesophageal electrogram, allowed tentative diagnosis of the tachycardia mechanism. A 12-lead ECG was recorded either during spontaneous or induced tachycardia, as well as during transesophageal atrial pacing at increasing rates. Electrical alternans occurred spontaneously in eight patients (33%, group A): five with accessory pathway reentry (mean VA: 136 +/- 43 msec), and three with AV nodal reentry (mean VA: 48.3 +/- 12 msec). Tachycardia rate ranged between 170 and 230 beats/min (mean 200.7 +/- 16). In two patients, alternation of the QRS occurred only in the presence of a heart rate exceeding 180 and 190 beats/min, respectively. The amplitude of QRS remained stable during tachycardia in 16 patients (67%, group B): 14 had accessory pathway reentry (mean VA: 137.5 +/- 32 msec), and two had AV nodal reentry (mean VA: 45 +/- 7 msec). In this group, the tachycardia rate ranged from 150 to 210 beats/min (mean 175 +/- 12). Incremental transesophageal atrial pacing up to rates equal to that of tachycardia was performed in five patients from group A and in five patients from group B. Electrical alternans could not be induced in both groups with pacing at progressively increasing rates.(ABSTRACT TRUNCATED AT 250 WORDS)     

Atrial and Ventricular Vulnerability in a Patient with the Wolff-Parkinson-White Syndrome

An electrophysiologic study was carried out in a patient with the Wolff-Parkinson-White syndrome and a history of spontaneous atrial fibrillation but with no evidence of organic cardiac disease. A single induced premature ventricular depolarization resulted in ventricular tachycardia followed by ventricular fibrillation. Similarly, atrial pacing or premature atrial stimulation resulted in frequent episodes of atrial fibrillation or flutter, The atrial and ventricular effective refractory periods were 180 ms and < 160 ms, respectively, at a driven cycle length of 480 ms. Intravenous administration of procainamide resulted in lengthening of the refractory periods and failure to induce either atriaJ or ventricular arrhythmias with pacing. In most patients with enhanced atrioventricular nodal or accessory atrioventricular nodal bypass, the mechanism of ventricular tachycardia is related to an inordinately rapid ventricular response during supraventricular arrhythmias. In our patient, a unique mechanism was apparent: atrial and ventricular vulnerability to fibrillation was associated with extremely short myocardial effective refractory periods. The relationship of this finding to sudden cardiac death bears further study.     

Rate Stabilization by Right Ventricular Pacing in Patients with Atrial Fibrillation

A recent study of de Jongste has demonstrated the lengthening of short R-R intervals in patients with atrial fibrillation by right ventricular pacing. We have further analyzed the data from this study and specifically looked at the effect of right ventricular pacing on the R-R interval instability and heart rate. At the cost of only a slight increase in mean heart rate, a major reduction of the R-R interval instability can be obtained by right ventricular pacing. Based on these findings, we have developed and evaluated an automatic pacing rate algorithm, which continuously varies the stimulation rate in order to stabilize the otherwise irregular rhythm in patients with atrial fibrillation.     

Entrainment of Ventricular Tachycardia by Sinus Rhythm

Entrainment of ventricular tachycardia (VT) may be manifest as fixed and progressive QRS fusion with ventricular and, rarely, atrial pacing. Only a single example of spontaneous VT entrainment by another rhythm, rapid atrioventricular nodal tachycardia, has been reported. This article describes an example of fixed and progressive QRS fusion between conducted sinus rhythm and VT consistent with entrainment. In contrast to entrainment with pacing, entrainment of VT by sinus rhythm occurred with drug-mediated arrhythmia slowing and demonstrated progressive QRS fusion at a constant cycle length. However, it did not demonstrate unfused but entrained QRS complexes. The resulting short PR interval and wide QRS mimicked a preexcited rhythm.     

