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PubMed1981

The mechanism of flutter electrical alternans.

We have had the opportunity to observe the occurrence of flutter electrical alternans in which two distinct populations of flutter waves are present and which alternate in 1:1 and 2:1 patterns. The flutter alternans whether 2: or 3:1, was concordant with the pattern of preceding ventricular conduction (ventriculophasic variation). This concordance occurred reproducibly and remained consistent. Our example of flutter alternans probably represents mechanical artefact caused by catheter movement during ventricular mechanical systole. We reproduced this pattern consistently at a slower rate during coronary sinus pacing. These findings appear to suggest an explanation for certain types of so-called atrial flutter electrical alternans.

Atrial Flutter↗

PubMed1996

Pacing therapy for atrial tachyarrhythmias.

The use of pacing techniques for the treatment of atrial tachyarrhythmias has been advocated for more than 30 years. Although it has played a beneficial role in the management of paroxysmal supraventricular tachycardia (PSVT) in drug-refractory patients, tachycardia acceleration and development of atrial fibrillation has been the major drawback. With the availability of radiofrequency catheter ablation therapy, the use of implantable antitachycardia devices for PSVT is currently negligible. From retrospective and small control studies it has been shown that atrial or dual-chamber pacing in patients with sick sinus syndrome has been associated with a lower incidence of paroxysmal atrial flutter or fibrillation than in those who received a ventricular pacemaker. Furthermore, recent studies have reported the potential benefit of reducing frequency of paroxysmal atrial flutter and fibrillation with multisite atrial pacing. As a result, there is a resurgence of research interest in antitachycardia pacing for prevention of atrial tachyarrhythmias. This paper briefly describes the basic aspects of antitachycardia pacing, reviews the data on the use of implantable antitachycardia devices for PSVT and the selection of patients, and assesses the current status of research on atrial pacing for prevention of paroxysmal atrial flutter and fibrillation.

Atrial Flutter↗

PubMed2003

[Ventricular fibrillation induction by transesophageal stimulation in a patient with valvular heart disease].

Rapid atrial transesophageal stimulation is currently used to stop atrial flutter or tachycardia. We report a case complicated of ventricular fibrillation. It is possible to pace the ventricles by transesophageal stimulation in 2-10% of cases. The ventricular stimulation might be dangerous in patients with heart disease. Therefore, transesophageal stimulation must be performed in specialized environment.

Aged↗

PubMed1976

[Treatment of rhythm disorders by fenoxedil hydrochloride].

Fenoxedil chlorhydrate (FC), which is used as a treatment for cerebral circulatory failure and peripheral vascular disease, has been given to 100 patients with a cardiac arrhythmia: atrial fibrillation (78 cases), atrial flutter (4 cases), atrial tachysystole (2 cases), ventricular extrasystoles (12 cases), and supraventricular extrasystoles (4 cases). FC has been prescribed alone, or as a complement to current anticoagulant or digitalis treatment; combination with prenylamine, amiodarone, dysopyramide or a drug of the quinidine group must always be avoided, and the potassium level checked and corrected if necessary before treatment. In 78 cases of atrial fibrillation, the authors found that sinus rhythm was restored in 58 (74.4%); four cases of flutter were restored, and one case out of two of atrial tachycardia. In case of supraventricular and ventricular extrasystoles the results are less clear, and merit a further study with a larger number of cases. The electrocardiographic disorders encountered in this series have been evaluated: lenghthening of the QT interval, disorders of atrioventricular conduction, sinus inhibition. They were either produced by or aggravated by the FC. No cases of axis deviation were encountered. The authors make mention of the complications observed by other authors, but draw a distinction between the prescription of FC in cases of cerebral vascular insufficiency, without previous knowledge of the exact cardiac status of the patient (otherwise there is a risk of severe accidents), and the use of FC in cases of arrhythmia which have undergone full assessment before the drug is used. According to this study, FC appears to be a very effective anti-arrhythmic agent, but its use demands very rigorous clinical and electrocardiographic supervision.

