Effects of Procainamide on Refractoriness, Conduction, and Excitable Gap in Canine Atrial Reentrant Tachycardia

The effects of procainamide were studied in a model of atrial flutter around the tricuspid valve in seven open chest, chloralose-anesthetized dogs (31 ± 3 kg). A Y-shaped incision in the intercaval area extending to the right atrial appendage was made and five bipolar electrodes were sutured on the atrial epicardium around the tricuspid valve. Reentry tachycardia was induced in the absence and presence of drug by burst pacing. Procainamide (5 mg/kg bolus followed by 0.075 mg/kg/min infusion) produced stable plasma levels (38 ± 9μ) during the study. At a pacing cycle length of 200 msec, mean (± SD) diastolic threshold at the five sites increased from 1.6 ± 1,5 to 2,0 ± 1.7 mA and mean atrial effective refractory period from 128 ± 9 to 140 ± 16 msec on drug (P < 0.05). Procainamide prolonged the cycle length of atrial flutter from 144 ± 10 to 160 ± 13 msec and slowed conduction velocity during atrial flutter around the tricuspid valve from 73 ± 6 to 66 ± 6 cm/sec (P < 0.05). A reset response curve was determined by introducing premature stimuli during atrial flutter. Procainamide prolonged effective refractory period during atrial flutter from 101 ± 13 to 116 ± 17 msec but did not change the duration of the excitable gap (38 ± 9 vs 40 ± 18 msec). Although the reset response curve was predominantly increasing, in six of seven experiments there was present a flat portion at long coupling intervals approaching the atrial flutter cycle length that comprised 23%± 10% of the excitable gap. Procainamide shifted the reset response curve upward and to the right but did not change its slope or the duration of the flat portion. Thus, in the majority of experiments the reset response curve in atrial flutter about the tricuspid valve in vivo suggests that procainamide prolongs atrial flutter cycle length directly by slowing conduction through fully excitable tissue rather than indirectly by increasing refractoriness at the head of the wave front.     

Emergency Department Use of Intravenous Procainamide for Patients with Acute Atrial Fibrillation or Flutter

Objectives Acute atrial fibrillation and flutter are very common arrhythmias seen in emergency department (ED) patients, but there is no consensus for their optimal management. The objective of this study was to examine the efficacy and safety of intravenous (IV) procainamide for acute atrial fibrillation or flutter.
Methods This health records review included a consecutive cohort of ED patients with acute-onset atrial fibrillation or atrial flutter who received IV procainamide at one university hospital ED during a five-year period. The standard clinical protocol involved IV infusion of 1 g of procainamide over 60 minutes, followed by electrical cardioversion if necessary. A trained observer extracted data from the original clinical records. Outcome measurements included conversion to sinus rhythm, adverse events, and relapse up to seven days.
Results The 341 study patients had a mean age of 63.9 years (SD ± 15.5 years), and 56.6% were male. The conversion rates were 52.2% (95% confidence interval = 47% to 58%) for 316 atrial fibrillation cases and 28.0% (95% confidence interval = 13% to 46%) for 25 atrial flutter cases. Mean dose given was 860.7 mg (SD ± 231.2 mg), and median time to conversion was 55 minutes. Adverse events occurred in 34 cases (10.0%): hypotension, 8.5%; bradycardia, 0.6%; atrioventricular block, 0.6%; and ventricular tachycardia, 0.3%. There were no cases of torsades de pointes, cerebrovascular accident, or death. Most patients (94.4%) were discharged home, but 2.9% of patients returned with a recurrence of atrial fibrillation within seven days.
Conclusions This study of acute atrial fibrillation or flutter patients treated in the ED with IV procainamide suggests that this treatment is safe and effective in this setting. Procainamide should be prospectively compared with other ED strategies.     

