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PubMed1993

Delayed restoration of atrial function after conversion of atrial flutter by pacing or electrical cardioversion.

It is often suggested but never proven that atrial function is not affected during atrial flutter, nor after its conversion to normal sinus rhythm. To evaluate this hypothesis, a prospective study was performed in 22 patients (age range 20 to 88 years) with atrial flutter. Diastolic transmitral flow was analyzed with echo-Doppler before and after conversion. After randomization, conversion was attempted with overdrive pacing or up to two 50 J shocks. If the initial method was unsuccessful, a 200 J shock was administered. All patients were converted to sinus rhythm with this protocol. Shortly after conversion (at 1 and 6 hours), atrial contribution to ventricular filling was absent in 4 of 22 patients. In the remaining 18 patients, atrial contribution to ventricular filling was small. Atrial contribution to transmitral flow improved from 20 to 27% within 24 hours (p < 0.01) and increased further to 38% at 6 weeks (p < 0.005). Peak velocity of late diastolic filling increased from 0.28 m/s after 1 hour to 0.39 m/s after 24 hours (p < 0.0001) and improved even further during later follow-up. In 1 patient, an effective atrial systole was not observed until the 14th day. Cardiac output did not change significantly during the study period. No differences were observed between the conversion modalities. In conclusion, atrial dysfunction is present immediately after conversion of atrial flutter to normal sinus rhythm. This dysfunction occurs also after overdrive pacing and can last > 1 week. The findings suggest that stasis in the atria can remain temporarily present after successful conversion of atrial flutter to sinus rhythm.

Adult↗
PubMed1996

Safety and risk/benefit analysis of ibutilide for acute conversion of atrial fibrillation/flutter.

Safety data were reviewed from several controlled clinical trials of ibutilide, a new class III antiarrhythmic drug recently approved for the acute interruption of atrial fibrillation and flutter. Noncardiovascular adverse effects of ibutilide were similar in frequency to those with placebo. Cardiovascular adverse effects occurred in 24.9% of 586 ibutilide-treated patients as compared with 22.2% of 108 sotalol-treated patients, and 7.1% of 127 patients who received placebo. Polymorphous ventricular tachycardia, diagnosed as torsades de pointes, was more common with ibutilide than with placebo or sotalol treatment. It occurred in 4.3% of patients, including 1.7% whose torsades de pointes was sustained and required cardioversion. In the ibutilide group, 4.9% of patients had nonsustained monomorphic ventricular tachycardia compared with 3.7% of patients who received sotalol and 0.8% of patients who received placebo. All of the sustained arrhythmias except 1 occurred within 1 hour of the end of ibutilide infusion, and all were successfully terminated without sequelae. In a multiple logistic regression analysis, bradycardia, low body weight, and history of congestive heart failure were predictive of the occurrence of torsades de pointes. Hypotension, conduction block, bradycardia, and all other cardiovascular adverse effects all occurred at similar rates in the ibutilide- and placebo-treated groups. For patients who failed to convert while receiving ibutilide, there was no decrease in the efficiency of cardioversion, nor was there an increase in the mean energy requirements for subsequent electrical cardioversion. Analysis of a 3-month follow-up study showed that patients receiving ibutilide had similar outcomes compared with patients receiving placebo. One placebo-treated patient died. Other than torsades de pointes, ibutilide has a very good safety profile. Under the proper clinical conditions, this complication of ibutilide therapy can be rapidly diagnosed and effectively treated.

Anti-Arrhythmia Agents↗
PubMed1990

Giant P wave in a patient with right ventricular cardiomyopathy.

A P wave of 7.5 mm in lead I and 12.5 in V1 was detected in a 28-year-old man, with a progressive cardiomegaly since the age of 14 years. At last admission he had minor symptoms, and a systolic murmur consistent with tricuspid regurgitation. The electrocardiogram showed an extremely tall P wave and a QRS of a very low amplitude; T waves were inverted on the precordial leads. These ECG features, and subsequent investigations, were consistent with right ventricular cardiomyopathy with massive tricuspid regurgitation, and right atrial abnormality.

Adult↗
PubMed1996

Effects of oral propafenone administration before electrical cardioversion of chronic atrial fibrillation: a placebo-controlled study.