Limitations to Activation of the Antitachycardia Burst Pacing Function of the Symbios 7008 Pacemaker in the Universal (DDD) Mode

The Symbios 7008 antitachycardia pacemaker was implanted in five patients for control of supraventricular tachycardia. Shortly after implantation in the first two patients, it was noted that the burst pacing sequence was not automatically activated by tachycardia when the pacemaker was in the DDD mode. Data from these two and the subsequent three patients were evaluated to explain this observation. The problem was primarily related to the operation of the device during the postventricular atrial refractory period. In all patients, the atrial electrogram encroached upon the programmed postventricular atrial refractory period because VA conduction during SVT was less than the lowest programmable interval (155 ms). Atrial events occurring during this interval will not trigger the tachycardia termination sequence. In all five patients, the size of the atrial electrogram decreased substantially (48 +/- 10%; mean +/- SD) during supraventricular tachycardia compared to sinus rhythm. In at least two of the five patients, decreased atrial size during supraventricular tachycardia may also have resulted in intermittent failure of atrial sensing during tachycardia, even at the most sensitive setting (0.6 mV). The latter may remain a problem even if the technical fault in SVT detection in the DDD mode were corrected. Two related problems were noted in the DDD mode: ventricular events during rapid SVT do not reset the low rate interval, resulting in random low rate pacing; and, automatic prolongation of atrial refractory period by two successive ventricular events without an intervening atrial sensed event compounds problems of atrial sensing. All of these problems were easily circumvented in all patients by noninvasive reprogramming to the DVI mode in which supraventricular tachycardia detection is based on ventricular sensing. These findings have implications for the future design of such devices.     

Sustained inhibition of a DDD pacemaker at rates below the programmed lower rate during automatic PVARP extension

A patient with a Pacesetter Paragon III DDD pacemaker exhibited sustained pacemaker inhibition at rates below the programmed lower rate during sinus rhythm with marked first degree AV block. In this device, a pacemaker defined ventricular extrasystole initiates automatic extension of the postventricular atrial refractory period to 480 ms and the atrial escape interval to 830 ms regardless of the programmed lower rate. Sustained pacemaker inhibition at rates below the programmed lower rate occurred because the P wave fell continually in the extended postventricular atrial refractory period, and the conducted QRS complex initiated a pacemaker ventricular extrasystole response with atrial escape interval extension. This process continued as long as the P wave stayed within the extended postventricular atrial refractory period, no ventricular extrasystole disrupted the sequence, and the R-R interval of spontaneous beats was shorter than the extended atrial escape interval. Such a pacemaker response should not be misinterpreted as device malfunction.     

Nonclinical Ventricular Tachycardia in the WolflF-Parkinson-White Syndrome

Between September 1980 and June 1984 we assessed the specificity of induction of ventricular tachycardia (VT) with one or two ventricular extrastimuli in a consecutive series of 148 patients undergoing electrophysiological assessment for the Wolff-Parkinson-White (WPW) syndrome by standard electrophysiological techniques. Fifteen patients (10%) had six or more beats of VT induced by one ventricular extrastimulus after a ventricular drive (9 patients), two ventricular extrastimuli during reciprocating tachycardia (6 patients), and during a single atrial extrastimulus (1 patient). None of the six men and nine women, aged 16-61 years, had apparent heart disease. VT lasted for 20 +/- 14 (mean +/- standard deviation) cycles with a cycle length of 235 ms +/- 27 and was generally polymorphic. One patient had ventricular fibrillation. These patients were compared to 15 age- and sex-matched patients studied in the same time period. There was no difference in anterograde effective refractory period of the accessory pathway (316 +/- 92 vs 319 +/- 68 ms), ventricular effective refractory period (218 +/- 12 vs 227 +/- 23), shortest pacing cycle length maintaining 1:1 anterograde conduction over the accessory pathway (306 +/- 132 vs 320 +/- 67) or minimum R-R interval between preexcited beats during atrial fibrillation (280 +/- 68 vs 294 +/- 105). All patients are alive and well over a follow-up interval of 20 +/- 11 months on no antiarrhythmic therapy (13 patients) or on propranolol (2 patients).(ABSTRACT TRUNCATED AT 250 WORDS)     

Performance of Basic Ventricular Tachycardia Detection Algorithms in Implantable Cardioverter Defibrillators; Implications for Device Programming

Around 20% of patients with third generation implantable cardioverter defibrillators receive inappropriate therapy, usually triggered by atrial fibrillation. This is because the criteria used for ventricular tachycardia detection by current implantable cardioverter defibrillators are based on the analysis of a sequence of RR intervals and may be inappropriately satisfied by supraventricular tachyarrhythmias. Algorithms for ventricular tachycardia detection were challenged against the full RR interval sequences from 482 spontaneous episodes of atrial fibrillation and 260 spontaneous episodes of ventricular tachycardia to determine their ability to discriminate between the arrhythmias. The sensitivities and specificities of the algorithms were calculated over a wide range of programmable parameters. For a given window length and detection interval, the most stringent algorithms, that required all beats to be classified as "fast", were more specific than those allowing a proportion of "normal" intervals, even after adjustment for differing sensitivity. These differences were less marked for faster tachycardias. Specificity increased with the detection window length to a limit of approximately 18 beats. We conclude that ventricular tachycardia is detected with the highest specificity if all beats in an analyzed sequence are required to be "fast" even after lengthening of the tachycardia detection interval to maintain sensitivity. Further improvement in algorithm performance may require the incorporation of criteria such as tachycardia onset and stability.     

