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PubMed1992

[Accidental ventricular fibrillation during transesophageal atrial overdrive].

Transesophageal atrial overdrive stimulation is a widely used technique for the interruption of atrial flutter and supraventricular tachyarrhythmias. We describe a case of 60 year old man with a previous myocardial infarction, suffering from angina during effort after aortocoronary bypass who presented several episodes of atrial flutter treated with success by transesophageal atrial overdrive stimulation using swallowing electrodes. During the treatment of the last episode of atrial flutter, after a 5 s burst at 300 b/min ventricular fibrillation occurred and was promptly interrupted by DC shock. This is the first case in our experience and probably the first report of ventricular fibrillation induced by swallowing electrodes. Possible mechanisms as pharmacological interactions, accidental ventricular stimulation, etc, are discussed. In conclusion, even though the risk of dangerous arrhythmias is very low, transesophageal atrial overdrive stimulation should be performed by experts in an equipped room.

Angina Pectoris↗
PubMed2007

Antithrombotic and interventional treatment options in cardioembolic transient ischaemic attack and ischaemic stroke.

Peer-reviewed data pertaining to anti-thrombotic and interventional therapy for transient ischaemic attack (TIA) or ischaemic stroke patients with non-valvular atrial fibrillation, atrial flutter, interatrial septal abnormalities, or left ventricular thrombus were reviewed. Long-term oral anticoagulant therapy with warfarin is the treatment of choice for secondary stroke prevention following TIA or minor ischaemic stroke in association with persistent or paroxysmal non-valvular atrial fibrillation or atrial flutter. If warfarin is contraindicated, long-term aspirin is a safe, but much less effective alternative treatment option in this subgroup of patients with cerebrovascular disease. Management of young patients with TIA or stroke in association with an interatrial septal defect is controversial. Various treatment options are outlined, but readers are encouraged to include these patients in one of the ongoing randomised clinical trials in this area. It is reasonable to consider empirical anticoagulation in patients with TIA or ischaemic stroke in association with left ventricular thrombus formation following myocardial infarction or in association with idiopathic dilated cardiomyopathy. If warfarin is prescribed, one should aim for a target international normalised ratio of 2.5 (range 2-3) to achieve the best balance between adequate secondary prevention of cardioembolic events and the risk of major haemorrhagic complications.

Age Factors↗
PubMedDate not supplied

Proarrhythmic effects of class Ic drugs.

Three cases managed with class Ic antiarrhythmic drugs but with subsequent aggravation of arrhythmias are reported herein. A 58-year-old man given 300 mg of flecainide for atrial flutter developed sinus arrest and transient ventricular fibrillation. A 42-year-old man with a postoperative condition of tetralogy of Fallot who received 300-mg doses of flecainide for sustained ventricular tachycardia had spontaneous sustained ventricular tachycardia. A 74-year-old man given 150 mg of propafenone for atrial tachycardia developed sustained ventricular tachycardia. The present cases illustrate that class Ic drugs may exacerbate ventricular arrhythmias, and their use may reveal concealed sinus node dysfunction. This may be due to marked slowing of conduction and prolonged ventricular refractoriness, which are characteristic of the class Ic drugs; also, it is probable that the patients' underlying cardiac conditions served as contributing factors.

Adult↗
PubMed1981

Paroxysmal atrial flutter and fibrillation associated with preexcitation syndrome: treatment with ajmaline.

Ajmaline was administered intravenously to six patients with the Wolff-Parkinson-White syndrome for the acute management of paroxysmal atrial flutter (three patients) or fibrillation (three patients) with a fast ventricular response (over the accessory pathway). Ajmaline increased refractoriness in the accessory pathway in all three patients with atrial flutter and stopped the flutter in one. The drug completely abolished preexcitation in two of the three patients with atrial fibrillation, decreasing the means ventricular rate of 240 and 300 beats/min to 110 and 180 beats/min, respectively. In the third patient with atrial fibrillation, ajmaline increased refractoriness over the accessory pathway, decreasing the mean ventricular rate of 300 beats/min to 160 beats/min. In two patients ajmaline was continued as an intravenous maintenance infusion until sinus rhythm was restored. It is concluded that ajmaline is an effective drug for the acute management of atrial flutter or fibrillation with a fast ventricular response in patients with the Wolff-Parkinson-White syndrome.

Adult↗
PubMed2004

Novel pore mutation in SCN5A manifests as a spectrum of phenotypes ranging from atrial flutter, conduction disease, and Brugada syndrome to sudden cardiac death.

