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PubMed1975

Atrial activity during exercise in patients with atrial flutter or atrial fibrillation.

The atrial activity was studied at rest and during exercise in 6 patients with atrial flutter and in 7 patients with atrial fibrillation. In the latter, a special recording technique was used which permitted identification of the f-waves. No increase in the frequency of the atrial waves was found. Thus the increase of the ventricular rate during work in patients with atrial flutter or atrial fibrillation seems to be caused by a change in the atrio-ventricular conduction.

Adult↗
PubMed1990

Clinical evaluation in therapy of patients with atrial fibrillation or flutter.

The weight of evidence clearly indicates that both atrial fibrillation and atrial flutter are due to a reentrant mechanism. Atrial fibrillation seems almost certainly due to multiple circulating reentrant wavelets of the leading circle type, whereas atrial flutter appears to be caused by single reentrant circuit located in the right atrium. The diagnosis of both atrial fibrillation and atrial flutter should always be possible using either old or new techniques. The interruption of atrial flutter should be possible using pacing or direct current cardioversion techniques, and the conversion of atrial fibrillation to sinus rhythm also is most often possible by direct current cardioversion or antiarrhythmic drug therapy. Long-term antiarrhythmic drug therapy to suppress recurrent atrial fibrillation and atrial flutter may be a problem, but availability of newer antiarrhythmic agents holds promise for finding an effective regimen. Catheter ablation techniques may be used to cause complete heart block in the treatment of either atrial fibrillation or atrial flutter when these rhythms cannot be satisfactorily suppressed and are associated with unacceptably rapid ventricular response rates. Finally, recent data suggest that atrial flutter may be successfully treated on a chronic basis with an antitachycardia pacing device, may be cured with catheter ablation techniques applied to a critical portion of the atrial flutter reentry circuit, and may be treated successfully with innovative surgical techniques. The latter is also true for atrial fibrillation.

Anti-Arrhythmia Agents↗
PubMed2004

Masquerade: a malignant arrhythmia masquerading as benign.

Pseudoatrial flutter has been reported to have benign causes, but this is the first report of a malignant arrhythmia presenting as a benign arrhythmia. An 82 year old patient presented with ventricular tachycardia and electrical artefact appearing as atrial flutter. In this case, comparing the morphology of the QRS complexes in the rhythm strip with those in lead II showed the arrhythmia to be ventricular in origin and points to the importance of comparing all leads of the ECG before arriving at a diagnosis.

Aged↗
PubMed2004

Heart failure and sudden death in patients with tachycardia-induced cardiomyopathy and recurrent tachycardia.

BACKGROUND: Tachycardia-induced cardiomyopathy is a reversible cause of heart failure. We hypothesized that although left ventricular ejection fraction measurements normalize after heart rate or rhythm control in patients with tachycardia-induced cardiomyopathy, recurrent tachycardia may have abrupt and deleterious consequences. METHODS AND RESULTS: Patients with tachycardia-induced cardiomyopathy that developed over years were evaluated and treated. Tachycardia episodes and outcomes were assessed. Twenty-four patients were identified. All had NYHA functional class III heart failure or greater on presentation. One third were heart transplant candidates. There were 17 men and 7 women with a mean age of 46+/-16 years and mean left ventricular ejection fraction of 0.26+/-0.09 at the index visit. The cause was atrial fibrillation (n=13), atrial flutter (n=4), atrial tachycardia (n=3), idiopathic ventricular tachycardia (n=1), permanent junctional reciprocating tachycardia (n=2), and bigeminal ventricular premature contractions (n=1). Within 6 months of rate control or correction of the rhythm, left ventricular ejection fraction improved or normalized and symptoms abated in all. Five patients had tachycardia recur. In these patients, left ventricular ejection fraction dropped precipitously and heart failure ensued within 6 months, even though the initial impairment took years. Rate control eliminated heart failure and improved or normalized ejection fraction in 6 months. Three of 24 patients died suddenly and unexpectedly. CONCLUSIONS: Tachycardia-induced cardiomyopathy develops slowly and appears reversible by left ventricular ejection fraction improvement, but recurrent tachycardia causes rapid decline in left ventricular function and development of heart failure. Sudden death is possible.