Anti-Arrhythmia Agents↗

PubMed1987

Adenosine: a clinical experience and comparison with verapamil for the termination of supraventricular tachycardias.

The efficacy and side-effects of adenosine for treatment of supraventricular arrhythmias were compared to verapamil therapy in patients presenting to the emergency room. Clinical variables and the time interval from the initiation of treatment to the termination of the supraventricular tachycardia, as well as the time from the initial effective dose of medication to the termination of supraventricular tachycardia were compared for adenosine and verapamil. Adenosine was given to a total of 44 patients, 16 patients in the electrophysiology laboratory, and 28 patients in the emergency room for evaluation and termination of their tachycardia. In the electrophysiology laboratory, 7 patients had AV node reentry, 5 had Wolff-Parkinson-White syndrome, 2 of whom had atrial flutter and fibrillation but no bypass tract reentry, 1 had concealed bypass tract reentry, 1 had Lown-Ganong-Levine syndrome, 1 had intraatrial reentry, and 1 had an automatic atrial tachycardia. Twenty-five patients received adenosine in the emergency room and 3 patients in the hospital for 31 episodes of supraventricular arrhythmias. In the emergency room, 11 patients had supraventricular tachycardia due to AV node reentry, 3 had Wolff-Parkinson-White syndrome, 6 had atrial flutter or intra-atrial re-entry, 2 had ventricular tachycardia, and 3 had sinus tachycardia. In the hospital, 2 patients had atrial flutter and one had sinus tachycardia. The group of 14 patients with supraventricular tachycardia due to Wolff-Parkinson-White syndrome or AV node reentry presenting in the emergency room were compared in a retrospective manner to the patients treated with standard verapamil therapy with respect to time from initiation of therapy to termination of supraventricular tachycardia and time from effective dose of medication to the termination of supraventricular tachycardia, as well as side-effects. There was no significant difference between the two groups with respect to clinical variables. Adenosine converted 18 of 18 episodes of supraventricular tachycardia in 14 patients 24.6 +/- 9.6 seconds from the administration of the effective dose (0.104 +/- 0.024 mg/kg) and a mean of 4.4 +/- 2.0 minutes from the initiation of therapy. Verapamil converted 29 of 32 episodes of supraventricular tachycardia in 20 patients, 10.9 +/- 7 minutes from the administration of the effective dose, and a mean of 16.8 +/- 20 minutes from the initiation of therapy using a mean of 8.4 +/- 3.4 mg of IV verapamil.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗

PubMed1993

Transesophageal cardioversion.

With the use of a novel quadripolar esophageal electrode system, we have attempted 131 transesophageal cardioversions in 105 patients: 109 episodes were atrial fibrillation, 16 episodes were atrial flutter, 2 episodes were supraventricular tachycardia, and 4 episodes were ventricular tachycardia. The mean predicted transesophageal impedance (+/- SEM) of 52.6 +/- 1.1 omega was significantly lower than the mean predicted transthoracic impedance (+/- SEM) of 63.1 +/- 1.6 omega (n = 104; p < 0.01). Of the 88 patients who presented with atrial fibrillation as the initial arrhythmia, successful transesophageal cardioversion (maximal delivered transesophageal energy of 100 J in 84 patients and 200 J in 4 patients) was recorded in 70 (79.5%); transesophageal cardioversion required a mean delivered energy of 63.1 +/- 4.2 J and a mean peak current of 20.3 +/- 0.6 A. Transthoracic countershock (maximal delivered energy of 360 J) was attempted in 17 of 18 patients when the transesophageal approach had been unsuccessful; countershock was successful in 10 patients, which yielded an overall success rate of 92.0% (mean successful delivered energy [transesophageal and transthoracic] of 85.3 +/- 7.8 J). All episodes of atrial flutter, supraventricular tachycardia, and ventricular tachycardia were successfully terminated with the use of the esophagus. This esophageal electrode system permits low-energy countershock of atrial and ventricular tachyarrhythmias.

Adult↗

PubMed1993

[Intravenous ablation of the atrio-ventricular junction in patients with supraventricular tachyarrhythmias].