OBJECTIVES: The purpose of this study was to determine the clinical and biophysical characteristics of a novel SCN5A mutation. BACKGROUND: Brugada syndrome and isolated cardiac conduction defect have been linked to SCN5A mutations. METHODS: Eleven members of a western European family underwent electrophysiologic investigations and mutation analysis of the SCN5A gene. Wild-type and mutant SCN5A channels were expressed in HEK293 cells, and whole cell currents were studied using patch clamp procedures. RESULTS: A novel mutation, R376H, in the first pore segment of SCN5A variably causes Brugada syndrome and/or conduction disease in a single family. Biophysical analysis demonstrated a significant current reduction for the mutant, a pathophysiologic profile consistent with Brugada syndrome and isolated cardiac conduction defect. Among 11 family members, 9 were carriers of the mutation. The proband's initial presentation was a saddleback Brugada ECG, atrial flutter, and diffuse conduction disturbances. He had no inducible ventricular arrhythmias but experienced sudden cardiac death. His brother was affected by atrial flutter and had a clear conduction disorder, but he did not display baseline or evocable ECG signs of Brugada syndrome. He received an implantable cardioverter-defibrillator that delivered one appropriate shock after 1 year of follow-up. The phenotype in the family members was highly variable and ranged from noninducible and inducible asymptomatic carriers of the mutations to isolated conduction disease and to symptomatic Brugada syndrome. CONCLUSIONS: We describe the functional characterization of a novel SCN5A pore mutation, R376H, with variable clinical expression in the same family. Differentiating between electrophysiologic entities (Brugada syndrome-isolated cardiac conduction defect) is more challenging. Recognition of factors modifying the clinical presentation may be important for clinical decision making.

Adolescent↗
PubMed1975

Verapamil and the heart: Pharmacological and Therapeutic Considerations.

Verapamil is a new anti-anginal and anti-arrhythmic drug whose pharmacological actions can be related to its specific blocking effect on the transmembrane transport of calcium ions. Intravenous verapamil slows the ventricular rate in atrial fibrillation and flutter with an occasional patient reverting to sinus rhythm. The drug promptly terminates most cases of paroxysmal supraventricular tachycardias. It is likely to become the initial agent of choice in the acute treatment of this arrhythmia. Verapamil is not effective in ventricular tachycardia or in atrial fibrillation complicating the WPW syndrome. Few side effects are encountered following intravenous verapamil expecially when the drug is given slowly. Verapamil is also effective in angina in a dose of 120mg tds orally. Little is known of the metabolism and pharmacokinetic of verapamil but the available experience in arrhythmias clearly justifies further study.

Angina Pectoris↗
PubMed1997

Arrhythmia and mortality after the Mustard procedure: a 30-year single-center experience.

OBJECTIVES: Our purpose was to assess the risk factors for late mortality, loss of sinus rhythm and atrial flutter after the Mustard operation. BACKGROUND: The Mustard operation provides correction of cyanosis with low surgical risk in transposition of the great vessels. However, right ventricular failure, loss of sinus rhythm, atrial flutter and death are frequent long-term complications. METHODS: Records of 534 children who underwent the Mustard operation at a single center since 1962 were reviewed for demographic, anatomic, electrocardiographic and physiologic predictors and outcomes. RESULTS: There were 52 early deaths (9.7%). Survival analysis was undertaken for 478 early survivors with a mean follow-up interval of 11.6 +/- 7.2 years. There were 77 late deaths (16.1%), with sudden death (n = 31) the most frequent cause. Survival estimates were 89% at 5 years and 76% at 20 years of age. Risk factors were an earlier date of operation, operative period arrhythmia and an associated ventricular septal defect. Risk (hazard) of late death declined in the first decade, with further peaks in the second decade. Sinus rhythm was present in 77% at 5 years and 40% at 20 years. Loss of sinus rhythm was associated with previous septectomy, postoperative bradycardia and late atrial flutter. Freedom from atrial flutter was 92% at 5 years and 73% at 20 years of age. Risk factors for atrial flutter were the occurrence of perioperative bradyarrhythmia, reoperation and loss of sinus rhythm during follow-up. Risk of atrial flutter demonstrates a late increase. CONCLUSIONS: Ongoing loss of sinus rhythm and late peaks in the risk of atrial flutter and death necessitate continued follow-up.

Arrhythmias, Cardiac↗
PubMed1978

[2 or 3 level blocks in the Tawara node during atrial tachycardia].