The Upper Link of Human Common Atrial Flutter Circuit Definition by Multiple Endocardial Recordings during Entrainment

Common atrial flutter is due to a macroreentry circuit in the right atrium, but the cranial path of the circuit has not been defined. The objectives of this article are to determine the cranial turning point of flutter activation in relation to a hypothetic obstacle, the superior vena cava opening, by examining the changes in activation sequence produced by entrainment from different points. In 13 cases of common atrial flutter with typical counter-clockwise right atrial circuits confirmed by endocardial mapping the atrium was paced from the high posterior and mid-septal walls. Entrainment was confirmed by simultaneous recordings of 6–7 right atrial electrograms. Changes in sequence of electrograms from high septum and high anterolateral walls was sought. Electrogram sequence and morphology did not change with entrainment at the posterior wall with respect to the basal flutter or mid-septal wall entrainment. Pacing "below" the superior vena cava did not advance the anterior wall electrogram in relation to the septal electrogram. These findings suppport the concept that common Putter activation turned around (cranial and anterior to) the superior vena cava opening, and not around the free end of a line of block below the superior vena cava in the posterior wall. Common atrial flutter activation rotates cranial (and anterior) to the superior vena cava opening, through the "right atrial roof" The line of functional block should span from inferior to superior vena cava openings.     

Relation Between Left Atrial Size and Secondary Atrial Arrhythmias After Successful Catheter Ablation of Common Atrial Flutter

Catheter ablation ptovides an effective cure for patients with typical atrial flutter. However, these patients may have the potential to develop atrial tachyarrhythmias other than common atrial flutter. This study examines clinical and echocardiographic predictors for the occurrence of uncommon atrial flutter or atrial fibrillation after abolition of common atrial flutter. The study population comprised 17 patients (12 men, 5 women, age 32–74 years) who underwent successful radiofrequency catheter ablation of common atrial flutter. Common atrial flutter did not recur in any patient during a median follow-up time of 8 (range 1–25) months. Within a median of 7 (range 1–223) days, however, symptomatic atrial tachyarrhythmias occurred in 8 of 17 patients (47%): uncommon atrial flutter (n = 4); atrial fibrillation (n = 3); and both uncommon atrial flutter and atrial fibrillation in one patient. Preablation left atrial volume was significantly larger in patients who developed secondary arrhythmias compared with patients who remained in sinus rhythm (57.9 ± 15.6 vs 43.7 ± 16.4 cm³, P < 0.05). Enlarged left atrial volume dichotomized at 51 cm³ independently predicted postablation atrial arrhythmias (x²=5.11, rel. risk = 5.3, P < 0.05). On Kaplan-Meier analysis, time to occurrence of postablation atrial arrhythmias was significantly shorter in patietits with enlarged left atrium (P < 0.02). In conclusion, symptomatic uncommon atrial flutter and atrial fibrillation develops in a substantial proportion of patients after successful ablation of common atrial flutter. Out of a series of clinical and echocardiographic parameters, preablation left atrial size is the best predictor for the occurrence of these postablation atrial arrhythmias.     

Atrial Flutter: Lessons from Surgical Interventions (Musing on Atrial Flutter Mechanism)

We report our experience with seven patients who underwent direct surgical ablation of problematic common flutter. Intraoperative mapping was obtained in four patients. Surgical techniques varied over time. A circular incision of the right atrium was performed in the first patient. Two patients had epicardial cryoablation of the isthmus between the inferior vena cava and the tricuspid valve annulus. Four patients had extensive endocardial cryoablation of the isthmus. There were no immediate postoperative complications. One patient had atrial fibrillation 2 months postoperatively and underwent a corridor operation 1 year later. The other six patients are free of arrhythmias without antiarrhythmic drugs. Surgical ablation confirmed that the common form of atrial flutter is associated with a right atrial macroreentrant circuit. One of our intraoperative endocardial maps suggested that variant reentrant circuits can be associated with variant forms of flutter.     

