Analysis of obstetric complications reported to the National Patient Insurance Association in Finland from 1987 to 1995

OBJECTIVE: To review comparative studies evaluating oral propafenone for restoring sinus rhythm in recent onset atrial fibrillation. DATA SOURCES: A MEDLINE search of the English-language literature (1966 to 1996) along with any referenced articles not identified by MEDLINE. STUDY SELECTION: Because intravenous propafenone is not marketed in Canada, only studies evaluating oral propafenone were included. Studies were selected if they compared oral propafenone with placebo or other antiarrhythmic agents for converting recent onset atrial fibrillation to normal sinus rhythm. DATA SYNTHESIS: Propafenone is often used as a first-line agent for pharmacological cardioversion of atrial fibrillation. In earlier studies, the efficacy of propafenone in restoring sinus rhythm was reported to be low with conversion rates of 6% to 62%. Many of these studies were noncomparative and often included patients with refractory, chronic atrial fibrillation or employed suboptimal doses of propafenone. More recently propafenone has been evaluated in the treatment of recent onset atrial fibrillation by using a single 600 mg oral loading dose. Success rates of 76% at 8 h and 83% at 12 h following the loading dose are reported. The incidence of atrial flutter during active treatment was similar to that with placebo, with the majority exhibiting 2:1 or greater atrioventricular conduction ratios and heart rates 150 beats/min or less. CONCLUSIONS: A single 600 mg oral dose of propafenone is highly effective at restoring sinus rhythm in patients with acute onset atrial fibrillation with few adverse effects. The small studies reviewed cannot lead to definitive conclusions about the safety of propafenone without prior administration of agents for rate control.     

Effect of aminophylline in patients with atropine-resistant late advanced atrioventricular block during acute inferior myocardial infarction

BACKGROUND: Advanced atrioventricular (AV) block is a frequent complication in patients with acute inferior myocardial infarction (AIMI). This conduction abnormality is associated with narrow QRS complex in conducted or junctional escape beats, suggesting that the site of block is the AV node; however, its pathophysiology has not been properly established. HYPOTHESIS: This study investigated the effect of aminophylline in eight patients (5 men, 3 women, age range 51 to 78 years, mean 67.5 +/- 8.8 years) with atropine-resistant late advanced AV block during AIMI. METHODS: Advanced AV block was late in appearance in all patients, starting 2 to 5 days after AIMI, and consisted of second-degree Mobitz II type in two patients and of complete AV block in six patients; all patients had narrow QRS complexes. Before aminophylline administration, all patients had a temporary pacemaker installed which was switched off throughout the study. They were given intravenous atropine (1 mg) that was found to be ineffective. One-half h after atropine, the first aminophylline injection (240 mg) was given intravenously over 10 min. One h following the first injection, a second aminophylline dose (240 mg) was administered. Electrocardiographic rhythm strips were obtained before and after drug administration, and the type of AV block and atrial and ventricular rate were noted. RESULTS: Aminophylline restored 1:1 conduction with first-degree AV block in six patients, Mobitz I AV block in one patient, and normal sinus rhythm in one patient. Mean atrial and ventricular rates before aminophylline were 104 +/- 16 beats/min and 57 +/- 9 beats/min, respectively, and after drug administration 95 +/- 25 beats/min and 89 +/- 17 beats/min, respectively, (p = 0.012). CONCLUSION: These results indicate that aminophylline improves AV conduction in atropine-resistant late advanced AV block complicating AIMI.     

Electropharmacologic effects of class I and class III antiarrhythmia drugs on typical atrial flutter: insights into the mechanism of termination

