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.     

Optimization of Pacing Algorithms to Prevent and Treat Supraventricular Tachyarrhythmias

Preventive atrial pacing and antitachycardia pacing have been proposed for the treatment of atrial fibrillation and associated arrhythmias in patients with indications for device implantation. Preventive algorithms provide overdrive atrial pacing, reduction of atrial premature beats, and prevent short-long atrial cycles with good patient tolerance. However, clinical trials testing preventive algorithms have shown contradictory results, possibly because of different trial designs, end points and patient populations. Factors probably responsible for neutral results include an already high atrial pacing percentage with the conventional DDDR mode, suboptimal atrial pacing site, and the deleterious effects of high percentages of right ventricular apical pacing. Atrial antitachycardia pacing therapies are effective in treating organized atrial tachyarrhythmias (that precede atrial fibrillation), mainly when delivered early after the onset particularly if the tachycardia is relatively slow. Antitachycardia pacing therapies might influence atrial fibrillation burden, but clinical studies have shown conflicting results about this issue. Consistent monitoring of atrial and ventricular rhythm including progression to persistent forms of atrial arrhythmias, variability of atrial arrhythmia recurrence patterns and onset mechanisms as well as antitachycardia pacing efficacy should be recorded in the stored device memory and used for optimal individual programming of these new functions.     

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.     

The Induction of Atrial Flutter and Fibrillation and the Termination of Atrial Flutter by Esophageal Pacing

In patients with Wolff-Parkinson-White syndrome (WPW), it is important to assess the ventricular response during atrial flutter or fibrillation since conduction across the accessory pathway during these atrial rhythms may cause hemodynamic impairment or life-threatening ventricular arrhythmias. We have recently reported the effective use of an esophageal electrode in pacing the atrium. In this study we praspectively assessed the ability to induce atrial flutter and fibrillation by esophageal pacing in 23 patients with WPW or other electrophysiological abnormalities. An esophageal bipolar electrode with 29 mm interelectrode distance was positioned in the esophagus to record the most rapid and largest esophageal electrogram (mean distance of 36.6 ± 2.9 cm (SD) from the nares). Pacing was performed at cycle lengths of 40–340 ms (mean 166 ± 72), pulse durations of 7.0–9.9 ms, and currents of 10–25 mA. Atrial flutter alone was induced in 6 patients, fibrillation alone in 11 patients, and both arrhythmias in 5 patients, In one patient neither flutter nor fibrillation was induced by esophugeal pacing, and fibrillation was induced only with difficulty using intracavitary pacing. Of the 11 patients with flutter, the arrhythmia was terminated in 8 by esophageal pacing at cycle lengths of 160–220 ms fmean 176 ± 18 ms). All patients tolerated the procedure well with only mild to moderate discomfort. Therefore, esophageal pacing appears to offer an effective, well tolerated method of initiating atrial fibrillation and flutter and terminating atrial flutter and offers a potentially useful noninvasive method of following patients serially.     

Double Atrial and Double Ventricular Responses During Slow-Fast Fast-Slow Atrioventricular Nodal Reentrant Tachycardia

A case was described with fast-slow form of atrioventricular nodal reentrant tachycardia as related with simultaneous fast and slow pathway conduction both antegrade and retrograde. Fast-slow form of tachycardia was induced by premature right atrial stimulation or incremental right ventricular pacing when the last paced beat conducted to the atria via both fast and slow pathways of the atrioventricular node causing double atrial response. Fast-slow form of tachycardia was spontaneously shifted to slow-fast form when the atrial echo, possibly through the retrograde intermediate pathway, was conducted antegradely over the fast and slow pathways simultaneously, producing double ventricular response.     

Dose-ranging studies of clofilium, an antiarrhythmic quaternary ammonium

Clofilium, a new quaternary ammonium antiarrhythmic without apparent ganglion-blocking effect, was evaluated in 25 patients, 22 with a history of ventricular arrhythmias and three with paroxysmal supraventricular arrhythmias. The study, including programmed atrial and ventricular stimulation, was carried out before and after infusion of 20 to 240 micrograms/kg IV as a single dose. Continuous Holter monitoring was carried out the day before the study through the fourth day after study, and laboratory parameters were monitored for up to 2 wk. There were no changes in intra-atrial and intraventricular conduction times or in AH or HV intervals. There were increases in QT interval, atrial effective refractory period, and ventricular refractory period. The atrioventricular nodal effective refractory period was unchanged. No side effects were noted, nor were changes in blood pressure or laboratory parameters. Monitoring revealed no change in frequency of premature ventricular complexes between the 24 hr before drug infusion and the 96 hr thereafter. In one patient refractoriness of the His-Purkinje system was increased and in two patients atrial fibrillation converted to sinus rhythm after clofilium. Three patients had sustained ventricular tachycardia with programmed stimulation before clofilium infusion; none had more than three repetitive ventricular responses after it. Clofilium increases atrial and ventricular effective refractory period without changing conduction time and, despite no apparent change in premature ventricular complex frequency, it can abolish the ability to induce ventricular tachycardia by programmed stimulation and is also well tolerated.     