Shift of Atrial Reentrant Tachycardia with Transient Entrainment to an Uncommon and a Common Type of Atrial Flutter

Atrial reentrant tachycardia (ART) which demonstrated transient entrainment shifted to an uncommon type of atrial flutter (AF) with premature atrial stimulation, and then returned to ART spontaneously, Subsequently, this ART shifted to a common type of AF by rapid atrial pacing, which was further transformed into an uncommon type of AF and finally terminated by rapid atrial pacing. The mechanism of AF in clinical cases is still controversial, but in this case, AF, both uncommon and common types, is considered due to macro-reentry within the atria. To explain (he shift of ART to AF and mutual transformation between common and uncommon type of AF, we made a schematic figure of reentry loop within (he atria of ART and AF.     

Persistent Atrial Fibrillation Converts to Common Type Atrial Flutter during CFAE Ablation

Background: Catheter ablation of persistent and long‐standing persistent atrial fibrillation (AF) is still challenging. So far different ablation techniques have been reported, including pulmonary vein isolation, additional linear lesions, ablation of complex fractionated atrial electrograms (CFAE), and combinations of these techniques. During ablation of CFAE, the occurrence of left atrial (LA) tachycardia is well known. The occurrence of right atrial flutter on the other hand is less well described. Methods: Here, we report three patients who had been ablated because of symptomatic persistent atrial fibrillation. Summary: In all patients, AF changed into a cavotricuspid isthmus = dependent right atrial flutter during ablation of CFAE in the LA. (PACE 2010; 33:304–308)     

Catheter Ablation of Atrial Flutter Circuits

Atrial flutter (AF) mapping has shown circular activation in the right atrium (RA), wilh a "counterclockwise" rotation in a frontal view. The myocardial isthmus between the inferior vena cava and the tricuspid valve (IVC-T) closes the activation circuit in its caudal end. The reproducibility of this activafion pattern, and the fact that some "rare" AF with a "clockwise" rotation of activation use the same circuit, suggests that reentry is greatly facilitated by the anatomical arrangement of the caudal end of the RA. This suggested that ablation of the IVC-T isthmus may interrupt AF and prevent its recurrence. We have applied radiofrequency (RF) current to the IVC-T isthmus in nine patients, producing sudden interruption of activation at this point in five (all those treated with large surface electrode catheters). in three others, RF produced acceleration or disorganization, leading to interruption. Preliminary follow-up data suggest a favorable effect on AF recurrence, either by preventing it, or by making antiarrhythmic drugs effective.     

Conversion of Atrial Flutter: Rapid Atrial Pacing as a Bedside Technique

Eleven patients with atrial flutter underwent intracardiac right atrial pacing at bedside in an attempt to terminate this dysrhythmia. Nine of the eleven patients were converted to sinus rhythm; the remaining two patients were converted to atrial fibrillation with a slower ventricular rate. There were no complications. The potential hazards of direct current cardioversion (anesthesia, fractures, muscle strain, myocardial injury, etc.) were avoided. In contrast to rapid atrial pacing in the electrophysiology laboratory, the bedside technique did not require a special laboratory setting, electronic or x-ray equipment, or technical personnel. Transportation of critically ill patients was obviated. Atrial flutter can be converted at the bedside to a more favorable rhythm; the expediency, safety, and low cost of this bedside cardioversion technique not only makes it feasible, but also it is often the procedure of choice.     