BACKGROUND: Acute effects of class I and class III antiarrhythmia drugs on the reentrant circuit of typical atrial flutter are not fully studied. Furthermore, the critical electrophysiologic determinants of flutter termination by antiarrhythmia drugs are not clear. METHODS AND RESULTS: The study population consisted of 36 patients (mean age, 53+/-17 years) with clinically documented typical atrial flutter. A 20-pole "halo" catheter was positioned around the tricuspid annulus. Incremental pacing was performed to measure the conduction velocity along the isthmus and lateral wall, and extrastimulation was performed to evaluate atrial refractory period in the baseline state and after intravenous infusion of ibutilide, propafenone, and amiodarone. Efficacy of these drugs in conversion of typical atrial flutter and patterns of termination were also determined. Ibutilide significantly increased the atrial refractory period and decreased conduction velocity in the isthmus at short pacing cycle length. It terminated atrial flutter in 8 (67%) of 12 patients after prolongation of flutter cycle length due to increase (86+/-19%) of conduction time in the isthmus. Propafenone predominantly decreased conduction velocity with use dependency and significantly increased atrial refractory period, but it only converted atrial flutter in 4 (33%) of 12 patients. Amiodarone had fewer effects on atrial refractory period and conduction velocity than did ibutilide and propafenone, and it terminated atrial flutter in only 4 (33%) of 12 patients. Termination of typical atrial flutter was due to failure of wave front propagation through the isthmus, which occurred with cycle length oscillation, abruptly without variability of cycle length, or after premature activation of the reentrant circuit. CONCLUSIONS: Ibutilide, with a unique increase in atrial refractoriness, was more effective in conversion of atrial flutter than were propafenone and amiodarone.     

Effects of azimilide dihydrochloride on circus movement atrial flutter in the canine sterile pericarditis model

INTRODUCTION: The effects of a Class III agent, azimilide dihydrochloride, on atrial flutter circuits were studies in a functional model of single loop reentrant atrial flutter using dogs, 3 to 5 days after production of sterile pericarditis. METHODS AND RESULTS: A computerized mapping system was used to construct activation maps from 138 to 222 epicardial sites in the right atrium. Doses of 3, 10, and 30 mg/kg i.v. azimilide dihydrochloride were analyzed in 8 dogs in which sustained atrial flutter lasting more than 30 minutes was induced by burst pacing. Atrial flutter was always due to single loop circus movement reentry in the lower right atrium. At 3 mg/kg, azimilide dihydrochloride terminated atrial flutter in 2 dogs; however, atrial flutter was reinduced. At 10 mg/kg, atrial flutter was terminated in all 8 dogs but was reinduced in 4 dogs with slower rate. At 30 mg/kg, atrial flutter was terminated in the remaining 4 dogs and could not be reinduced. Atrial flutter cycle length always increased prior to termination. Isochronal activation maps showed that the increase in cycle length was due to additional conduction delays in the slow zone of the reentrant circuit. The site of termination was always located within the slow conduction zone situated in the lower right atrium between the line of functional conduction block and the AV ring. Effective refractory periods (ERPs) were measured at selected sites in the slow zone and normal zone at twice diastolic threshold for the 10 mg/kg dose. Azimilide preferentially prolonged ERP in the slow zone (42.4 +/- 20.1 msec, mean +/- SD) compared with the normal zone (23.3 +/- 15.4 msec, P < 0.0001). The increase in cycle length corresponded with the increase in ERP in the slow zone. CONCLUSIONS: In a functional model of circus movement atrial flutter, azimilide dihydrochloride terminates and prevents reinduction of atrial flutter by a preferential increase in refractoriness leading to further conduction delay and conduction block in the slow zone of the functional reentrant circuit.     

Rate adaptive atrial pacing in the bradycardia tachycardia syndrome

In 42 patients (26 men, 16 women; mean age 69 +/- 10 years), who were paced and medicated with antiarrhythmic drugs for the bradycardia tachycardia syndrome, chronotropic response and AV conduction with rapid atrial pacing during exercise were studied. Patients were included if they had no second- or third-degree AV block, no complete bundle branch or bifascicular block, and a PQ interval < or = 240 ms during sinus rhythm at rest. The interval between the atrial spike and the following Q wave (SQ) was measured in the supine position at rest with an AAI pacing rate of 5 beats/min above the sinus rate (SQ-R + 5), and at the end of exercise with 110 beats/min (SQ-E110). Bicycle ergometry was performed using the Chronotropic Assessment Exercise Protocol with the pacemakers being programmed to AAI with a fixed rate of 60 beats/min. Chronotropic incompetence was defined as peak exercise heart rate: (1) < 100 beats/min; (2) < 75% of the maximum predicted heart rate; or (3) the heart rate at half the maximum workload < 60 + 2 beats/min per mL O2/kg per minute (calculated O2 consumption). During exercise, one patient developed atrial fibrillation. Chronotropic incompetence was present in 71% (29/41) of the patients according to definition 2, and in 76% (31/41) according to definition 1 or 3. Ten out of 41 patients (24%) exhibited a second-degree AV block with atrial pacing at 110 beats/min at the end of exercise. Only 9 out of the remaining 31 patients (29%) showed a physiological adaptation of the SQ-E110, and 21 patients (68%) exhibited a paradoxical increase of the SQ interval with rapid atrial pacing at the end of exercise as compared to the SQ-R + 5. These observations indicate that the pacing system to be used in most patients paced and medicated for the bradycardia tachycardia syndrome should be dual chamber, and the option of rate adaptation should be considered.     