Wavelength and Atrial Vulnerability: an Endocavitary Approach in Humans

If atrial vulnerability parameters are well defined, wavelength (WL) measurement (conduction velocity x refractory period), has never been assessed through an endocavitary electrophysiological exam.
We investigated 30 patients (14 female, mean age 63.4 ± 13 y.o.), 10 with paroxysmal atrial fibrillation (PAF group), 10 with ischemic cerebral injury (ICI group) by comparison with 10 controls (C group).
The upper to lower right atrium conduction time and velocity were measured in the right atrium with a decapolar electrode catheter applied along the free wall. Others parameters correlated to atrial excitability were also taken into account: effective (ERP) and functional refractory periods (FRP); spontaneous or paced atrial electrogram (AI) or extrastimulated atrial electrogram (A2) widths, ERP/ A2 ratio, provocative atrial testing. Measurements were taken in sinus rhythm and in 600 – 460 ms paced cycle lengths. If ERP, FRP, Al widths are the same in the 3 groups, PAF and ICI groups have a significant increased conduction time and lower conduction velocity, leading to a shorter A1 WL during 600 and 460 ms paced rhythms (p 0.05) and A 2 WL during 460 ms paced rhythm. The provocative testing was positive in 60% of PAF and ICI groups, and there is a significant correlation between arrhythmia induction and 600 ms A1 WL or 460 ms A2 WL.
This electrophysiological study suggests the possibility of an approach in humans of wavelength concept and proves the presence of correlation between a short wavelength and atrial spontaneous or induced arrhythmias. A no-arrhythmia band (A1 WL > 17 cm during 600 ms paced rhythm, Al WL > 16 cm or A2 WL > 12cm during 460 ms paced rhythm) and a fibrillation-band (A1 WL < 12 cm during 600 and 460 ms pacing, A 2 WL < 7 cm during 460 ms pacing) can be defined. Therefore, the ICI group has the same atrial pattern as the AF group.     

Safety of High Energy Internal Cardioversion for Atrial Fibrillation

High energy internal cardioversion has been proposed as an alternative method to cardiovert drug refractory or external cardioversion refractory atrial fibrillation. However, the safety of this technique has not been clearly evaluated. We reviewed findings in 53 patients who underwent 55 sessions of high energy internal cardioversion (2 patients underwent 2 sessions] for termination of longstanding atrial fibrillation. Shocks energy varied from 70–270 J. Three patients had 3 shocks during the same session, 5 had 2, and 47 only 1. Success rate was 89% (success was defined as immediate conversion to normal sinus rhythm).
Low cardiac output occurred in two patients, and resulted in the death of one of these individuals, a patient with significant hypertrophic cardiomyopathy and heart failure. The other patient recovered completely. In 11% of the cases, shock induced transient atrioventricular block, necessitating ventricular pacing until sinus rhythm was restored. In three patients, a moderate but asymptomatic and uncomplicated pericardial effusion was diagnosed on echocardiogram. Finally, four patients had side effects related to venous puncture, which resolved spontaneously. These results suggest that high energy internal cardioversion is effective for conversion of atrial fibrillation. However, the technique may not be optimal in patients with advanced hypertrophic cardiomyopathy and in such cases the technique should be used carefully and only in the case of failure of external cardioversion; no more than two shocks should be delivered during the same procedure. Temporary ventricular pacing should be provided in all patients and an echocardiogram should be performed before patients are being discharged.     

Coincident Idiopathic Left Ventricular Tachycardia and Atrioventricular Nodal Reentrant Tachycardia: Control by Radiofrequency Catheter Ablation of the Slow Atrioventricular Nodal Pathway

A healthy 37-year-old male presented with a history of frequent palpitations and sustained wide QRS complex tachycardia with a right bundle branch block and left axis morphology. Serial electrophysiological studies revealed two inducible tachycardias, which were shown to represent atrioventricular nodal reentrant tachycardia and idiopathic left ventricular tachycardia. Transformation from one tachycardia to the other occurred spontaneously as well as following atrial or ventricular pacing. Radiofrequency catheter ablation of the slow atrioventricular nodal pathway resulted in cure of atrioventricular nodal reentrant tachycardia and the prevention of spontaneous recurrence of ventricular tachycardia, suggesting a role of atrioventricular nodal reentrant tachycardia in triggering the clinical episodes of ventricular tachycardia. The patient has remained asymptomatic without antiarrhythmic therapy for 8 months.     

