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The influence of electrical cardioversion on superoxide anions (O2-) production by polymorphonuclear neutrophils, hydrogen peroxide (H2O2) plasma level and malondialdehyde serum concentration.

We studied the influence of electrical cardioversion on unstimulated and stimulated superoxide anion production by polymorphonuclear neutrophils in 22 patients with atrial flutter or atrial fibrillation. We also estimated hydrogen peroxide plasma level, as well as malondialdehyde serum concentration, in these subjects. We noted an increase in spontaneous production of superoxide anions from 14.9 +/- 1.8 nmol/10(6) neutrophils per 20 min to 21.37 +/- 2.7 nmol/10(6) neutrophils per 20 min (P = 0.002) in neutrophils obtained after electrical cardioversion. Similarly, stimulated production of O2- also increased after electrical cardioversion (41.8 +/ 3.4 nmol/10(6) neutrophils per 20 min vs. 59.0 +/- 5.9 nmol/10(6) neutrophils per 20 min, P = 0.0027). Moreover, hydrogen peroxide plasma level increased significantly after electrical cardioversion (39.9 +/- 6.2 mumol/l vs. 53.4 +/- 7.6 mol/l, P = 0.003). Serum malondialdehyde concentration also increased after countershock (2.56 +/- 0.26 nmol/ml vs. 2.94 +/- 0.26 nmol/ml, P = 0.023). These results seem to indicate that electrical cardioversion may lead to polymorphonuclear neutrophils activation, increased H2O2 production and lipid peroxidation.

Adult↗

Transesophageal cardioversion of resistant atrial arrhythmias.

One hundred and thirty five episodes of atrial flutter and atrial fibrillation resistant to transthoracical cardioversion were treated in 127 patients with asynchronized direct current shocks via an esophageal electrode constructed by us. Sinus rhythm was restored in 105 (77.8%) cases. The mean defibrillating voltage was 4.3 kV. Complications were not observed.

Atrial Fibrillation↗

Pediatric dysrhythmias.

Arrhythmias in children are less common than in adults but are increasing because of successful repair of congenital heart diseases. Supraventricular tachycardia is the most common symptomatic pediatric tachyarrhythmia. Atrial flutter and atrial fibrillation in children are attributed largely to structural heart disease. Bradycardia is defined as a heart rate less than the lower limit of normal for a child's age, and the most common cause is sinus bradycardia. Despite the infrequent occurrence of arrhythmias, it is crucial to expeditiously identify and treat certain rhythm abnormalities because they can lead to further decompensation.

Anti-Arrhythmia Agents↗

Clinical implications of differences in pharmacodynamic action of polar and nonpolar cardiac glycosides.

The principal effects of cardiac glycosides probably can be classified as parasympathomimetic or sympathomimetic. Data from animals and from man suggest that polar cardiac glycosides, such as ouabain and digoxin, possess greater parasympathomimetic (vagal) cardiac effect for a given amount of sympathomimetic (positive inotropic) cardiac effect than do less polar cardiac glycosides, such as digitoxin. Polar glycosides therefore offer some advantage in uncomplicated paroxysmal atrial tachycardia and in uncomplicated atrial flutter and atrial fibrillation when the principal desired effect is reduction in the number of atrial impulses reaching the ventricles or conversion to normal sinus rhythm. Non-polar glycosides offer an advantage when positive inotropicity is desired but when there is some degree of atrioventricular block or when inappropriate sinus bradycardia or anorexia, nausea, or vomiting are present. Ecotopic impulse formation when due to cardiac glycosides is a toxic manifestation of excessive sympathomimetic effect, but is aggravated by vagal-induced sinus bradycardia, so that both parasympathomimetic and sympathomimetic capability of cardiac glycosides must be considered when dealing with myocardial electrical instability.

Animals↗

Efficacy and safety of long-term oral flecainide acetate in patients with responsive supraventricular tachycardia.

In 102 patients with inducible supraventricular tachycardia (SVT), 56 women and 46 men aged 20-86 (mean, 52) years, underwent electrophysiologic study. SVTs observed at electrophysiologic study were atrial flutter or atrial fibrillation (32%), the "slow-fast" form of atrioventricular (AV) nodal reentrant tachycardia (45%), orthodromic AV reentrant tachycardia (25%), and atrial tachycardia (9%). More than 1 SVT occurred in some patients. Spontaneous symptomatic SVT frequency prior to oral flecainide varied from 3/day to 1/3 months (mean, 3/month). At electrophysiologic study and during SVT, intravenous flecainide, 2 mg/kg body weight, was given at an infusion rate of 10 mg/min up to a maximum dose of 150 mg. Patients were commenced on oral flecainide if SVT termination occurred during intravenous flecainide administration and if reinitiation was not possible after the total dose of flecainide had been given. In patients with AV nodal reentrant tachycardia and AV reentrant tachycardia further criteria for commencing oral flecainide were SVT termination by ventricular-atrial conduction block and persistent ventricular-atrial block after intravenous flecainide administration. Initial oral flecainide dosage was determined by assessing ability to reinitiate SVT after 50 mg, 100 mg, and the total dose of intravenous flecainide had been given. Eighty-nine patients (87%) remained free of symptomatic SVT over a mean follow-up period of 3.9 years (range, 3 months to 6.5 years). Two thirds were still taking the original dosage of flecainide and the rest were SVT-free on a higher dosage. Oral dosages ranged from 50 to 300 mg/day (median dosage, 100 mg twice daily) Nine patients experienced minor side effects, including, lethargy, dizziness, headache, and blurred vision. There were no deaths and no reports of major proarrhythmic events or other major adverse effects.