Detection of BK polyomavirus genotypes in healthy and HIV-positive children

BACKGROUND: Atrial flutter is a common arrhythmia which frequently recurs after cardioversion and is relatively difficult to control with antiarrhythmic agents. AIMS: To evaluate the success rate, recurrence rate and safety of radiofrequency, (RF) ablation for atrial flutter in a consecutive series of patients with drug refractory chronic or paroxysmal forms of the arrhythmia. METHODS: Electrophysiologic evaluation of atrial flutter included activation mapping with a 20 electrode halo catheter placed around the tricuspid annulus and entrainment mapping from within the low right atrial isthmus. After confirmation of the arrhythmia mechanism with these techniques, an anatomic approach was used to create a linear lesion between the inferior tricuspid annulus and the eustachian ridge at the anterior margin of the inferior vena cava. In order to demonstrate successful ablation, mapping techniques were employed to show that bi-directional conduction block was present in the low right atrial isthmus. RESULTS: Successful ablation was achieved in 26/27 patients (96%). In one patient with a grossly enlarged right atrium, isthmus block could not be achieved. Of the 26 patients with successful ablation, there has been one recurrence of typical flutter (4%) during a mean follow-up period of 5.5 +/- 2.7 months. This patient underwent a successful repeat ablation procedure. Of eight patients with documented clinical atrial fibrillation (in addition to atrial flutter) prior to the procedure, five continued to have atrial fibrillation following the ablation. There were no procedural complications and all patients had normal AV conduction at the completion of the ablation. CONCLUSIONS: RF ablation is a highly effective and safe procedure for cure of atrial flutter. In patients with chronic or recurrent forms of atrial flutter RF ablation should be considered as a first line therapeutic option.     

The development of sinoatrial dysfunction in pacemaker patients with isolated atrioventricular block

The purpose of this paper is the assessment of sinus node competence over time in patients with isolated atrioventricular block (AV block). Patients implanted with AV synchronous pacemakers for isolated AV block between December 1993 and June 1995 were prospectively evaluated at predischarge, 6 weeks, and subsequent 6 months follow-up with respect to atrial rate monitors/24-hour Holter and modified exercise test. Patients unable to maintain AV synchronous pacing or complete a modified exercise test were excluded. Sinus node competency is interpreted as: (1) absence of atrial brady- or tachyarrhythmia, (2) ability to achieve a minimum heart rate of 100 beats/min with modified exercise test or during daily activities. There were 58 patients (22 women), mean age 71.0 +/- 13.8 with an average follow-up of 30.4 months (11-40). Three patients did not complete a modified exercise test, 4 patients were lost to follow-up, and 2 patients were unable to maintain AV synchronous pacing. Of the remaining 49 patients, 3 developed chronic or paroxysmal atrial fibrillation. No patient developed significant bradyarrhythmias. All patients achieved a heart rate of > or = 100 beats/min modified exercise test. In our group of patients with isolated AV block within a moderate follow-up period, development of sinoatrial dysfunction was rare (6%). A longer follow-up is required to delineate the natural history of sinoatrial dysfunction in patients with isolated AV block.     