Atrial and Ventricular Pressures in Atrial Flutter

The hemodynamic effects of atrial flutter (AF) are unknown. The purpose of the present study was to investigate the changes in atrial and ventricular pressures after induction of AF. In 23 patients with paroxysmal AF (age 59 ± 9 years), a hemodynamic study was performed both during sinus rhythm and after induction of the tachyarrhythmia. During AF, 13 patients showed a fixed 2:1 AV conduction and 10 patients showed variable conduction. Mean right and left atrial pressures increased (P < 0.001) and right and left ventricular end-diastolic pressures decreased (P < 0.001) after induction of AF. Roth the increase in mean atrial pressures and the decrease in ventricular end-diastolic pressures were present either in the patients with fixed 2:1 AV (heart rate: 133 ± 15 beats/min) or in those with variable conduction (heart rate 96 ± 15 beats/min), but were more marked in the former. AF produces an impairment of atrial function, as evidenced by the increase in mean atrial pressures and reduction in ventricular end-diastolic pressures in the absence of an elevated heart rate. The mechanisms responsible for the increase in mean atrial pressures are unknown; however, atrial contractions against closed AV valves seem to play an important role.     

Comparison of Right Atrial and Peripheral Procainamide Infusion Levels in Patients with Spontaneous or Induced Atrial Fibrillation

As part of a new effort to develop an implantable drug infusion pacing system to treat atrial fibrillation, this study examined the effects of rapid intracardiac procainamide infusion in humans with pacing-induced atrial fibrillation. Twenty patients with atrial fibrillation for >5 minutes during an EP study received 500mg of procainamide either via a peripheral venotis infusion (n=5) or directly in the right atrium (n=15). Peak coronary simis and femoral vein procainamide blood levels (mean ± SEM) during 10, 5, and 3.3 minute central infusions were 17.0 ± 4.1, 25.1 ± 4.5, 45.6 ± 5.1 and 11.3 ± 3.2, 17.1 ± 6.4, 18.7 ± 5.0, respectively. In contrast, peak coronary sinus and femoral procainamide levels following the 5 minute intravenous infusion were 17.7 ± 5.1 and 9.3 ± 2.1. Changes in QT, QTc, QRS, and RI intervals were similar at each infiision rate. Systolic blood pressures (BP) decreased more with higher procainamide infusion rates but similar when comparing intravenous versus central drug administration at the same rate. The mean ± SEM decreases in blood pressure with the 10, 5, and 3.3 min procainamide infusions were 12f5, 20f11, and 39f14, respectively. Conversion to sinus rhythm was not a primary endpoint given the often transient nature of acute atrial fibrillation in this setting. We conclude that significantly higher femoral vein and coronary sinus procainamide levels can be achieved by central rather than peripheral drug infusion. These data support that concept that rapid central infitsion of anti-arrhythmic therapy can result in high intracardiac levels of antifibrillatory agents for the treatment of paroxysmal atrial fibrillation.     

High Resolution Recordings of Atrial Flutter

We present high resolution tracings of atrial flutter which, to our knowledge, have not been previously described. Two patients have been studied; in both cases atrial activity was made by waves similar to each other, differing only in voltage. We discuss the nature of these waves, which are probably related to continuous atrial activity, with a segregation into small and large waveform activity. It is concluded that high resolution recordings may be valid support for the interpretation of atrial flutter activity.     

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.     

Atrial Flutter Mapping and Ablation II. Radiofrequency Ablation of Atrial Flutter Circuits

The definition of the anatomical substrate of reentry in at rial flutter has allowed the recognition of narrow, critical areas of the circuit, where radiofrequencv ablation can interrupt reentry. In common flutter the isthmus between the inferior vena cava and the tricuspid valve appears the best target, but ablation between the coronary sinus and tricuspid valve can also be effective in some cases. In atypical flutter using the same circuit as common flutter in a “clockwise” direction, ablation of the same isthmus is effective. Flutter interruption is the main objective, but it does not mean complete isthmus ablation. If flutter remains inducible, new applications are delivered in the isthmus, until it is made noninducible. Complications are rare. Despite attaining noninducibility, flutter may recur, and new procedures may he needed to prevent recurrence. Atrial fibrillation can occur in up to 30% of the cases during follow-up, but it is generally well controlled with antiarrhythmic drugs, that were ineffective to treat flutter before ablation. In reentry circuits based on surgical atrial scars, ablation of an isthmus between the scar and the inferior vena cava can also be effective. Left atrial circuits are not known well enough to guide successful ablation.     