Adult↗
PubMed2000

Esmolol versus diltiazem in the treatment of postoperative atrial fibrillation/atrial flutter after open heart surgery.

BACKGROUND: Supraventricular tachyarrhythmias are common after open heart surgery. Possible causative factors for these arrhythmias include operative trauma, atrial ischemia, electrolyte imbalances, pericardial irritation, and excess catecholamines. Two agents commonly used to control ventricular rate in atrial fibrillation or atrial flutter (AF/AFL) are beta-blockers and calcium channel blockers. METHODS AND RESULTS: This randomized study was designed to compare the safety and efficacy of intravenous diltiazem versus intravenous esmolol in patients with postoperative AF/AFL after coronary bypass surgery and/or valve replacement surgery. A comparative cost analysis was also performed. Thirty patients received either esmolol (n = 15) or diltiazem (n = 15) for AF/AFL. During the first 6 hours of treatment, 66.6% of esmolol-treated patients converted to sinus rhythm compared with 13.3% of the diltiazem-treated patients (P <.05). At 24 hours, 66.6% of the diltiazem group converted to SR compared with 80% of the esmolol group (not significant). Drug-induced side effects, time to rate control (<90 beats/min), number of patients requiring cardioversion, and length of hospitalization were similar for the two groups. The drug cost/successfully treated patient for esmolol versus diltiazem was $254 versus $437 at 6 hours and $529 versus $262 at 24 hours. CONCLUSIONS: Although this is a small study, it suggests that esmolol is more effective in converting patients to normal sinus rhythm than diltiazem during the initial dosing period. No differences in conversion rates were observed between the two groups after 24 hours. Additional studies are needed to confirm whether esmolol is the initial drug of choice in patients with postoperative AF/AFL after coronary bypass surgery.

Adrenergic beta-Antagonists↗
PubMed1995

[Sedation and anesthesia in dogs and cats with cardiovascular disease. II. Anesthesia planning with respect to pathophysiology, heart arrhythmia].

The purpose of this study was to review the incidence of cardiac arrhythmias in 137 anesthetized dogs and 13 anesthetized cats with congenital or acquired heart disease that were referred for correction of following procedures: patent ductus arteriosus (PDA-ligation, 28%), cardiac catheterization with angiogram and angioplasty (22%), pacemaker implantation (18%), exploratory lateral thoracotomy (8.7%), correction of right aortic arch (ring anomaly, 3.3%), correction of subvalvular aortic stenosis (2.7%), correction of PDA with coil in patients with mitral regurgitation and congestive heart failure (2%), pericardectomy and removal of heart base tumor (2%), and palliative surgery for ventricular septal defect (VSD, 0.7%). The anesthetic plan considered the risks of anesthesia based upon the pathophysiology of cardiac lesions and the anesthetic drug effects on the cardiovascular system. Recommendations are made for dogs with decreased cardiac contractility, cardiac disease with volume overload, cardiac disease with pressure overload, and pericardial tamponade. The percentages of animals and their associated cardiac arrhythmias after premedication and during and after anesthesia were: sinus bradycardia (15.3%), sinus tachycardia (3.3%), atrial flutter (0.7%), atrial fibrillation (0.7%), premature ventricular contraction (14%), and ventricular tachycardia (1.3%). Prompt therapy was given to a percentage of animals in order to control arrhythmia and support cardiovascular system, by using atropine or glycopyrrolate (14%), lidocaine (17.3%), and dopamine (14.7%).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1986

Intravenous adenosine in the treatment of supraventricular tachycardia: a dose-ranging study and interaction with dipyridamole.

Increasing doses of adenosine were given by rapid intravenous bolus to seven patients with spontaneous supraventricular tachycardia. Adenosine restored sinus rhythm in 10 of 14 episodes of narrow complex tachycardia. In those patients in whom adenosine produced only transient ventricular slowing the underlying rhythm was atrial flutter. Transient dyspnoea occurred in all patients. In two patients taking dipyridamole the mean dose of adenosine which produced an electrophysiologic effect (restoration of sinus rhythm or ventricular slowing to under 100 beats min-1) was 1.0 +/- 0.52 mg, whereas in other patients the mean dose was 8.8 +/- 2.6 mg, suggesting potentiation of the action of adenosine by dipyridamole.