A wide, complex look at cardiac dysrhythmias

The diagnosis and treatment of cardiac dysrhythmias answers the following four questions: Is the patient stable? Is the rate fast or slow? Are the ventricular complexes wide or narrow? Is the rhythm regular or irregular? The most common narrow complex regular tachycardias are sinus tachycardia, atrial flutter, atrial tachycardia that blocks, and paroxysmal supraventricular tachycardia. Carotid sinus massage is useful in differentiation. Irregular narrow-complex tachycardias are usually atrial fibrillation. An ultra-rapid wide-complex or polymorphous irregular tachycardia is likely to be atrial fibrillation with ventricular preexcitation.

Wide-complex regular tachycardias present a special challenge, since wide beats may result from supraventricular or ventricular impulse formation. Ventricular tachycardia is more likely than supraventricular tachycardia in the presence of underlying ischemic heart disease, atrioventricular dissociation, fusion or capture beats, or a very broad (greater than .14 seconds) QRS complex. Still, misdiagnosis is common; the most costly mistake is over-diagnosis of SVT.

In emergencies, where vital organ hypoperfusion is present, the origin of the impulse and the name of the dysrhythmia are unimportant. With the exception of sinus tachycardia, all life-threatening, rapid tachycardias should be terminated by electrical cardioversion.     

Dual Atrio-ventricular Nodal Pathways and Atrial Fibrillation

The determinants of the ventricular rate during atrial fibrillation were studied in a group of eleven patients demonstrating dual A-V nodal pathways during atrial stimulation. The shortest R-R interval and the mean ventricular cycle length during at least 1 min of pacing-induced atrial fibrillation were compared: a) to the effective and functional refractory period of the fast pathway; b) to the effective refractory period of the slow pathway determined during atrial stimulation, at two or more different basic cycle lengths of pacing; and c) to the shortest cycle length during atrial stimulation followed by 1:1 A-V conduction. A group of 8 patients not demonstrating dual A-V nodal pathway-curves during atrial stimulation was used as a control. In both groups the shortest R-R interval during atrial fibrillation was best predicted by the shortest cycle length followed by 1:1 A-V conduction during atrial stimulation. The mean ventricular cycle length during atrial fibrillation was not accurately predicted by any of the variables studied. The similar results in patients with and without dual A-V nodal pathways suggest that concealed conduction from one to another A-V nodal pathway does not play a role in determining the ventricular response during atrial fibrillation in patients with dual A-V nodal pathways.     

Unusual Electrocardiographic Findings Associated with Type A Wolff-Parkinson-White Syndrome

A 50-year-old woman with Wolff-Parkinson-White (WPW) syndrome presented with unusual electrocardiographic (ECG) findings following the termination of paroxysmal supraventricular tachycardia. The ECG showed three different QRS complexes and irregular R-R intervals. These QRS complexes consisted of: (1) narrow QRS; (2) wide QRS with delta wave; and (3) wide QRS with left bundle branch block (LBBB). The mechanisms of these findings, revealed by electrophysiological study, were: (1) intermittent anterograde left-sided accessory pathway conduction; (2) rate-dependent ipsilateral LBBB; and (3) intermittent retrogradely conducted atrial echoes that occurred due to intraventricular conduction delay resulting from LBBR. Cases of WPW syndrome with these unusual ECG findings, which were clearly interpreted by electrophysiological study, are rare.     

Wide QRS Tachycardia Due to AV Nodal Reentry and a "Bystander" Bypass Tract with Slow Conduction Properties

An unusual mechanism for recurrent, wide QRS complex supraventricular tachycardia is described in this report. A 25-year-old man with normal PR and QRS intervals during sinus rhythm was shown to have preexcitation with a left bundle branch block pattern during tachycardia and during atrial pacing. Electrophysiologic studies demonstrated slow and decremental conduction properties in an accessory "bystander" AV pathway utilized for antegrade conduction during AV nodal reciprocating tachycardia. The differential diagnosis of this tachycardia is discussed in detail.     