Since the first successful therapeutic DC ablation of the AV junction in 1986, we have treated 20 symptomatic patients with drug-refractory supraventricular tachyarrhythmias (average of 6 antiarrhythmic drugs prior to the ablation attempt). The primary rhythm disturbances necessitating ablation were: AV nodal reentrant tachycardia (50% of pts), atrial flutter or fibrillation, with an uncontrolled rapid ventricular response (40%), atrioventricular reentrant tachycardia using an accessory pathway (20%), atrial tachycardia (10%), and junctional reciprocating tachycardia (5%). Percutaneous catheter ablation of the AV junction was made by Gallagher's method. The USCI 4-polar catheter (7F) was used in 40% of pts, and bipolar Cordis catheter (5F) in the remaining 60%. 70% of pts received either one or two shocks, usually of 200 or 300 J during one session. Another 25% received stored cumulative energy from 800 to 1200 J (in two sessions), and one patient--1800 J (during three sessions). In 85% of pts, the immediate post-ablation conduction was third-degree AV block with the escape pacemaker, ranging from 20 to 50 beats/min., which was infra-His in 57%, and supra-His in 43% of pts. In 15% of pts were either first-degree AV block (10%) or normal AV conduction (5%). A His bundle deflection more than 0.2 mV was predictive of successful production of third-degree AV block. Except a mild and transient increase of indicating enzymes (CPK and CPK-MB) we did not observe any other serious complications directly related to the ablalation procedure. Follow-up study included 19 pts (time range from 2 to 56 months, mean 28).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1997

Long-term management of atrial fibrillation.

In the past decade, catheter ablation techniques and implantable devices have revolutionized the treatment of ventricular arrhythmias, junctional arrhythmias, and atrial flutter. For most patients presenting with atrial fibrillation (AF), the treatment available today is similar to that used a century ago, although nonpharmacologic strategies of therapy have begun to emerge for selected cases. There have been important recent advances in our understanding of the pathophysiology of AF and its complications, and it may be possible to improve patient management by refinement of the way in which current drugs are used.

Adrenergic beta-Antagonists↗

PubMed1991

Efficacy and safety of intravenous and oral propafenone in pediatric cardiac dysrhythmias.

Propafenone was administered to 58 patients with a mean age of 3.2 years (range 0.1 to 16). Mean intravenous dose was 1.2 mg/kg body weight (range 0.3 to 1.5 mg). The final mean oral maintenance dose was 308 mg/m2 body surface area (range 200 to 600 mg/m2, 16.8 mg/kg body weight). After intravenous application, propafenone was effective in 21 of 36 patients; atrial flutter was converted in 1 of 5 patients, and reentry supraventricular tachycardia was controlled in 15 of 25 patients. Propafenone was partially or completely effective in 3 of 4 patients with chaotic atrial tachycardia. Junctional ectopic tachycardia was suppressed in 2 infants. Thirty-seven patients had oral treatment with a mean follow-up of 2.2 years. Propafenone was effective in 33 of 37 patients (89%); atrial flutter was controlled in 2 patients, ventricular ectopy was suppressed in 1 of 2 patients. In reentry supraventricular tachycardia, propafenone was effective in 25 of 28 patients. Chaotic atrial tachycardia (n = 3) and junctional ectopic tachycardia (n = 2) were controlled after successful intravenous therapy. Systemic side effects were rare. Two patients developed a proarrhythmic effect, and 1 patient with ventricular ectopy after repair of tetralogy of Fallot died suddenly during propafenone maintenance therapy.

Administration, Oral↗

PubMed1991

Prevention of arrhythmias after noncardiac thoracic operations: flecainide versus digoxin.