Focal Right Atrial Dysplasia and Atrial Flutter in a Patient with Myotonic Dystrophy

Focal dysplasia of the right atrium was identified postmortem in a 22-year-old man with myotonic dystrophy and sudden death. Antemortem cardiac abnormalities included a single syncopal episode associated with atrial flutter with exercise-induced 1:1 atrioventricular conduction, sinus node dysfunction, and mild mitral valve prolapse. Pathologically there was only mild conduction system disease and the ventricular myocardium was normal. Right atrial dysplasia, previously unreported in myotonic dystrophy, appears to have been an arrhythmogenic lesion in this patient, serving as a morphological substrate for reentry.     

Combined Transesophageal Left Atrial Pacing and Antiarrhythmic Therapy in the Treatment of Atrial Flutter

In order to terminate atrial flutter (AF) overdrive transesophageal left atrial pacing (TELAP) was performed in 760 patients with paroxysmal AF. There were 315 women and 415 men (mean age 59 years). In 260 patients, TELAP was used in an outpatient setting. Approximately half of the patients (51 %) had coronary artery disease and/or arterial hypertension, and 23% of the patients had no structural heart disease. The duration of AF ranged between 1 hour and 1 month. TELAP was performed in 312 patients without any antiarrhythmic drug (AAD) administration (group I) and in 448 patients after administration of AAD (procainamide and/or amiodarone) in conventional doses (group II). TELAP resulted in immediate return of sinus rhythm in 85 patients (27%) of group I and in 222 patients (50%) of group II (P < 0.001). TELAP converted AF to atrial fibrillation (AFIB) in 185 of group I and in 214 (48%) of the group II patients (P < 0.01). In addition, within 1–2 days after TELAP AFIB converted to sinus rhythm spontaneously or after AAD in 87 patients of group I (28%) and in 84 (19%)of the group II patients (P < 0.01). In general, sinus rhythm was restored in 172 (55%) of the group I and in 306 (68%) of the group II patients (P < 0.005). AF was converted to AFIB in 98 (31 %) of the group I and in 130 (29%) of the patients in group II patients (NS). TELAP was ineffective in 42 (13.5%) of the group I and in 12 (3%) of the group II patients (P < 0.001). TELAP was an effective noninvasive method for the treatment of recent onset AF. Our experience showed that after TELAP, sinus rhythm was restored in most of the patients with paroxysmal AF within 1–2 days. In some patients TELAP converted AF to AFIB, making it easier to control the heart rate with AAD. Treatment with AAD before TELAP increased its effectiveness.     

Sinus Node Recovery After 25 Years of Atrial Flutter

PALMA, E.C., et al. : Sinus Node Recovery After 25 Years of Atrial Flutter. This case report demonstrates that the sinus node can recover relatively quickly even after being suppressed by atrial flutter for 25 years, and that a permanent pacemaker may not always be necessary in all patients with sinus arrest after a successful atrial flutter ablation.     

Procainamide Induced Change of the Width of the Zone of Entrainment and its Relation to the Inducibility of Reentrant Ventricular Tachycardia