OBJECTIVES: Our aim was to evaluate the benefits and risks of administering propafenone before electrical defibrillation for chronic atrial fibrillation. BACKGROUND: In this context, an antiarrhythmic drug-although potentially useful in preventing early recurrence of arrhythmia-could adversely affect the defibrillation threshold and reduce the cardioversion success rate. METHODS: We randomly assigned 100 patients with chronic atrial fibrillation to oral treatment with either placebo (51 patients) or 750 mg/day of propafenone (49 patients) for 48 h before administration of direct current shock. After successful cardioversion, all patients received propafenone therapy and were followed up for 48 h. RESULTS: Before defibrillation, three patients in the propafenone group (6.1%) had reversion to sinus rhythm and one had sustained ventricular tachycardia. Shock efficacy (82.4% vs. 84.4%) and the cumulative effective energy (395 +/- 258 vs. 421 +/- 236 J) were not different between the placebo and propafenone groups. In the propafenone group, 11 patients had their arrhythmia transformed into atrial flutter and required a lower energy level for arrhythmia conversion than did the other patients with continued atrial fibrillation (245 +/- 197 vs. 493 +/- 215 J, p < 0.01); the latter patients showed a trend (p < 0.10) toward higher energy requirements than that of patients who received placebo. The incidence of asymptomatic bradyarrhythmias was higher in the propafenone group (28.9% vs. 7.1%, p < 0.02), but more patients who received placebo had early recurrence of atrial fibrillation (16.7% vs. 0%, p < 0.02). Two days after cardioversion, more patients given propafenone (73.5% vs. 52.9%, p < 0.05) were discharged from the hospital with sinus rhythm. During the in-hospital stay, propafenone was withdrawn from six patients (6.6%) because of side effects. CONCLUSIONS: Propafenone, given before electrical cardioversion for chronic atrial fibrillation does not affect the mean defibrillation threshold or the rate of successful arrhythmia conversion. It decreases the recurrence of atrial fibrillation early after shock, thus allowing more patients to be discharged from the hospital with sinus rhythm.

Administration, Oral↗
PubMed2001

Prognostic implications of right atrial ischemic dysfunction in patients with biventricular inferior infarction: transesophageal echocardiographic analysis.

In order to determine the effect of right atrial dysfunction on clinical outcome, six patients with inferior myocardial infarction with extension to right ventricle and right atrium involving only obstructions of the right coronary artery were examined with transesophageal echocardiography (TEE) at the time of the event. Five of the patients were reexamined 15 to 55 months later. Two patients underwent thrombolysis and maintained ratios of right-to-left ventricular diameters of less than 1, as well as normal convexity of the interatrial septum. One patient had spontaneous reperfusion of the right coronary artery, reduction in right ventricular diameter, and normalization of interatrial septum. Another patient underwent delayed angioplasty and manifested a diminished wall movement score (WMS) in the follow-up echocardiogram. One patient died during his first hospitalization with significant right ventricular dilatation, inverted convexity of the interatrial septum, and right atrial thrombosis. The last patient died during follow-up with right ventricular dilatation, increased WMS, right atrial akinesis, and inverted interatrial convexity. Serial TEE examination of patients with infarction of the left ventricular inferior wall is a safe technique for determining the degree of the extension of the ischemic process to the right chambers.

Adult↗
PubMed1985

[Reevaluation of pacemaker-induced reentry tachycardias: incidence, mechanisms and therapy].

To reassess incidence, mechanisms and therapeutic possibilities in the treatment of pacemaker-induced reentry tachycardias (RT) in patients with the second generation of DDD-pacemakers, 35 consecutive patients were studied prospectively by measuring VA conduction at implant and searching for RT clinically and by repeat 24-hour ECG monitoring. Reprogramming to the VVI mode because of atrial flutter and to the AAI mode because of lead displacement was necessary in 2 and 1 of the patients respectively. RT were detected in 7/32 patients (22%), 4 of whom were symptomatic. The triggering mechanism of RT was premature ventricular contraction in 4 patients, premature atrial contractions in 1, loss of atrial sensing in 1, and remained unclear in 1. Unlike the 30% of patients of an earlier consecutive series with first generation of physiologic PM who had RT and required permanent reprogramming to VVI stimulation in 10% of cases, RT was abolished in all patients maintaining physiologic pacing by prolonging the atrial refractory period, shortening the av delay, adjusting atrial output or atrial sensing, or by antiarrhythmic therapy.

Aged↗
PubMed1993

[Arrhythmia and syndrome of obstructive sleep apnea in adults].