Permanent Rapid Atrial Pacing to Control Supraventricular Tachycardia

A case is reported of a patient who had continuous supraventricular tachycardia with a ventricular rate of about 170. The arrhythmia was refractory to drugs and DC countershock, and did not convert with atrial pacing. Rapid atrial stimulation controlled the ventricular rate by simulating atrial fibrillation (pacing at 300-400/min), or by simulating a faster atrial tachycardia with 2:1 conduction (pacing at 205-210/min). This form of therapy was used on a permanent basis for more than five months.     

Holter Documented Sudden Death in a Patient with an Implanted Defibrillator

A 68-year-old man with recurrent attacks of monomorphic ventricular tachycardia (VT) received a pacer cardioverter defibrillator featuring antitachycardia pacing and cardioversion/defibrillation. Over 300 episodes of VT were successfully terminated by antitachycardia pacing. During Holter monitoring the patient experienced supraventricular tachycardia with delivery of multiple antitachycardia pacing, cardioversion, and defibrillation therapies ending with the death of the patient. The following factors played a role in the unfortunate outcome of this patient: 1. triggering of VT therapy by an unexpected high sinus rate; 2. atrial fibrillation induced by cardioversion therapy; 3. a gradual and continuous increase in rate during atrial fibrillation possibly caused by repeated VT and ventricular fibrillation therapies and/or by a thrombus, found at autopsy, in a bypass graft; and 4. the limited ability of presently available defibrillators to distinguish between ventricular and supraventricular arrhythmias.     

Safety of Transvenous Low Energy Cardioversion of Atrial Fibrillation in Patients with a History of Ventricular Tachycardia: Effects of Rate and Repolarization Time on Proarrhythmic Risk

The objective of this study was to assess the safety and efficacy of transvenous low energy cardioversion of atrial fibrillation in patients with ventricular tachycardia and atrial fibrillation and to study the mechanisms ofproarrhythmia. Previous studies have demonstrated that Cardioversion of atrial fibrillation using low energy, R wave synchronized, direct current shocks applied between catheters in the coronary sinus and right atrium is feasible. However, few data are available regarding the risk of ventricular proarrhythmia posed by internal atrial defibrillation shocks among patients with ventricular arrhythmias or structural heart disease. Atrial defibrillation was performed on 32 patients with monomorphic ventricular tachycardia and left ventricular dysfunction. Shocks were administered during atrial fibrillation (baseline shocks), isoproterenol infusion, ventricular pacing, ventricular tachycardia, and atrial pacing. Baseline shocks were also administered to 29 patients with a history of atrial fibrillation but no ventricular arrhythmias. A total of 932 baseline shocks were administered. No ventricular proarrhythmia was observed after well-synchronized baseline shocks, although rare inductions of ventricular fibrillation occurred after inappropriate T wave sensing. Shocks administered during wide-complex rhythms (ventricularpacing or ventricular tachycardia) frequently induced ventricular arrhythmias, but shocks administered during atrial pacing at identical ventricular rates did not cause proarrhythmia. The risk of ventricular proarrhythmia after well-synchronized atrial defibrillation shocks administered during narrow-complex rhythms is low, even in patients with a history of ventricular tachycardia. The mechanism of proarrhythmia during wide-complex rhythms appears not to be related to ventricular rate per se, but rather to the temporal relationship between shock delivery and the repolarization time of the previous QRS complex.     

Use of the Esophageal Lead in the Diagnosis of Mechanisms of Reciprocating Supraventricular Tachycardia

Recent studies have emphasized the role of concealed accessory pathways in reciprocating supraventricular tachycardia. Diagnosis has generally required multicatheter electrophysiologic study. We recorded esophageal electrograms during study in 16 patients with reciprocating tachycardia due to reentry using an accessory atrioventricular pathway, and in 12 patients with reciprocating tachycardia due to reentry in the AV node. The interval from onset of ventricular depolarization to earliest atrial activation (V-AMIN), earliest atrial activity on the esophageal lead (V-AESO), and high right atrium (V-HRA) was measured. No patient with RT due to an accessory atrioventricular pathway had a V-AMIN or V-AESO less than 70 ms, or a V-HRA less than 95 ms. In contrast, 11 of 12 patients with reentry in the AV node had V-AESO intervals less than 70 ms. Esophageal recording during reciprocating tachycardia provides a simple screening procedure available to all practicing physicians to exclude the diagnosis of accessory atrioventricular pathways in the genesis of paroxysmal supraventricular tachycardia.