Renal-hepatic-pancreatic dysplasia: an autosomal recessive malformation

BACKGROUND: Pharmacological conversion of paroxysmal atrial fibrillation is frequently necessary. The aim of this study was to compare intravenous propafenone, a class Ic antiarrhythmic agent, with placebo in paroxysmal atrial fibrillation (AF) of recent onset (< 72 h). PATIENTS AND METHODS: We randomly allocated 75 patients, aged 18 to 70 years, with paroxysmal AF to receive intravenous propafenone (2 mg/kg in 15 min followed by 1 mg/kg in 2 h) or the matching placebo. Patients were followed for 3 h. Exclusion criteria were the presence of one of the following: clinical heart failure, recent acute myocardial infarction, hypotension, atrioventricular block, Wolff-Parkinson-White syndrome, or current treatment with antiarrhythmic agents or digitalis. RESULTS: No sign of heart disease was found in 74.7% of the patients. Echocardiographically determined left atrium diameter was similar in the two groups. Conversion to sinus rhythm occurred in 24 of 41 patients allocated to propafenone and in 10 of 34 patients allocated to placebo (odds ratio 3.2, 95% confidence intervals 1.3-7.9; p < 0.01). Mean conversion time was 34 +/- 29 and 71 +/- 55 min, respectively, for propafenone and placebo. Mean heart rate in nonconverters decreased from 146 to 109 beats/min in patients treated with propafenone while it remained virtually unchanged in those treated with placebo. Only minor side effects were noted. CONCLUSIONS: Intravenous propafenone is an effective therapeutic option for restoring sinus rhythm in patients with paroxysmal AF of recent onset.     

A simple technique for selective radiofrequency ablation of the slow pathway in atrioventricular node reentrant tachycardia

OBJECTIVES: A simple technique was designed for radiofrequency ablation therapy of atrioventricular (AV) node reentrant tachycardia. BACKGROUND: This technique was based on the hypothesis that slow pathway conduction reflects conduction through the compact node and its posterior atrial input. METHODS: A total of 100 consecutive patients were studied; there were 37 men and 63 women, with a mean age of 48 +/- 15 years. All 100 patients had induction of sustained tachycardia with (51 patients) or without (49 patients) administration of isoproterenol or atropine, or both. The ablation catheter was initially manipulated to record the largest His bundle deflection from the apex of Koch's triangle. It was then curved downward and clockwise to the area of the compact node when His deflection was no longer visible and the ratio of atrial to ventricular electrogram was < 1. The radiofrequency current was delivered from the 4-mm tip electrode a mean of 5 +/- 7 times at a power of 25 +/- 4 W for a duration of 21 +/- 4 s. The total fluoroscopic time was 19 +/- 11 min. RESULTS: Selective ablation (56 patients) or modification (26 patients) of the slow pathway without affecting anterograde and retrograde fast pathway conduction was achieved in 82 patients. Ablation or modification of both the retrograde fast pathway and the slow pathway but with preservation of anterograde fast pathway conduction was noted in 12 patients. Ablation or modification of the retrograde fast pathway alone or both anterograde and retrograde fast pathway conduction was noted in three patients. Complete AV node block occurred in three patients. Seventy-three patients had no induction of echo beats or tachycardia and 24 patients had induction of a single echo beat after ablation. Follow-up study was performed in 62 patients 76 +/- 18 days after ablation. Thirty-nine patients had no induction of echo beats or tachycardia, 22 had induction of echo beats alone and 1 patient had induction of sustained tachycardia. CONCLUSION: Selective ablation of the slow AV node pathway can be achieved by a simple procedure with a high success rate and few complications.     

Combination of sotalol and quinidine in a canine model of torsades de pointes: no increase in the QT-related proarrhythmic action of sotalol