Cardiac arrhythmias are known complications of thoracic operations. The prophylactic value of flecainide administered as a constant-rate, intravenous infusion (0.15 mg.kg-1.h-1) after a loading dose (2 mg.kg-1) was compared with digoxin (10 micrograms.kg-1 for 12 hours, then 0.25 mg.24 h-1) in a randomized study in 30 patients using Holter monitoring during the first 72 hours after operation. Drug monitoring was performed every day to keep a serum level of flecainide of 200 to 600 ng.mL-1 and a digoxin level of 0.8 to 2 ng.mL-1. Failure, defined as the appearance of atrial fibrillation or flutter or the development of complex ventricular arrhythmias (Lown IVb and V), was observed in one patient in the flecainide group (7%) and in 7 patients in the digoxin group (47%) (p less than 0.05). It is concluded that flecainide is more efficient than digoxin in preventing and treating cardiac arrhythmias after thoracic operations. At the dosage used side effects related to flecainide or digoxin were not observed.

Arrhythmias, Cardiac↗

PubMed2003

Acute pulmonary edema after cardioversion of cardiac arrhythmias.

OBJECTIVE: To examine the occurrence of acute pulmonary edema after cardioversion of arrhythmias. METHODS: Cases, case series, and related articles on the subject identified through a comprehensive literature search were examined. RESULTS: Thirty cases (23 males) of post cardioversion acute pulmonary edema were identified. The mean age was 53.8 +/- 13 years (range, 18 to 75 years). Underlying arrhythmias were atrial fibrillation (69%), atrial flutter (24%), supraventricular tachycardia (4%), and ventricular tachycardia (4%). The duration of arrhythmia preceding cardioversion varied widely ranging from 1 day to 13 years. Twenty-six (87%) patients had concomitant cardiovascular disease comprising of coronary artery disease (38%), rheumatic heart disease (23%), cardiomyopathy (23%), and hypertension (8%). Direct current electrical cardioversion was used in 28 (93%) patients and pacing in two (7%) patients. Occurrence of pulmonary edema was independent of the amount of energy used for cardioversion (range 20 to 1280 Joules, mean 263 +/- 27 Joules). Short acting general anesthetic drugs were administered in 14 (47%) and sedation in eight (27%) patients. Sinus rhythm was established in 23 (77%) patients. Duration to develop pulmonary edema after cardioversion was available in 23 patients and ranged from immediately to 96 h. Pulmonary edema occurred within 15 min after cardioversion in 22%, within 3 h in 30%, within 24 h in 30%, within 48 h in 17% and within 96 h in remaining 4% of patients. Three patients required mechanical ventilation. CONCLUSION: The rare complication of acute pulmonary edema after cardioversion has been reported mostly in patients with underlying cardiac disease, and is independent of the amount of energy used for cardioversion.

Acute Disease↗

PubMed1990

Cardiac rhythm disturbances early after orthotopic heart transplantation: prevalence and clinical importance of the observed abnormalities.

To precisely define the incidence, type and consequences of cardiac arrhythmias early after heart transplantation, 25 cardiac transplant recipients were monitored continuously for 728 days from the day of surgery to discharge or death. A subset of 15 patients had sinus node function studies with overdrive suppression performed weekly at the time of endomyocardial biopsy. Results revealed sinus bradycardia in 10 patients (40%) and junctional bradycardia in 6 (24%). Supraventricular tachycardia in the form of atrial tachycardia, atrial fibrillation and atrial flutter occurred in 11 patients (44%). Ventricular tachycardia occurred in 15 patients (60%) and was nonsustained in all. Cardiac pacing for 1,403 h was used in nine patients with a pulse rate less than 50 beats/min; seven recovered and permanent pacing was instituted in two. In the subgroup that had sinus node function studies, seven patients were identified with clinical bradyarrhythmia; each had abnormal sinus node recovery time (greater than 1,400 ms) and abnormal corrected sinus node recovery time (greater than 525 ms) in at least one study. These seven patients also had a significantly prolonged ischemic time (236 +/- 26 versus 159 +/- 68 min, p less than 0.01). In conclusion, cardiac arrhythmias, particularly ventricular tachycardia and bradyarrhythmia, occur more commonly early after orthotopic heart transplantation than has previously been reported. Sinus node dysfunction due to prolonged organ ischemic time, antiarrhythmic drug use or surgical trauma, alone or in combination, may contribute to these arrhythmias.

Arrhythmia, Sinus↗

PubMed1988

Experience with flecainide for the treatment of cardiac arrhythmias in children.