Cardiac surgery for arrhythmias

Cardiac arrhythmia surgery was initiated in 1968 with the first successful division of an accessory AV connection for the Wolff-Parkinson-White Syndrome. Subsequent surgical procedures included the left atrial isolation procedure and the right atrial isolation procedure for automatic atrial tachycardias, discrete cryosurgery of the AV node for AV nodal reentry tachycardia, the atrial transection procedure, corridor procedure and Maze procedure for atrial fibrillation, the right ventricular disconnection procedure for arrhythmogenic right ventricular tachycardia, the encircling endocardial ventriculotomy, subendocardial resection procedure, endocardial cryoablation, the Jatene procedure, and the Dor procedure for ischemic ventricular tachycardia. Because of monumental strides in the treatment of most refractory arrhythmias by endocardial catheter techniques during the past decade, the only remaining viable surgical procedures for cardiac arrhythmias are the Maze procedure for atrial fibrillation and the Dor procedure for ischemic ventricular tachycardia. Nevertheless, the 25-30 years of intense activity in the field of cardiac arrhythmia surgery provided the essential foundation for the development of these catheter techniques and represent one of the most exciting and productive eras in the history of medicine. In one short professional career, we have witnessed the birth of arrhythmia surgery, its adolescence as an "esoteric" specialty, its prime as an enlightening yet exhausting period, and finally its waning years as a source of knowledge and wisdom on which better methods of treatment have been founded. One could hardly ask for a more rewarding experience.     

Modification of the DDD Pacing Mode to Prevent Junctional Reentry Tachycardia: Computer Modelling Experiments

This paper examines the possibility of using short atrioventricular (AV) delay dual chamber pacing to prevent junctional reentry tachycardia mediated by an accessory pathway or by an intra-AV nodal circuit. For this purpose, a clinically realistic computer simulation model of cardiac rhythm and heart-pacemaker interactions has been used. The computational experiments compared the actions of two pacemaker models: (A) a clinically realistic DDD mode operating with quasi-Wenckebach prolongation of the AV delay; and (B) a new modification of the DDD mode introducing independent counters for the atrial and ventricular refractory periods of the heart, and the possibility of instantaneous or shortly delayed atrial pacing triggered by a sensed or paced ventricular event. The pathological phenomena modelled in the experiments simulate different possibilities of tachycardia initiation. These disorders include: (1) single atrial premature beats (APBs), (2) salvos of APBs, (3) closely coupled pairs of APBs, (4) ventricular premature beats initiating an antidromic reentry tachycardia, and (5) ventricular ectopic beats initiating an AV nodal reentry tachycardia. The computational results prove that many possible mechanisms of initiation of junctional reentry tachycardia are beyond the prophylactic capabilities of current sophisticated DDD pacemakers (A). The results also show that the suggested pacing mode (B) improves anti-tachycardia prophylaxis even when responding to complex pathological episodes of the natural cardiac activity. Future development of the suggested mode (B) is discussed.     

Treatment of Ventricular and Supraventricular Tachyarrhythmias by Transcutaneous Cardiac Pacing

The efficacy of noninvasive transcutaneous cardiac pacing (TCP) in the treatment of tachyarrhythmic events was tested in 24 patient: 14 with ventricular tachycardia, seven with supraventricular tachycardia and three with atrial flutter. Six (42.9%) ventricular tachycardias were interrupted: in two of the ten patients on whom underdrive pacing was attempted and in all four cases in which overdrive stimulation was possible. Five of the six supraventricular tachycardias utilizing an atrioventricular bypass tract were interrupted, while the TCP was unsuccessful on the only patient with atrioventricular nodal reentrant tachycardia. TCP failed to interrupt the arrhythmia in the three cases of atrial flutter. No clinically significant untoward effects (in particular tachycardia acceleration or ventricular fibrillation) were observed, except for a tolerable thumping sensation on the chest during pacing. In four patients, TCP effects on cardiac activation was evaluated by endocavitary recording: while the mean ventricular threshold was 70 mA, atrial capture was possible on only two patients at a current intensity of 140 and 150 mA. We consider our preliminary experience with TCP in the treatment of tachycardias encouraging. The technique was easily and rapidly usable and it was immediately successful in the majority of atrioventricular reentrant tachycardias and in a relevant percentage of ventricular tachycardias. In this latter setting TCP was mostly effective in the slower tachycardias where overdrive pacing was possible. A further experience with devices provided by higher pacing rates is warranted.     