Adenosine↗
PubMed1982

[Closed chest interruption of A-V conduction in the treatment of refractory supraventricular tachyarrhythmias. A clinical contribution].

The AA. describe a technique for interrupting the A-V conduction using a direct-current shock delivered from a cardioversion unit to the A-V junctional tissue by means of a conventional electrode-catheter. The method was used in 2 patients with refractory supraventricular tachycardias. After the procedure both patients received a programmable A-V sequential pacemaker. The first patient, with cardiomyopathy and intermittent W-P-W syndrome, had a 2-year history of iterative reciprocating tachycardia and occasional episodes of atrial flutter-fibrillation. The second patient, with coronary heart disease, had recurrent episodes of atrial flutter for at least 2 years. In patient 1 the shock caused a suprahisian first-degree block. Atrial pacing at 580 ms cycle length provoked a 2:1 block and ventricular pacing showed no retrograde conduction. The patient, who is not pacemaker-dependent, is now free from reciprocating tachycardia and, during atrial flutter-fibrillation episodes, the ventricular rate varies from 62 to 75 bpm. In patient 2 the shock caused a persistent complete A-V block and neither antegrade nor retrograde conduction was observed during atrial and ventricular pacing. During a long episode of atrial flutter, there was a complete A-V block with a ventricular rate between 40 and 48 bpm. The follow-up is 9 months in both patients. We conclude that the technique used, which does not require open heart surgery, can be effectively used in patients with disabling supraventricular tachyarrhythmias resistant to drug treatment.

Amiodarone↗
PubMed1975

[Pacemaker treatment of tachyarrhythmias by programmed rate-related interval stimulation(author's transl)].

Programmed rate-related interval stimulation proved to be a low-risk method when applied to 74 patients with drug-resistant ventricular tachycardia or runs of ventricular extrasystoles as precursors of tachycardia. Atrial flutter was converted to atrial filbrillation and sinus rhythm by atrial interval-related multiple stimulations. Tachycardias, which could not be terminated by simple or double stimulation, were successfully suppressed by sequential ventricular R-R related multiple stimulations. Rare-related stimulation has proved to be an alternative method of treating tachy-arrhythmias unresponsive to conventional means.

Aged↗
PubMed1994

Isolated congenital left ventricular diverticulum in an adult. A case report.

A sixty-three-year-old man presented himself with atrial flutter and congestive heart failure. Cardiac catheterization revealed that left ventricular diverticulum was located on the anterobasal wall with narrow connection to the left ventricular cavity. Coronary angiography revealed normal coronary arteries. The patient had been asymptomatic until adult life with no other thoracoabdominal or cardiac anomalies. This is an extremely rare finding in the adult population.

Atrial Flutter↗
PubMed1980

Response of atrial flutter to overdrive atrial pacing and intravenous disopyramide phosphate, singly and in combination.

Ten patients who suffered spontaneous paroxysms of atrial flutter were investigated by electrophysiological techniques. Two had overt Wolff-Parkinson-White syndrome; three Lown-Ganong-Levine syndrome; and one a concealed accessory atrioventricular connection. Atrial flutter was initiated, at study, by right atrial pacing and electrograms from the right atrium and coronary sinus were observed for at least five minutes to ensure stable flutter in both atria. Atrial flutter was terminated by 2.5 s or 5 s bursts of atrial pacing at rates 10, 50, or 100 beats/min faster than the intrinsic flutter rate in only two patients. Atrial flutter, which was reinitiated in two patients, was then treated with intravenous disopyramide phosphate, 2 mg/kg body weight, infused over five minutes. In all 10 patients the atrial rate slowed from a mean of 310 +/- 39 beats/min to 217 +/- 27 beats/min and atrial flutter terminated in one case. Though the mean ventricular rate fell from 161 +/- 52 beats/min to 156 +/- 45 beats/min the atrioventricular conduction ratio fell from 2.17 +/- 0.86 to 1.55 +/- 0.59 and four patients were left with symptomatically significant increases of ventricular rate. In seven of nine patients overdrive atrial pacing, repeated after disopryamide, resulted in the conversion of atrial flutter to sinus rhythm. In this study, overdrive atrial pacing and intravenous disopyramide, singly and in combination, terminated atrial flutter in nine of the 10 patients and it is suggested that this method may provide an effective alternative to direct current cardioversion.