INTRODUCTION: Clinical treatment with a combination of Class IA and III antiarrhythmic drugs is not recommended, as they both favor bradycardia-dependent proarrhythmic events such as torsades de pointes (TdP). However, this theoretical additive effect on ventricular repolarization has never been demonstrated and could be questioned as other Class I drugs, such as mexiletine, a Class IB drug, limit the number of sotalol-induced TdP in dogs with AV block, suggesting the possibility of an antagonistic action of Class I properties against Class III effects. METHODS AND RESULTS: We compared the electrophysiologic and proarrhythmic effects of sotalol (Class III) alone and combined with quinidine (Class IA) in a canine model of acquired long QT syndrome. Seven hypokalemic (K+: 3 +/- 0.1 mEq/L) dogs with chronic AV block had a demand pacemaker implanted and set at a rate of 25 beats/min. They were submitted to two (sotalol-alone and sotalol-plus-quinidine) experiments 48 hours apart using a randomized cross-over protocol. They were pretreated with quinidine (10 mg/kg + 1.8 mg/kg per hour) or saline infused throughout the experiment, and given sotalol (4.5 mg/kg + 1.5 mg/kg per hour) for 2 hours, 30 minutes after the beginning of the pretreatment infusion during both experiments. Ventricular and atrial cycle lengths were similarly increased by sotalol after quinidine or saline. The sotalol-induced prolongation of the QT interval was significantly shorter in quinidine-pretreated dogs (24 +/- 7 msec after quinidine vs 40 +/- 8 msec after saline). Fewer dogs developed TdP: significantly during the first hour of infusion (1/7 sotalol-plus-quinidine vs 6/7 sotalol-alone dogs, P < 0.05) but nonsignificantly during the second hour (3/7 vs 6/7). CONCLUSION: In this model, the sotalol-plus-quinidine combination is at least no more arrhythmogenic than either of the drugs given alone.     

Characterization of the excitable gap in human type I atrial flutter

OBJECTIVES: We sought to characterize the excitable gap of the reentrant circuit in atrial flutter. BACKGROUND: The electrophysiologic substrate of typical atrial flutter has not been well characterized. Specifically, it is not known whether the properties of the tricuspid valve isthmus differ from those of the remainder of the circuit. METHODS: Resetting was performed from two sites within the circuit: proximal (site A) and distal (site B) to the isthmus in 14 patients with type I atrial flutter. Resetting response patterns and the location where interval-dependent conduction slowing occurred were assessed. RESULTS: Some duration of a flat resetting response (mean +/- SD 40.1 +/- 20.9 ms, 16 +/- 8% of the cycle length) was observed in 13 of 14 patients; 1 patient had a purely increasing response. During the increasing portion of the resetting curve, interval-dependent conduction delay most commonly occurred in the isthmus. In most cases, the resetting response was similar at both sites. In three patients, the resetting response differed significantly between the two sites; this finding suggests that paced beats may transiently change conduction within the circuit or the circuit path, or both. CONCLUSIONS: Some duration of a flat resetting response was observed in most cases of type I atrial flutter, signifying a fully excitable gap in all portions of the circuit. The isthmus represents the portion of the circuit most vulnerable to interval-dependent conduction delay at short coupling intervals.     

Characterization of low right atrial isthmus as the slow conduction zone and pharmacological target in typical atrial flutter

BACKGROUND: Previous electrophysiological studies in patients with typical atrial flutter suggested that the slow conduction zone might be located in the low right atrial isthmus, which is a path formed by orifice of inferior vena cava, eustachian valve/ridge, coronary sinus ostium, and tricuspid annulus. The conduction characteristics during atrial pacing and responses to antiarrhythmic drugs of this anatomic isthmus were unknown. METHODS AND RESULTS: Forty-four patients, 20 patients with paroxysmal supraventricular tachycardia (group 1) and 24 patients with clinically documented paroxysmal typical atrial flutter (group 2), were studied. A 20-pole halo catheter was situated around the tricuspid annulus. Incremental pacing from the low right atrium and coronary sinus ostium was performed to measure the conduction time and velocity along the isthmus and lateral wall in the baseline state and after intravenous infusion of procainamide or sotalol. In both groups, conduction velocity in the isthmus during incremental pacing was significantly lower than that in the lateral wall before and after infusion of antiarrhythmic drugs. Furthermore, gradual conduction delay with unidirectional block in the isthmus was relevant to initiation of typical atrial flutter. Compared with group 1, group 2 had a lower conduction velocity in the isthmus and shorter right atrial refractory period. Procainamide significantly decreased the conduction velocity, but sotalol did not change it. In contrast, sotalol significantly prolonged the atrial refractory period with a higher extent than procainamide. After infusion of procainamide, the increase of conduction time in the isthmus accounted for 52+/-19% of the increase in flutter cycle length, and 5 of 12 patients (42%) had spontaneous termination of typical flutter. After infusion of sotalol, typical flutter was induced in only 6 of 12 patients (50%) without significant prolongation of flutter cycle length. CONCLUSIONS: The low right atrial isthmus with rate-dependent slow conduction properties is critical to initiation of typical human atrial flutter. It may be the potentially pharmacological target of antiarrhythmic drugs in the future.     