In atrial flutter (or paroxysmal atrial tachycardia), the ventricular response is dependant on the passage through 3 superposed zones of conduction in the Tawara node, the zone of decremential conduction being the central zone N. When the ventricular response is between half and a quarter of the atrial rate there are two possible explanations: type B alternate Wenckebach period (mobitz I block in the central zone N, 2/1 block at the nodo-ventricular junction) or type A alternate Wenckebach period (Mobitz I block in the central zone N and 2/1 block at the atrio-nodal junction). These two responses may alternate in the same patient depending on the drug therapy or vagal activity due to a phenomenon similar to the "GAP" phenomenon. Inexactitudes in the working out of the arithmetic formulae may easily be explained by a certain degree of concealed conduction of blocked activation in one zone or more rarely by hisian extrasystoles. Type A alternate Wenckebach periods are always easier to construct than type B. Perfect 3/1 atrial flutter can only be explained by a type B alternate Wenckebach period with a 3/2 period with a 3/2 period in the N zone and a 2/1 block in the NH zone. When the ventricular rhythm is permanently very slow or when the RR intervals are greater than four times the atrial cycle, 3 zones of block are usually at issue (the third being located in the inferior part of the node or superior part of the bundle of His). Examples of 5/1, 6/1 flutter are thereby analysed. Rapid atrial pacing after termination of the atrial arrhythmia allows a better analysis of its mechanism and the successive reproduction of conduction defects in each zone of block.

Atrioventricular Node↗
PubMed2000

[Non-contact mapping: a simultaneous spatial detection in the diagnosis of arrhythmias].

The non-contact mapping device (Ensite, Endocardial Solution) enables a simultaneous, spatial detection of the myocardial depolarization. An isopotential map is visualized in the 3D reconstruction of the cardiac chamber. The analysis of focal premature beats, of unstable arrhythmias and of macro reentry mechanisms is possible. The current article demonstrates the use of the non-contact mapping device for analysis and ablation of atrial flutter, premature beat associated atrial fibrillation and of ventricular tachycardias.

Arrhythmias, Cardiac↗
PubMed1996

[Complications of radiofrequency ablation: A French experience. Le Groupe de Rythmologie de la Société Francaise de Cardiologie].

The multiplication of the indication of radiofrequency for curative or palliative treatment of cardiac arrhythmias motivated the Rhythmology Working Group to set up a register of the complications related to this technique. Five thousand six hundred and eighty nine cases from 19 French centres were recensed up to March 1996. There were 2765 ablations of a Bundle of Kent, 1579 ablations of slow pathways, 621 ablations of atrial flutter, 25 ablations of atrial tachycardia, 200 ablations of ventricular tachycardia and 499 ablations of the Bundle of His. Eighty five complications (1.5%), two of which were lethal (0.04%), were reported. The complications of catheterization (27% of all complications) were pneumothorax (n = 6), arterial thrombosis (n = 3), venous thrombosis with and without pulmonary embolism (n = 8), haematoma (n = 2), femoral pseudoaneurysm (n = 1), arteriovenous fistula (n = 1), infection (n = 2), valvular disease with mitral or aortic regurgitation (n = 3). Other complications were specific to the ablation itself:skin burns at the site of the patch (n = 2), ventricular fibrillation (n = 3), coronary events (n = 2), vascular events (n = 2), tamponade (n = 12), one of which was lethal, and transient or permanent complete atrioventricular block (n = 32) complicating ablation of antero and posteroseptal accessory pathways, atrial flutter and slow intranodal reentry pathways (n = 25). One lethal cerebral haemorrhage occurred the day after an ablation procedure. It was not possible to identify a predictive factor in these complications apart from the operator's experience. There were 1.4% of complications in Kent bundle ablations, 1.9% in ablation of slow pathway, 0.6% in atrial flutter and tachycardia, 1.5% for ventricular tachycardia and 1.9% for Bundle of His. The authors concluded that the prevalence of complications, though small with minimal risk of mortality (0.04%), should incite physicians to reserve this technique for symptomatic patients or those with potentially lethal arrhythmias.

Arrhythmias, Cardiac↗
PubMed1990

Clinical experience with a new software-based antitachycardia pacemaker for recurrent supraventricular and ventricular tachycardias.

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

Adult↗
PubMed1994

[Results of oral sotalol therapy in children with supraventricular and ventricular arrhythmias].

Experience with oral sotalol, a beta-blocker with class III-antiarrhythmic properties, is limited in the pediatric population. Sotalol was administered to 32 patients with a mean age of 8.7 years (range 1 day-19.9 years). Mean dosage was 4.6 (1.5-9.4) mg/kg or 122.1 (52-306) mg/m2, respectively. In 27/32 patients, at least 1 antiarrhythmic agent had failed to control the dysrhythmia before sotalol was started. Cardiac diagnoses included normal heart (n = 16), status after correction of congenital heart disease (n = 13), and cardiomyopathy (n = 3). Success (based on symptoms and 24-h electrocardiogram) was achieved in 16/18 patients with reentry supraventricular tachycardia, in 7/8 patients with atrial flutter, and in 4/6 patients with ventricular tachycardia. During a mean follow-up of 15.6 (2-78) months, proarrhythmia occurred in five (16%) patients (symptomatic bradycardia n = 2, QT-prolongation and ventricular extrasystoles n = 1, ventricular extrasystoles n = 1, 2 degrees av-block n = 1), requiring dosage reduction (n = 3), cessation of treatment (n = 1) and pacemaker implantation in one patient, respectively. Symptomatic hypotension was noted in two patients, in whom therapy had to be stopped. Sotalol was a very effective agent for the treatment of various pediatric cardiac dysrhythmias. However, incidence of proarrhythmic effects warrants close electrocardiographic monitoring.