Adult↗
PubMed2001

Multicenter experiences with a single lead electrode for dual chamber ICD systems.

Monitoring of atrial signals improves the accuracy in identifying supraventricular tachyarrhythmias to prevent inappropriate therapies in patients with implantable ICDs. Since difficulties due to the additional atrial lead were found in dual chamber ICD systems with two leads, the authors designed a single pass VDD lead for use with dual chamber ICDs. After a successful animal study, the prototype VDD lead (single coil defibrillation lead with two additional fractally coated rings for bipolar sensing in the atrium) was temporarily used in 30 patients during a German multicenter study. Atrial and ventricular signals were recorded during sinus rhythm (SR), atrial flutter, AF, and VT or VF. The implantation of the lead was successful in 27 of 30 patients. Mean atrial pacing threshold was 2.5 +/- 0.9 V/0.5 ms, mean atrial impedance was 213 +/- 31 ohms. Atrial amplitudes were greater during SR (2.7 +/- 1.6 mV) than during atrial flutter (1.46 +/- 0.3 mV, P < 0.05) or AF (0.93 +/- 0.37 mV, P < 0.01). During VF atrial "sinus" signals had significantly (P < 0.01) lower amplitudes (1.4 +/- 0.52 mV) than during SR. The mean ventricular sensing was 13.3 +/- 7.9 mV and mean ventricular impedance was 577 +/- 64 ohms. Defibrillation was successful with a 20-J shock in all patients. In addition, 99.6% of P waves could be detected in SR and 84.4% of flutter waves during atrial flutter. During AF, 56.6% of atrial signals could be detected without modification of the signal amplifier. In conclusion, a new designed VDD dual chamber lead provides stable detection of atrial and ventricular signals during SR and atrial flutter. Reliable detection of atrial signals is possible without modification of the ICD amplifier.

Aged↗
PubMed1993

[The clinico-electrocardiographic prodromes of fatal cardiac arrhythmias in patients with an acute myocardial infarct].

The authors made a retrospective analysis of case histories of 201 patients who had died of fatal cardiac arrhythmias. The predictors of their death were ventricular fibrillation in 133 (66.2%) patients, asystole in 68 (32.8%), electromechanical dissociation in 2 (1%). Terminal sinus tachycardia, atrial fibrillation and flutter, the second-third degree atrioventricular block, the third-fifth grade ventricular extrasystole were the most common clinical and electrocardiographic prodromes of ventricular fibrillation. In the development of the latter, various mixed disturbances of cardiac rhythm and conduction in combination with prolonged Q-T interval were of more unfavorable value. Asystole was more frequently preceded by the second-third degree atrioventricular block, complete bundle branch block, third-fifth grade ventricular extrasystole, atrial fibrillation and flutter, and various mixed disturbances of cardiac rhythm and conduction. Cardiac arrhythmias and conduction disturbance with prolonged Q-T interval were found to be precursors of asystole in 84.8%.

Adult↗
PubMed1975

[Four years of clinical experience with the cardio-eurhythmic action of verapamil in intravenous administration].

Personal clinical experience using Verapamil intravenously in 200 patients with a number of arrhythmia conditions is reported. The effectiveness of the drug in controlling supraventricular paroxysmal tachycardia and high ventricular frequency atrial fibrillation in particular is pointed out. Good results were also obtained in atrial flutter, in sinus tachycardia, in extrasystole conditions and, at times, in ventricular paroxysmal tachycardia. Clinical experience limits contraindications to atrioventricular block, severe shock, excessive digitalization, and the associated use of beta block substances.