Clinical Experience with a New Software-Based Antitachycardia Pacemaker for Recurrent Supraventricular and Ventricular Tachycardias

The Intermedics Intertach 262-12 tachycardia reversion pulse generator was implanted in 14 patients (six male, eight female, mean age at implantation 45 +/- 16 years) with recurrent symptomatic tachycardias. Six patients had atrioventricular (AV) nodal reentrant tachycardia, three patients had orthodromic tachycardia with Wolff-Parkinson-White syndrome, two had circus movement tachycardia via a concealed bypass tract, two had ventricular tachycardia, one patient had atrial flutter. Mean duration of symptoms before implantation was 8 +/- 4 years and mean number of antiarrhythmic drug trials was 3.5 +/- 1. The primary tachycardia response made consisted of autodecremental pacing in one patient, burst pacing in two patients, and adaptive scanning of the initial delay or burst cycle length in eleven patients. The secondary tachycardia response mode consisted of autodecremental pacing in four patients, burst pacing in three patients and burst scanning in four patients. Tachycardia response was automatic in all but one patient with ventricular tachycardia. During a follow-up period of 30.5 +/- 10.6 months, one patient with ventricular tachycardia died from a nonarrhythmic cause. Reinterventions were necessary due to electrode fracture in one patient and due to pacemaker software defect in another one. Two patients underwent surgical cure of their arrhythmia: one patient with atrial flutter and one patient with AV nodal reentry tachycardia, 24 months and 11 months postpacemaker implantation, respectively. Four patients required digitalis to prevent pacing induced atrial fibrillation. Other proarrhythmic effects were not encountered. The pacemaker proved to be a versatile system with reliable tachycardia detection and termination functions. It provided a valuable adjunctive therapy in these selected patients.     

Organized incessant atrial arrhythmias in the setting of severe, isolated biatrial scarring

Introduction: Diffuse transmural fibrosis and scarring limited to the area without atrial dilation or significant structural heart or other systemic disease has not been reported. We present three cases of a syndrome characterized by refractory organized atrial arrhythmias, diffuse atrial scarring with electrical silence, and mechanical paralysis in the absence of atrial dilation or any systemic or neurodegenerative disorders.
Methods: Patients referred for electrophysiology study of atrial arrhythmias were included. Electroanatomic mapping with the Carto system (Biosense Webster, Diamond Bar, CA, USA) and magnetic resonance imaging ( MRI) with scar sequencing were performed.
Results: There was no family or personal history of cardiac, muscular, or developmental diseases. All patients had organized atrial arrhythmias. Echocardiograms showed atrial standstill with normal atrial and ventricular dimensions. No other structural abnormalities were noted. Carto mapping revealed severe biatrial diffuse scarring. The left atrial (LA) was less affected than the right atrial (RA). MRI findings confirmed biatrial scarring. During tachycardia, islands of dissociated electrical activity could be seen in the right atria. Entrainment mapping was not performed in the atria as high-output pacing could not capture the atria. Coronary sinus entrainment demonstrated the coronary sinus (CS) not to be critical to the tachycardia. Ablation was targeted toward channels of low voltage but was not successful in any cases. All required atrioventricular (AV) nodal ablation with pacing.
Conclusion: An association between biatrial cardiomyopathy and scarring with normal atrial dimensions has been described. Since severe scarring has not been reported with organized arrhythmias this may represent a new syndrome.     

Differentiation of Arrhythmias in the Dog by Measurement of Activation Sequence Using an Atrial and Two Ventricular Electrodes

Timing of atrioventricular activation and ventricular dispersion identifies and discriminates between beats of different origin. In eight dogs, three bipolar epicardial electrodes recorded left atrial and left and right ventricular depolarizations simultaneously during arrhythmias induced by programmed electrical stimulation and coronary artery occlusion and release. The interval between the left atrial and left ventricular intrinsic deflections (V₁-V₂) and between the left ventricular and right ventricular intrinsic deflections (V₁-V₂) of each heat was measured. Recordings were of normal sinus rhythm (NSR) (mean of five beats in 8/8 dogs), atrial flutter (AFL) (five beats of one episode), atrial fibrillation (AF) (144 beats in 29 episodes in 7/8), monomorphic ventricular tachycardia (MVT) (24 beats with six morphologies in 2/8), polymorphic ventricular tachycardia (PVT) (63 beats in 15 episodes in 5/8) and premature ventricular contractions (PVC) (29 beats with 29 morphologies in 5/8). Supraventricular rhythms can be differentiated from ventricular rhythms by V₁-V₂ timing. The mean difference in V₁-V₂ during AFL and AF vs NSR was 1 ms (range of 0–3 ms). The change from sinus during MVT ranged from 38 to 43 ms (m 31 ms) and during PVC 10 to 75 ms (m 38 ms). Thirty-five of 35 of these ectopic ventricular morphologies exhibited 10 ms or more timing difference compared to corresponding beats of NSR. PVT was consistently distinguished from supraventricular rhythms and MVT by the variability of V₁-V₂,A-V₁ intervals can be used to distinguish supraventricular arrhythmias from sinus rhythm; a 32 ms difference existed for AFL. AF could be detected by the variability in AV₁. One atrial and two ventricular leads can provide a means of differentiating normal sinus rhythm from supraventricular and ventricular arrhythmias that may be applicable to implantable antitachycardia devices.     