Comparison of S(-)-bupivacaine with racemic (RS)-bupivacaine in supraclavicular brachial plexus block

Control of heart rate in critically ill patients who develop atrial fibrillation or atrial flutter can be difficult. Amiodarone may be an alternative agent for heart rate control if conventional measures are ineffective. We retrospectively studied intensive care unit patients (n = 38) who received intravenous amiodarone for heart rate control in the setting of hemodynamically destabilizing atrial tachyarrhythmias resistant to conventional heart rate control measures. Atrial fibrillation was present in 33 patients and atrial flutter in 5 patients. Onset of rapid heart rate (mean 149 +/- 13 beats/min) was associated with a decrease in systolic blood pressure of 20 +/- 5 mm Hg (p <0.05). Intravenous diltiazem (n = 34), esmolol (n = 4), or digoxin (n = 24) had no effect on heart rate, while reducing systolic blood pressure by 6 +/- 4 mm Hg (p <0.05). The infusion of amiodarone (242 +/- 137 mg over 1 hour) was associated with a decrease in heart rate by 37 +/- 8 beats/min and an increase in systolic blood pressure of 24 +/- 6 mm Hg. Both of these changes were significantly improved (p <0.05) from onset of rapid heart rate or during conventional therapy. Beneficial changes were also noted in pulmonary artery occlusive pressure and cardiac output. There were no adverse effects secondary to amiodarone therapy. Intravenous amiodarone is efficacious and hemodynamically well tolerated in the acute control of heart rote in critically ill patients who develop atrial tachyarrhythmias with rapid ventricular response refractory to conventional treatment. Cardiac electrophysiologic consultation should be obtained before using intravenous amiodarone for this purpose.     

Neurohumoral and hemodynamic mechanisms of diuresis during atrioventricular nodal reentrant tachycardia

Thirty-two consecutive patients with paroxysmal supraventricular tachycardias, with previously defined mechanisms of the tachycardias, were interviewed by noninvestigators about whether they experienced symptoms of diuresis during or at the termination of the tachycardias, to test the hypothesis that patients with AV nodal reentrant tachycardia would have a feeling of diuresis, polyuria, or both during or at the termination of the tachycardia. Twelve of the 13 patients with AV nodal reentrant tachycardia (92%), two of the 15 patients with AV reentrant tachycardia (13%), and one of the 4 patients with atrial flutter associated with 2:1 AV conduction (25%) felt diuresis during or at the termination of the tachycardias (AV nodal reentrant tachycardia vs other forms of tachycardia; P < 0.001). In 14 of the 32 patients, the right atrial pressure and plasma atrial natriuretic peptide (ANP) concentration were measured during both the tachycardias and sinus rhythm. The mean right atrial pressure during AV nodal reentrant tachycardia was significantly elevated compared to that during other forms of tachycardia (P < 0.01). The plasma ANP concentration during AV nodal reentrant tachycardia was also elevated significantly compared to that during other forms of tachycardias (P < 0.001). There were no significant differences in the cycle lengths of the tachycardias, age, left atrial dimensions, or the left ventricular ejection fraction between the AV nodal reentrant tachycardia and the other forms of tachycardia. We concluded that the feeling of diuresis during or at the termination of tachycardia was a more common symptom in patients with AV nodal reentrant tachycardia. The higher secretion of plasma ANP from the right atrium might be involved in the mechanism of this symptom.     