Arrhythmias, Cardiac↗
PubMed1992

Dissociation of atrioventricular conduction and refractoriness following application of radiofrequency energy to the canine atrioventricular node: acute and chronic observations.

The electrophysiology of AV nodal modification induced by radiofrequency energy (n = 5) or a sham procedure (n = 5) was studied in ten dogs. The five dogs that received radiofrequency energy had an AH prolongation > 100% from baseline values and this prolongation persisted throughout the 2-month study. The AV nodal functional refractory period was prolonged only acutely. These data indicate a dissociation between the effects on AV nodal conduction and refractoriness that was induced by this procedure. The five sham treated controls showed no acute or chronic electrophysiological changes. In the dogs that received radiofrequency energy, there was fibrosis of the approaches to the AV node and the region of the AV node itself. It is concluded that chronic modification of AV nodal conduction without concomitant changes in refractoriness can be induced by radiofrequency energy delivered in the proximal portion of the AV node. It would be anticipated that this procedure would not decrease the ventricular response to atrial fibrillation or flutter, may be effective in preventing AV nodal reentrant tachycardia by interfering with conduction either in the AV node or perinodal region. Since the AV node itself suffers at least moderate pathological damage, there may be an appreciable incidence of the late development of complete heart block after this procedure.

Animals↗
PubMed1999

Electrophysiological and antiarrhythmic effects of the atrial selective 5-HT(4) receptor antagonist RS-100302 in experimental atrial flutter and fibrillation.

BACKGROUND: Stimulation of 5-HT(4) receptors increases atrial chronotropic and inotropic responses. Whether other electrophysiological effects are produced is unknown. In humans and swine, 5-HT(4) receptors are present only in atrium. Therefore, the effects of a novel 5-HT(4) receptor antagonist, RS-100302, and the partial agonist cisapride on atrial flutter and fibrillation induced in swine were studied to delineate the role of the 5-HT(4) receptor in modulating atrial electrophysiological properties and the antiarrhythmic potential of RS-100302. METHODS AND RESULTS: In 17 anesthetized, open-chest, juvenile pigs, atrial flutter or fibrillation was induced by rapid right atrial pacing with or without a right atrial free wall crush injury, respectively. Atrial effective refractory period (ERP), conduction velocity, wavelength, and dispersion of refractoriness were determined during programmed stimulation via a 56-electrode mapping plaque sutured to the right atrial free wall. Ventricular electrophysiological parameters were also measured. All electrophysiological parameters were measured at baseline and after infusion of RS-100302 and cisapride. In the atrium, RS-100302 prolonged mean ERP (115+/-8 versus 146+/-7 ms, P<0.01) and wavelength (8.3+/-0.9 versus 9.9+/-0.8 cm, P<0.01), reduced dispersion of ERP (15+/-5 versus 8+/-1 ms, P<0.01), and minimally slowed conduction velocity (72+/-4 versus 67+/-5 cm/s, P<0.01). These effects were all partially reversed by cisapride. RS-100302 produced no ventricular electrophysiological effects. RS-100302 terminated atrial flutter in 6 of 8 animals and atrial fibrillation in 8 of 9 animals and prevented reinduction of sustained tachycardia in all animals. CONCLUSIONS: The electrophysiological profile of RS-100302 suggests that it may have atrial antiarrhythmic potential without producing ventricular proarrhythmic effects.

Animals↗
PubMed2002

Alternating duration of ventricular paced cycles during automatic mode switching of a DDDR pacemaker.

This report describes the response of a Vitatron Diamond II DDDR pacemaker to atrial flutter in a patient who developed alternating duration of the ventricular paced cycles during automatic mode switching to the DDIR mode. This device activates mode switching on a beat-to-beat basis and exhibits "ventricular hysteresis" in the DDIR mode when an atrial sensed event is detected during the period corresponding with the AV delay prior to emission of the ventricular stimulus. Such unusual behavior must not be interpreted as pacemaker malfunction.

Atrial Flutter↗