Many nocturnal cardiac arrhythmias and conduction defects have been reported in the adult sleep apnoea syndrome. The most original is the great variability of the heart rate which is cyclical and related to the apnoeic episodes, and easily differentiated from simple respiratory sinus arrhythmia. It is characterised by an initial bradycardia followed by rebound tachycardia. The bradycardia is vagally dependent (inhibited by atropine) probably secondary to carotid chemoreceptor stimulation by the hypoxaemia. The tachycardia is mainly attributed to the cessation of vagal hypertonicity although catecholamine stimulation has been suggested. The origin of these changes is purely functional, regressing with treatment of apnoea (waking, tracheotomy), the maintenance of arterial oxygen concentrations with oxygen therapy and parasympathetic blockade (atropine). The intensity of the phenomenon is related to the degree of arterial desaturation, which is itself related to basal arterial saturation (SaO2) and the duration of the apnoeas. Prolonged systole due to paroxysmal sino-atrial or atrioventricular block may be observed at night in these patients. The influence of vagal overactivity is confirmed (suppression of vagotomy) with no organic pathology (diurnal absence, tracheotomy, normal electrophysiological testing) in favour of a relationship with apnoea. Though less common than conduction abnormalities, atrial arrhythmias (extrasystoles, flutter, fibrillation) are also possible complications of sleep apnoea. The absence of an organic substrate is indicated by their regression post-tracheotomy and the efficacy of atropine (again in favour of a vagally-induced mechanism). Finally, nocturnal ventricular hyper-excitabilty is sometimes observed, the probable mechanism being the association of severe hypoxaemias (SaO2 < 60%) and the increased sympathetic tone at the end of the apnoea.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

Electrophysiologic and antiarrhythmic effects of the new class III antiarrhythmic drug KCB-328 in experimental canine atrial flutter.

BACKGROUND: The electrophysiologic and antiarrhythmic effects of a new class III antiarrhythmic drug (KCB-328), a delayed rectifier potassium current (IKr) blocker with minimal reverse use-dependent effect on atrial repolarization, were evaluated in the canine night atrial crush-injury model of atrial flutter (AFL). METHODS: Ten anesthetized, open-chest dogs, were studied after right atrial crush-injury. Atrial effective refractory period (ERP), conduction velocity (CV), wavelength, and dispersion of refractoriness were determined during programmed stimulation (S1S2 at S1S1 = 200, 300, 400, and 500 msec) at four sites via a mapping plaque sutured on the right atrial free wall. Right and left ventricular ERP were similarly measured at single sites. Electrophysiological parameters were determined at baseline and following sequential cumulative doses of KCB-328 (10, 30, 100, and 300 microg/kg). RESULTS: Sustained AFL was inducible in 7/10 dogs by rapid pacing following baseline electrophysiologic measurements. KCB-328 significantly prolonged sinus cycle length, but had no effect on PR interval, and prolonged QTc only at the highest dose level. KCB-328 significantly prolonged atrial ERP and wavelength and ventricular ERP, and significantly reduced dispersion of atrial refractoriness. KCB-328 significantly prolonged AFL cycle length, and increasing doses progressively terminated sustained AFL and prevented its reinduction by pacing. No adverse hemodynamic or ventricular proarrhythmic effects were observed. CONCLUSIONS: The electrophysiologic profile of KCB-328 in this canine model of AFL, particularly its lack of reverse use-dependent effect on atrial refractoriness, suggests that it may have significant antiarrhythmic potential in treatment of atrial arrhythmias.

Animals↗
PubMed1982

[Value and methodology of electric stimulation in intracardiac examination of patients with ventricular pre-excitation syndrome].

The procedures involved in different techniques of cardiac electrostimulation for the diagnosis of the pre-excitement syndrome were examined in 154 patients. In a group of 150 patients with provoked (140) or spontaneous (10) tachycardia developing in response to endocardial electrocartography, the paroxysmal supraventricular tachycardia was noted in 95.5%, atrial flutter in 11.4%, atrial flutter-fibrillation in 5.7%, atrial fibrillation in 29.8%, A-V tachycardia in 3.7%. The methods of diagnostic cardiac electrostimulation are of great importance in determining the type, localization, electrophysiologic properties and mechanisms of heart rhythm disorders and in selecting a rational therapeutic method.

Atrioventricular Node↗
PubMed2003

Thromboembolic risk of patients referred for radiofrequency catheter ablation of typical atrial flutter without prior appropriate anticoagulation therapy.