Proarrhythmic Effects of Reactive Hypoglycemia

A patient with refractory atrioventric-ular nodal reentry tachycardia is reported in whom it was possible to document that reactive hypoglyce-mia was the trigger for aggravation of arrhythmia. Over a period of 6 years, a series of electrophysiological studies revealed that, when the patient was in a hypoglycemic state, initiation of tachycardia was easy and most importantly that tachycardia termination by extra-stimulus pacing always failed. Furthermore, atrial fibrillation was inducible or spontaneously occurred only when the blood glucose level was reduced by IV insulin administration.     

Noise Reversion of a Dual Chamber Pacemaker without Noise

Three patients are reported whose DDD pacemakers reverted to the asynchronous mode in the absence of skeletal muscle or electromagnetic (EMI) interference. In all three cases, the basic cardiac rhythm was atrial fibrillation with fast ventricular response due to intrinsic AV conduction. Noise reversion was triggered by the patients' own ventricular activity at cycle lengths shorter than the ventricular refractory period of the pulse generator. In one patient, asynchronous AV sequential pacing during atrial fibrillation was noted shortly after resuscitation from ventricular fibrillation; however, the initiation of the malignant ventricular arrhythmia by the pacemaker remains unproven. The mechanism of noise reversion by rapid cardiac activity and possible solutions to the problem by adequate pacemaker design are discussed.     

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.     

Tachycardia Recognition and Diagnosis from Changes in Right Atrial Pressure Waveform—A Feasibility Study

Implantable defibrillators either monitor heart rate or use a probability density function to detect ventricular fibrillation/tachycardia. As a result, they are unable to discriminate sinus tachycardia and atrial arrhythmias from malignant ventricular rhythms. We have assessed high fidelity fiber-optic pressure recordings in the right atrium during cardiac arrhythmias in 23 patients (mean age 44 years, 11 females) undergoing electrophysiological study. The unfiltered pressure signal was amplified and recorded on paper. During sinus rhythm, a constant amplitude deflection occurred during atrial systole (a wave). A characteristic waveform pattern was observed during each of the studied tachyarrhythmias, which included atrial flutter and fibrillation, atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, and ventricular tachycardia with and without ventriculoatrial conduction. The waveform pattern allowed clear visual discrimination of the underlying arrhythmia. Mean atrial pressure was increased during all arrhythmias and did not allow discrimination of the nature of the tachycardia. High fidelity pressure recordings produced characteristic appearances for pattern recognition of each arrhythmia studied. They allowed determination of the temporal relation between electrical and mechanical cardiac events and may have potential in the detection and recognition of cardiac arrhythmias.     

Rapid pacing results in changes in atrial but not in ventricular refractoriness

It is well known that atrial tachycardia causes atrial electrical remodeling, characterized by shortening of atrial effective refractory periods (AERPs) and loss of physiological adaptation of AERP to rate. However, the nature and time course of changes in ventricular effective refractory periods (VERP) caused by rapid rates are to be established. After being instrumented with epicardial electrodes on both atria and both ventricles nine goats were subjected to 1 week of rapid AV pacing with a rate of 240 beats/min and an AV delay of 100 ms. Pacing was only interrupted for measurement of left and right AERPs and VERPs at three basic cycle lengths (BCL) of 400 ms, 300 ms, and 200 ms during sinus rhythm in the conscious animal. Left and right AERPs decreased at all BCLs, reaching minimum values after 3 days (right AERP at BCL of 400 ms, 96 +/- 16 ms after 3 days vs 144 +/- 16 ms at baseline, P < 0.05). In contrast, both left and right VERPs did not change at any BCL. This study demonstrates a difference between the atria and ventricles with respect to tachycardia induced changes in refractoriness.