We treated 22 children, aged 3 days to 16 years 6 months (median 11 years 1 month), with flecainide for a variety of arrhythmias where a Class I agent was indicated. In 16, conventional antiarrhythmic treatment had failed. Structural heart disease was present in nine. The arrhythmia was paroxysmal re-entry atrioventricular tachycardia in nine; paroxysmal atrial tachycardia, flutter or fibrillation in five; paroxysmal ventricular tachycardia in five and frequent ventricular extrasystoles (with couplets) in three. Sinus rhythm was achieved in all four children who received flecainide during tachycardia (three received intravenous flecainide, one oral). During follow-up of 3-24 months (median 12 months), arrhythmia control was obtained in 13 children (59%). Combination therapy was used in seven of these; with digoxin in four and a beta blocker in three. Flecainide doses used in this study ranged from 1-11 mg kg-1 day-1 (median 4 mg kg-1 day-1), 25-297 mg m-2 day-1 (median 113 mg m-2 day-1). The median, pre-dose flecainide concentration in those responding to therapy was 225 micrograms l-1 and in those failing to respond was 417 micrograms l-1. An arrhythmogenic effect occurred in one child.

Adolescent↗

PubMed2003

CVT-510: a selective A1 adenosine receptor agonist.

Adenosine is an endogenous nucleoside that has potent antiarrhythmic effects on paroxysmal supraventricular tachycardia (PSVT) due to its negative dromotropic effects on the atrioventricular node. In addition to its electrophysiologic effects, adenosine has important effects on vascular smooth muscle cells, inflammatory cells, the central nervous system, and the kidney. Four known adenosine receptor subtypes (A1, A2A, A2B, and A3) mediate the pleiotropic effects of adenosine in humans. These receptors are coupled to a wide range of second messenger cascades. Activation of the A1 adenosine receptor accounts for the negative chronotropic and dromotropic effects of adenosine, whereas A2A, A2B and A3 adenosine receptor activation are responsible for such effects as coronary vasodilation, bronchospasm, inhibition of platelet aggregation, and neuronal stimulation. Elucidation of the specific properties of each of the adenosine receptor subtypes has led to the development of selective ligands as potential therapeutic agents. CVT-510, N-(3(R)-tetrahydrofuranyl)-6-aminopurine riboside, was developed as a selective A1 adenosine receptor agonist that specifically targets the atrioventricular node for termination of PSVT. Preliminary clinical trials have shown that CVT-510 is effective in terminating PSVT and eliminating many of the undesirable adverse effects of adenosine. CVT-510 is also being explored as a potential agent for controlling the ventricular rate of atrial fibrillation and flutter.

Adenosine↗

PubMed1994

Contraction-excitation feedback in atrial reentry: role of velocity of mechanical stretch.

To determine the effects of atrial stretch on atrial flutter, we analyzed variations in atrial flutter cycle length (CL) caused by ventricular contraction in five dogs with artificially induced atrioventricular block. In contrast to absence of variations in CL during sustained ventricular asystole, atrial stretch by ventricular contraction consistently produced phasic variations in CL. The variations were not confined to any specific atrial sites, but depended on the time of ventricular contraction relative to atrial activation phase. The phase-response curve of the variations was closely related to that of the velocity of changes in the atrial pressure with no time lags, but not to that of the atrial pressure itself. Pharmacological denervation did not abolish the variations. Conventional electrophysiological study revealed greater changes in intra-atrial activation time by atrial stretch at a short pacing cycle length than at a longer one, suggestive of changes in repolarization by mechanical stretch. In conclusion, atrial stretch caused by ventricular contraction produces phasic variations in CL, the extent of which depends on the velocity of the mechanical stretch of atrial muscles.

Animals↗

PubMed1988

Energy, current, and success in defibrillation and cardioversion: clinical studies using an automated impedance-based method of energy adjustment.