BACKGROUND: Radiofrequency catheter ablation of isthmus dependent atrial flutter is considered the therapy of choice. There is, however, controversy with regard to the thrombogenicity of atrial flutter in comparison with atrial fibrillation. METHODS: Consecutive patients scheduled for catheter ablation of documented typical atrial flutter receiving insufficient (INR < 2.0) or no anticoagulation during the three weeks preceding the procedure underwent multiplane transesophageal echocardiography (TEE). Patients with exclusive documentation of atrial flutter were classified as group I, whereas patients with additional documentation of atrial fibrillation were classified as group II. RESULTS: The study included 201 patients, 62 of whom were not on therapeutic anticoagulation (mean age 64 +/- 9 years, 87% men). In 10 of these 62 patients (16%), TEE detected a left atrial (LA) appendage thrombus in 4, or dense spontaneous echo contrast (SEC) in 6 patients. Comparison of patients with versus without SEC or thrombus, revealed a higher incidence of valvular heart disease (60% vs 26%, P = 0.05), but no differences with respect to age, gender, LA diameter, left ventricular end-diastolic diameter, or left ventricular ejection fraction. The incidence of positive TEE findings in group I was 1 in of 36 versus 9 of 26 in group II (3% vs 35%, P < 0.001), and the relative risk for thromboembolism in group II versus group I was 12.5 (95% CI: 3-55, P < 0.001). CONCLUSION: There is a significant risk for thromboembolism in patients referred for ablation of typical atrial flutter who have not been appropriately anticoagulated.

Anticoagulants↗
PubMed2005

Sinus node dysfunction concomitant with Brugada syndrome.

BACKGROUND: A genetic correlation between Brugada syndrome (BS) and sinus node dysfunction (SND) has been proposed, although the clinical and electrophysiologic characteristics of this concomitant condition are unknown. METHODS AND RESULTS: The study comprised 5 patients with symptomatic BS (4 with spontaneous episodes of ventricular fibrillation (VF) and 1 with syncope) of whom 3 had a documented sinus pause > 3 s (a 42- and 62-year-old man, and a 49-year-old woman). Only 1 of them had a family history of sudden death; 2 of them had also had an episode of atrial fibrillation or flutter. Electrophysiologic study demonstrated prolonged sinus node recovery time in 2 patients (2.6 s and > 5 s), in whom a cardiac pacemaker had been implanted before the diagnosis of BS was made after episodes of VF. Finally, all 3 patients received an implantable cardioverter defibrillator, including 2 upgrades from pacemaker. CONCLUSIONS: SND is not a rare concomitant disorder in BS and there is a possible genetic connection.

Adult↗
PubMed1994

Initial experience with mode switching in a dual sensor, dual chamber pacemaker in patients with paroxysmal atrial tachyarrhythmias.

Mode switching algorithms have been developed to avoid tracking of atrial fibrillation (AF) or flutter (AFL) during DDD(R) pacing. Upon recognition of AF or AFL, the mode is switched to a nontracking, sensor driven mode. The Vitatron Diamond model 800 pacemaker does this on a beat-to-beat basis. Atrial events occurring within a "physiological range" (+/- 15 beats/min) calculated from a running average of the atrial rate are tracked. When atrial events are not tracked the escape interval is either determined by the sensor(s) or by a fallback algorithm thereby preventing large increases in V-V interval during mode switching. Loss of atrioventricular (AV) synchrony by atrial premature beats and after an episode of AF or AFL is prevented by atrial synchronization pulses (ASP), which are delivered after a safe interval (timed out from the sensed premature atrial event) has expired and before delivery of the next ventricular stimulus. We implanted 26 such devices in 18 men and 8 women with symptomatic second- or third-degree AV block and paroxysmal AF or AFL. Their ages ranged from 18-84 years (mean 60), and the follow-up ranged from 2-13 months (mean 8). During pacemaker check-up, exercise testing or 24-hour Holter monitoring one or more episodes of mode switching was documented in 8 patients. In these 8 patients a smooth transition (ventricular rate) from sinus rhythm to AF or AFL was documented on one or more occasions, without inappropriate increase in ventricular rate in the DDDR mode. None of the patients complained of palpitations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Nonpharmacologic approaches to the treatment of atrial fibrillation and atrial flutter.