Atypical atrioventricular nodal reentry tachycardia with atrioventricular block mimicking atrial tachycardia: electrophysiologic properties and radiofrequency ablation therapy

INTRODUCTION: Fast-intermediate form AV nodal reentry tachycardia (AVNRT) sometimes may mimic atrial tachycardia or atrial flutter and render the diagnosis difficult when the tachycardia rate is fast and AV block occurs during tachycardia. METHODS AND RESULTS: A 45-year-old woman with paroxysmal supraventricular tachycardia was referred to this institution. Initially, the tachycardia was thought to be an atrial tachycardia because of: (1) a short cycle length of the tachycardia with 2:1 and Wenckebach AV block; (2) a difference in the atrial activation sequence during tachycardia and during ventricular pacing; and (3) failure of burst ventricular pacing to affect the atrial rate and the atrial activation sequence during tachycardia. An accurate diagnosis of fast-intermediate form AVNRT was subsequently made based on the finding that the tachycardia was induced following delivery of a third ventricular extrastimulus, which showed a sequence of V-A-H and a change on atrial activation sequence of the induced beat. Successful radiofrequency ablation was achieved only after accurate diagnosis of the tachycardia was made. CONCLUSION: Fast-intermediate form AVNRT sometimes may masquerade as atrial tachycardia. Accurate diagnosis is mandatory for successful ablation therapy.     

Isolated paralysis of the ramus marginalis mandibulae nervi facialis: clinical aspects, etiology, diagnosis and therapy. An overview]

INTRODUCTION: Little is known about the predictors of recurrent atrial flutter or fibrillation after successful radiofrequency ablation of typical atrial flutter. In addition, there is only limited evidence suggesting that elimination of atrial flutter would modify the natural history of atrial fibrillation in patients who experienced both of these arrhythmias. The aims of the present study were to investigate the long-term results of radiofrequency catheter ablation and to examine the predictors for late occurrence of atrial fibrillation in a large population with typical atrial flutter. METHODS AND RESULTS: The study population consisted of 144 patients (mean age 56 +/- 18 years) with successful ablation of clinically documented typical atrial flutter. In the first 50 patients, successful ablation was defined as termination and noninducibility of atrial flutter; for the subsequent 94 patients, successful ablation was defined as achievement of bidirectional isthmus conduction block and no induction of atrial flutter. The clinical and echocardiographic variables were analyzed in relation to the late occurrence of atrial flutter or fibrillation. Over the follow-up period of 17 +/- 13 months, 14 (9.7%) patients had recurrence of typical atrial flutter. In the first 50 patients, 8 (16%) had recurrence of atrial flutter, compared with only 6 (6%) of the following 94 patients. Patients with incomplete isthmus block had a significantly higher incidence of recurrent atrial flutter than those with complete isthmus block (6/16 vs 0/78, P < 0.0001) in the following 94 patients. There was no predictor for recurrence of atrial flutter after successful ablation as determined by univariate and multivariate analysis. Although successful ablation of atrial flutter eliminated atrial fibrillation in 45% of patients with a prior history of atrial fibrillation, 31 (21.5%) of 144 patients undergoing this procedure developed atrial fibrillation during the follow-up period. Univariate analysis revealed that three clinical variables were related to the occurrence of atrial fibrillation: (1) the presence of structural heart disease; (2) a history of atrial fibrillation before ablation; and (3) inducible sustained atrial fibrillation after ablation. By multivariate analysis, only a history of atrial fibrillation and inducible sustained atrial fibrillation could predict the late development of atrial fibrillation after atrial flutter ablation. CONCLUSION: Radiofrequency catheter ablation of typical atrial flutter is highly effective and associated with a low recurrence rate of atrial flutter, but atrial fibrillation continues to be a long-term risk for patients undergoing this procedure. The presence of structural heart disease and prior spontaneous or inducible sustained atrial fibrillation increases the risk of developing atrial fibrillation.     

Efficacy of intravenous propafenone in termination of atrial flutter by overdrive transesophageal pacing previously ineffective

Fifty patients with symptomatic type I atrial flutter in whom termination of the arrhythmia with transesophageal stimulation was unsuccessful were randomized to undergo a repeat procedure after intravenous propafenone (n = 25) or placebo (n = 25). Immediate sinus rhythm recovery rate was 36% in the propafenone group and 4% in the placebo group (p = 0.005), indicating that intravenous propafenone increases the rate of successful transesophageal stimulation and can be used when a first attempt at conversion is ineffective.     