Procainamide depresses conduction velocity and prolongs refractoriness in myocardium responsible for reentrant VT, but the mechanism by which the induction of VT is suppressed after procainamide administration remains to be determined. In the present study, the relationship between electrophysiological parameters and the noninducibility of VT was assessed during procainamide therapy with a special reference to the change of an excitable gap. Clinically documented monomorphic sustained VT was induced in 30 patients and, utilizing the phenomenon of transient entrainment. the zone of entrainment was measured as the difference between the cycle length of VTand the longest paced cycle length interrupting VT (block cycle length) which was determined as the paced cycle length decreased in steps of 10 ms, and used as an index of the excitable gap. The effective refractory period was measured at the pacing site and the paced QBS duration was used as an index of the global conduction time in the ventricle. The cycle length of VT, the block cycle length, and the width of the zone of entrainment were determined and compared between the responders and nonresponders. In 15 patients, these parameters were determined at the intermediate dose and related to subsequent noninducibility at the final dose. At the final doses of procainamide, VT was suppressed in 8 (26.7%) of 30 patients. However, the cycle length of VT, the block cycle length, and the width of the zone of entrainment were unable to predict the drug efficacy, i.e., noninducibility. The change in the effective refractory period at the pacing site or the width of the paced QRS duration was not different between the responders and nonresponders. Among the variables, only the width of the zone of entrainment showed a significant narrowing in the responders at the intermediate dose of procainamide, and it was smaller than that of the nonresponders. The significant narrowing of the width of the zone of entrainment was associated with the subsequent noninducibility of VT at the final dose. The present study showed that the baseline cycle length of VT, the block cycle length, the drug induced change of the effective refractory period, or the paced QRS duration was not a predictor of the noninducibility after procainamide administration. However, a significant narrowing of the width of the zone of entrainment at the intermediate dose was associated with the noninducibility of VT at the final dose.     

Accelerated AV Nodal Conduction with Use of Procainamide in Atrial Fibrillation

Background: Atrial fibrillation is a common dysrhythmia seen in the emergency department (ED). Chemical or electrical cardioversion may be performed on patients who have had atrial fibrillation for < 48 h duration and who are at low risk for thromboembolic events. Multiple studies suggest that intravenous procainamide is an appropriate agent in the treatment of acute atrial fibrillation due to its relatively low risk profile and high conversion rate. Objectives: A case is presented that demonstrates an adverse reaction to the use of intravenous procainamide for chemical cardioversion of atrial fibrillation in an otherwise hemodynamically stable patient. Case Report: We report a case of lone paroxysmal atrial fibrillation in a patient with a structurally normal heart who suffered paradoxical accelerated atrioventricular nodal conduction and secondary hypotension in response to procainamide administration. Conclusion: When administering procainamide for chemical cardioversion of atrial fibrillation, a low threshold should be maintained for administration of a complementary rate-controlling agent, and facilities for immediate electrical cardioversion always must be available.     

Assessment of Intersignal Variability for Discrimination of Atrial Fibrillation from Atrial Flutter

The analysis of endocardial signals obtained from an electrode located in the right atrium enabled by new dual chamber implantable cardioverter defibrillators may be helpful to provide additional therapies such as overdrive pacing or low energy atrial cardioversion for the treatment of concomitant atrial flutter (AFL) or atrial fibrillation (AF). Algorithms for discrimination of atrial tachyarrhythmias based on rate counting are of limited efficacy. The aim of this study was to assess the intersignal variability by using fast discrete wavelet transforms (FDWT) as a new method of discrimination of AF from AFL. Patients with spontaneous episodes of AF/AFL or patients who developed AF/AFL during an electrophysiological study were studied. The endocardial signals were recorded from the high right atrium using a transvenous 5 Fr bipolar electrode catheter (interelectrode spacing: 1 cm). The signals were digitized (2 kHz, 12-bit resolution) after amplification and filtering (40–500 Hz). Within data segments of 10-second duration, 25 consecutive signals were selected and normalized and FDWT was applied. Standard deviations of the wavelet coefficients (SD) from coarse scales (scale 4–8) were calculated. A total of 94 data segments (AF: 52, AFL: 42) from 28 patients were analyzed. SD at each considered scale was higher for AF than for AFL (P < 0.001). SD at scale 8 discriminated between AF from AFL with 100% sensitivity and specificity. We conclude that assessment of intersignal variability of bipolar endocardial recordings using FDWT is an effective method for the discrimination of AF from AFL. The implementation of this tool in a discrimination algorithm of an implantable device may help provide the appropriate differential therapy for atrial tachyarrhythmias.