The high prevalence of atrial fibrillation, the associated morbidity and mortality, the absence of safe and effective drug therapy, and an increased understanding of the pathophysiologic basis of atrial fibrillation and flutter have collectively led to the development of novel nonpharmacologic treatments for the management of these arrhythmias, including the CORRIDOR and MAZE surgical procedures, catheter-based ablation and modification of AV conduction, catheter-based ablation of atrial flutter and fibrillation, and internal atrial defibrillation. These surgical and catheter-based techniques offer potentially curative therapy while sparing the long-term risk of antiarrhythmic drug therapy. For patients with typical atrial flutter, catheter ablation affords to cure rate in excess of 70%. As technological innovations further facilitate identification and ablation of the critical isthmus in the floor of the right atrium, success rates should improve substantially. For patients with atrial fibrillation, AV junction ablation with implantation of a rate-responsive ventricular pacemaker should be considered palliative therapy, as should modification of AV junction conduction. The MAZE procedure offers very high cure rates, but because it currently involves open heart surgery, patient selection is critical. Catheter-based procedures emulating aspects of the MAZE procedure may one day offer cure rates comparable to those of the surgery itself, but additional research and technological development are necessary to further define and refine the minimal effective procedure, and then to facilitate the placement of contiguous, full-thickness lesions in precise three-dimensional configurations. In the interim, the implantable automatic atrial defibrillator may offer a means for rapidly restoring sinus rhythm without the risks of long-term antiarrhythmic drug therapy.

Atrial Fibrillation↗
PubMed2006

Clinical evaluation of adverse effects during bepridil administration for atrial fibrillation and flutter.

BACKGROUND: Bepridil hydrochloride (Bpd) has attracted attention as an effective drug for atrial fibrillation (AF) and atrial flutter (AFL). However, serious adverse effects, including torsade de pointes (Tdp), have been reported. METHODS AND RESULTS: Adverse effects of Bpd requiring discontinuation of treatment were evaluated. Bpd was administered to 459 patients (361 males, 63+/-12 years old) comprising 378 AF and 81 AFL cases. Mean left ventricular ejection fraction and atrial dimension (LAD) were 66+/-11% and 40+/-6 mm, respectively. Adverse effects were observed in 19 patients (4%) during an average follow-up of 20 months. There was marked QT prolongation greater than 0.55 s in 13 patients, bradycardia less than 40 beats/min in 6 patients, dizziness and general fatigue in 1 patient each. In 4 of 13 patients with QT prolongation, Tdp occurred. The major triggering factors of Tdp were hypokalemia and sudden decrease in heart rate. There were no differences in the clinical backgrounds of the patients with and without Tdp other than LAD and age, which were larger and older in the patients with Tdp. CONCLUSION: Careful observation of serum potassium concentration and the ECG should always be done during Bpd administration, particularly in elderly patients.

Age Factors↗
PubMed1986

Transvenous catheter ablation of the His bundle in ventricular tachycardia.

The usefulness of transvenous catheter ablation of the His bundle in three patients with recurrent ventricular tachycardia (VT), in which the initiating mechanism was recognized during a rapid atrial rhythm, is reported. Tachycardia was refractory to conventional treatment and required transthoracic direct-current shocks in all patients. In patient No. 1 double tachycardia (atrial flutter and VT) was documented and VT was easily induced by rapid atrial pacing. In patients Nos. 2 and 3 initiation of VT during junctional reciprocating and atrial tachycardia, respectively, was observed. Interruption of the His bundle was performed by means of fulguration. Stable atrioventricular (AV) block was observed in patient No. 1 after the ablative procedure; patient No. 2 showed anterograde conduction over a posterior septal accessory pathway with no evidence of conduction over the normal conduction system in both the anterograde and retrograde directions. In patient No. 3, transient AV block was observed; AV conduction resumed 2 days later and the cardiac rhythm showed persistent ectopic atrial tachycardia with second-degree AV block. Patients Nos. 1 and 2 underwent pacemaker implantation, but patient No. 2 was not pacemaker dependent. After the procedure, VT no longer occurred in any of the patients (follow-up: 2 years, 5 months, and 6 months).

Aged↗
PubMed2006

Modern management of arrhythmias.

The specialist management of arrhythmias has changed significantly over the past decade. This article outlines current management strategies for atrial flutter and atrial fibrillation, with particular emphasis on curative strategies with catheter ablation and the recent data on rhythm compared with rate control strategies. The expanding role of catheter ablation in the treatment of a wide variety of supraventricular and ventricular arrhythmias is discussed. The current evidence for implantable cardioverter defibrillators in the prevention of sudden cardiac death is summarised. The article also highlights the increasing recognition of a number of inherited syndromes that predispose to sudden cardiac death (for example, Brugada and long QT syndromes).

Anti-Arrhythmia Agents↗