Administration, Oral↗
PubMed2003

Oral loading single dose flecainide for pharmacological cardioversion of recent-onset atrial fibrillation.

The efficacy and safety of the single oral loading dose of flecainide for cardioversion of recent-onset atrial fibrillation was examined by reviewing the trials on the subject identified through a comprehensive literature search. Most of the trials used a single dose of 300 mg for oral loading. The success rate ranged from 57 to 68% at 2-4 h and 75 to 91% at 8 h after drug administration. The conversion time ranged from 110+/-82 to 190+/-147 min, depending on the duration of observation after drug administration, which in most trials was of 8 h. Single oral loading regimen of flecainide was significantly more efficacious than placebo, and was as efficacious as the single oral loading regimen of propafenone. Both the single oral loading and the intravenous loading regimens of flecainide were equally efficacious but the intravenous regimen resulted in an earlier conversion. Adverse effects reported were mild non-cardiac side effects, reversible QRS complex widening, transient arrhythmias and left ventricular decompensation. The transient arrhythmias were chiefly at the time of conversion and included appearance of atrial flutter and sinus pauses. No life-threatening ventricular arrhythmia or death was reported. The single dose oral loading regimen of flecainide appears to be effective for cardioversion of recent-onset atrial fibrillation with a relatively rapid effect within 2-4 h, and is free of serious complications in patients without structural heart disease. Patients with substantial structural heart disease were excluded from most of the trials.

Administration, Oral↗
PubMed2005

Neonatal cholestasis associated with fetal arrhythmia.

We evaluated the consequence of different types of fetal arrhythmia in the development of neonatal cholestasis. The charts of 38 children born at St. Justine Hospital between 1993 and 2001 with sustained and hemodynamically significant fetal arrhythmias were studied: 19 with supraventricular tachycardia, 14 with atrial flutter, and 5 with atrio-ventricular (AV) block. Six of these 38 children presented with cholestasis. The average duration of arrhythmia was 15.7 days in the noncholestatic group, compared with 40.3 days in the cholestatic group ( P <.05). The three infants with supraventricular tachycardia who developed cholestasis survived and resolved their cholestasis, whereas 2 of 3 infants with AV block died. No infant with atrial flutter developed cholestasis. We conclude that newborns who developed tachyarrhythmia during their fetal life can show transient neonatal cholestasis. In patients with AV block, severe and irreversible liver failure could be observed. In addition, extensive collapse of the stroma and the absence of hepatocytes (foie vide) also were observed in a patient with anti-Ro antibodies.

Arrhythmias, Cardiac↗
PubMed1996

[Exogenous adenosine as an anti-arrhythmia agent].

Adenosine has potent cardiac electrophysiologic effects including a negative chronotropic action on the sinus node and a predominant negative dromotropic action on the AV node. The latter property has mainly led to the use of adenosine as antiarrhythmic agent for the acute management of paroxysmal supraventricular tachycardia (PSVT) mediated by a reentrant mechanism involving the AV node. The effects of adenosine are dose-dependent and of very short duration since the half-life is less than 10s. The efficacy rates for termination of AV reentrant tachycardias were found to be 35% with 3 mg, 60-70% with 6 mg, 80% with 9 mg, and 90-95% with 12 mg adenosine. The AV nodal depressant effects of adenosine have also been used for determining the mechanism of wide QRS tachycardias for differentiating supraventricular tachyarrhythmias with aberrant conduction from ventricular tachycardia. Adenosine either terminates or slows almost all types of supraventricular tachyarrhythmias or it leads to unmasking of the underlying mechanism such as atrial flutter with aberrant conduction. One form of ventricular tachycardia, the idiopathic type originating from the right ventricular outflow tract can usually be terminated with adenosine due to its cAMP-mediated mechanism. Adenosine is helpful to detect or to increase preexcitation which is important for planning a catheter ablation procedure since the preexcitation pattern allows to localize the accessory pathway. Since the action of adenosine usually does not alter the accessory pathway conduction it is also useful for control ablation efficacy noninvasively in terms of antegrade conduction and during ventricular pacing for the retrograde conduction. Further evaluation and research is necessary for better understanding of adenosine action on the human atrial electrophysiology since it provokes atrial fibrillation in some patients, and of adenosine action on the different pathways in AV nodal reentrant tachycardias and some accessory pathways with decremental (AV nodal-like) conduction properties.

Adenosine↗