Conduction properties of the inferior vena cava-tricuspid annular isthmus in patients with typical atrial flutter

INTRODUCTION: A functional region of slow conduction located in the inferior right atrium has been postulated to be critical to the induction and maintenance of typical human atrial flutter. We reexamined the potential role of functional conduction delay in the annular isthmus between the tricuspid valve and the inferior vena cava; it is within this region that such delays have been postulated to occur, and where interruption of conduction by radiofrequency energy application has been shown to eliminate typical flutter. METHODS AND RESULTS: Thirty patients with type I atrial flutter (30 counterclockwise, 14 clockwise) were studied. Counterclockwise and clockwise isthmus activation times adjacent and parallel to the tricuspid valve were measured during three conditions: (1) atrial pacing in sinus rhythm, (2) atrial flutter, and (3) entrainment of atrial flutter. During pacing in sinus rhythm at progressively shorter cycle lengths, both counterclockwise and clockwise isthmus activation times remained unchanged; decremental conduction prior to flutter induction or loss of capture was not observed. Counterclockwise isthmus activation time did not significantly differ during flutter (68 +/- 23 msec), inferolateral tricuspid annulus pacing (71 +/- 23 msec), or entrainment of flutter (72 +/- 23 msec). Similarly, clockwise isthmus activation times did not significantly differ between flutter (65 +/- 22 msec), proximal coronary sinus pacing (73 +/- 21 msec), or entrainment of flutter (64 +/- 15 msec). CONCLUSION: Decremental conduction is not characteristic of activation through the isthmus when activation is assessed parallel and adjacent to the tricuspid annulus. Functional slowing or conduction delay does not develop in this region during typical atrial flutter.     

New diagnostic finding to assess para-Hisian pacing observed in a patient with a permanent form of junctional reciprocating tachycardia

Para-Hisian pacing, a useful method to differentiate conduction over an accessory pathway from conduction over the AV node, is assessed essentially by comparing the timing of local atrial electrograms between His-bundle captured beats and His-bundle noncaptured beats. We describe the case of a patient with a permanent form of junctional reciprocating tachycardia, in whom an atrial double potential was recorded only during the tachycardia at the right posterior septum. During para-Hisian pacing, a morphologic change in the atrial electrogram at the posterior septum was also identified, as well as a change in the retrograde atrial sequence. Since the morphologic change of atrial electrograms during para-Hisian pacing cannot be demonstrated in a patient without an accessory pathway, this new finding could be considered a new additional diagnostic criterion suggesting the presence of an accessory pathway.     

Different modes of cell death induced by 5-fluoro-2''-deoxyuridine in two clones of the mouse mammary tumor FM3A cell line

OBJECTIVES: To clarify the prevalence and mechanism of supraventricular tachycardia in patients with right atrial isomerism. BACKGROUND: Paired SA and dual atrioventricular (AV) nodes have been described in patients with right atrial isomerism. However, the clinical significance remains unclear. METHODS: From 1987 to 1996, a total of 101 patients (61 male, 40 female) and four fetuses were identified with right atrial isomerism. The diagnosis of supraventricular tachycardia exclude the tachycardia with prolonged QRS duration or AV dissociation, and primary atrial tachycardia. RESULTS: The median follow-up duration was 38 months (range 0.2-270 months). Supraventricular tachycardia was documented in 25 patients (24.8%) and one fetus (25%) (onset age ranged from prenatal to 14 years old; median 4 years old). Actuarial Kaplan-Meier analysis revealed that the probability of being free from tachycardia was 67% and 50% at 6 and 10 years of age, respectively. These tachycardias could be converted by vagal maneuvers in one, verapamil in seven, propranolol in four, digoxin in two, procainamide in one, and rapid pacing in five. Spontaneous conversion was noted in six (including the fetus). Seven cases had received electrophysiological studies. Reciprocating AV tachycardia could be induced in five and echo beats in one. The tachycardia in three patients was documented as incorporating a posterior AV node (antegrade) and an anterior or a lateral AV node (retrograde). Two of them received radiofrequency ablation. Successful ablation in both was obtained by delivering energy during tachycardia, aimed at the earliest retrograde atrial activity and accompanied by junctional ectopic rhythm. The patient with echo beats developed tachycardia soon after operation. CONCLUSIONS: Supraventricular tachycardia is common in patients with right atrial isomerism and can occur during the prenatal stage. Drugs to slow conduction through the AV node may help to terminate the tachycardia. Radiofrequency ablation is a safe and effective treatment alternative to eliminate tachycardia.