The purposes of this study were two. First, we wanted to evaluate in patients a technique for automated adjustment of selected energy for defibrillation or cardioversion based on transthoracic impedance. Second, we wanted to define the relationship of peak current and shock success in various arrhythmias. Applying a previously validated method of predicting transthoracic impedance in advance of any shock, we modified defibrillators to automatically double the operator-selected energy if the predicted impedance exceeded 70 omega. Success rates of shocks given for ventricular and atrial arrhythmias from these modified energy-adjusting defibrillators were compared with success rates for shocks given from standard defibrillators. We prospectively collected data on 347 patients who received a total of 1009 shocks. Low-energy (100 J) shocks given to high-impedance (greater than or equal to 70 omega) patients had a poor success rate; in such high-impedance patients significant improvement in shock success rate was achieved by the energy-adjusting defibrillators. For example, when 100 J shocks were selected for high-impedance patients in ventricular fibrillation the energy-adjusting defibrillators achieved a shock success rate of 75%, whereas standard defibrillators achieved a shock success rate of only 36% (p less than .01). Similar improvements were seen for ventricular tachycardia and atrial fibrillation. Thus, automated energy adjustment based on transthoracic impedance is a beneficial approach to defibrillation and cardioversion. For ventricular fibrillation, atrial fibrillation, and atrial flutter there was a clear relationship between peak current and shock success.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗

PubMed1996

Modulation of atrioventricular nodal function by metabolic and allosteric regulators of endogenous adenosine in guinea pig heart.

BACKGROUND: There has been increasing interest in the development of agents that utilize endogenous adenosine to exert their actions. We tested the hypothesis that substances that either potentiate the activity (allosteric enhancers) or increase the interstitial concentration (inhibitors of metabolism) of endogenous adenosine may cause event (tachycardia)-specific depression of AV nodal conduction. METHODS AND RESULTS: The frequency-dependent effects of iodotubercidin (ITU, an inhibitor of adenosine kinase), erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA, an inhibitor of adenosine deaminase), draflazine (a nucleoside transport blocker), and PD81,723 (an allosteric enhancer of the A1 adenosine receptor binding) on the stimulus-to-His bundle (SH) interval, a measure of AV nodal conduction, were determined in guinea pig hearts and compared with those of adenosine and diltiazem. All drugs depressed AV nodal conduction in a frequency-dependent manner. The ratios of SH interval prolongations at fast to slow pacing rates for draflazine, ITU + EHNA, PD81,723, adenosine, and diltiazem were 17.5 +/- 3.4, 11.1 +/- 5.0, 3.5 +/- 0.9, 10.1 +/- 2.8, and 8.3 +/- 3.5, respectively. Coincident with the prolongation of the SH interval at rapid pacing rates, draflazine and ITU + EHNA increased the epicardial fluid adenosine concentrations by 2.2- and 2.6-fold, respectively. In contrast, epicardial transudate levels of adenosine do not change in the presence of PD81,723. The AV nodal effects of draflazine, ITU, EHNA, and PD81,723 were reversed by the A1 adenosine receptor antagonist 8-cyclopentyltheophylline and adenosine deaminase, implicating endogenous adenosine acting at the A1 adenosine receptor. CONCLUSIONS: Adenosine-regulating agents that act in an event- and site-specific manner represent a novel drug design strategy that may potentially be valuable for the long-term treatment of supraventricular arrhythmias and control of ventricular rate during atrial fibrillation or flutter.

Adenosine↗

PubMed1984

Procainamide infusion and acute atrial fibrillation.

We report the use of intravenous procainamide infusion in the treatment of fifteen patients with acute atrial fibrillation. Procainamide was infused at 50 mg/min to a maximum of 20 mg/kg, with blood pressure and electrocardiographic monitoring. Ten patients responded, with a mean dose of 8.7 (standard deviation 4.3) mg/kg, four of these reverting to sinus rhythm after a low dose of less than 5.0 mg/kg. Hypotension was a common concomitant and was seen in four cases, but required termination of the infusion only in a patient with cardiomyopathy. An increase in ventricular rate or conversion to atrial flutter was not seen. Intravenous infusion of procainamide is a safe and moderately effective method of cardioversion in acute atrial fibrillation.

Acute Disease↗