Administration, Oral↗

Enhanced diagnosis of narrow complex tachycardias with increased electrocardiograph speed.

The objective of this study was to determine if the addition of rapid speed (50 mm/s) electrocardiograms (EKGs) improves the clinician's diagnostic accuracy of narrow complex tachycardias when compared to standard speed (25 mm/s) EKGs. We conducted a prospective, comparative trial. Forty-five difficult narrow complex tachycardias (heart rate range: 150-250 beats per minute) were printed at both 25 mm/s and 50 mm/s. Eight board certified emergency physicians initially interpreted the standard speed EKG (standard group) and chose a therapy for the hypothetical patient. These eight participants later interpreted the same 45 EKGs by using both the standard and rapid speed EKGs (rapid group) and again chose a therapy. The gold standard for each EKG was based on the patient's clinical diagnosis and was independently confirmed in all cases by a board-certified cardiologist. The rhythm distribution was as follows: atrial flutter (17), atrial fibrillation (11), paroxysmal supraventricular tachycardia (15), and sinus tachycardia (2). Participants were masked to all clinical information and EKG ratios. Diagnostic accuracy was compared by using McNemar's chi(2) test. Correct diagnosis improved from 226/360 (63%), in the standard group to 257/360 (71%) in the rapid group (difference in means 8.6%, p = 0.002). The incorrect use of adenosine was decreased from 43/240 (18%) in the standard group to 32/240 (13%) in the rapid group (difference in means 4.5%, p = 0.06). In conclusion, correct diagnosis of difficult narrow complex tachycardias was improved when EKGs at both 25 mm/s and 50 mm/s were used for interpretation. It appears that the simple technique of increasing the EKG paper speed, and thus effectively spacing out the rhythm, enhances the diagnostic ability of the observer.

Adenosine↗

Mechanisms underlying the development of atrial arrhythmias in heart failure.

There is an important association between heart failure and the development of atrial arrhythmias. Although most often associated with atrial fibrillation, there is some evidence to suggest an association between heart failure and other atrial arrhythmias and, in particular, atrial flutter and atrial tachycardia. The mechanisms by which these common atrial arrhythmias may arise in patients with heart failure are discussed.

Aged↗

Radiofrequency catheter ablation for the management of cardiac tachyarrhythmias.

Radiofrequency catheter ablation techniques allow for safe and highly effective curative therapy of a variety of cardiac dysrhythmias. The technique involves the delivery of a high-frequency, alternating electrical current through an intravascular catheter to sites of arrhythmogenic myocardium. This current induces resistive electrical heating of the tissue, resulting in discrete areas of myocardial destruction through coagulation and desiccation. Dysrhythmias most commonly treated with these techniques are atrioventricular nodal reentry and tachycardias related to accessory atrioventricular bypass tracts. For these dysrhythmias, success rates of 90% to 95% are achievable with a low (2% to 4%) risk of complications. Radiofrequency catheter ablation techniques also have been used to treat ventricular tachycardias, atrial flutter, ectopic atrial tachycardia, and sinus node reentry, albeit with lower success rates. These techniques are still evolving, alternate energy sources (such as microwave and laser) and improved catheter technology should enhance the technique's safety and efficacy for a wider range of dysrhythmias.

Atrial Flutter↗

A technique for measurement of the extent of spatial organization of atrial activation during atrial fibrillation in the intact human heart.

Atrial fibrillation (AF) is a common clinical problem, associated with considerable morbidity and mortality, for which effective management strategies have yet to be devised. The absence of objective measures to guide selection of antiarrhythmic drug therapy for maintenance of sinus rhythm leaves only clinical endpoints (either beneficial or detrimental) for assessment of drug action, with occasional catastrophic consequences. As part of an attempt to provide an objective framework for the assessment of antiarrhythmic drug action on the electrophysiologic determinants of atrial fibrillation, we have developed a measure of the spatial organization of atrial activation processes during atrial fibrillation. By recording activation sequences at multiple equally spaced locations on the endocardial surface of the atria during atrial fibrillation in humans and determining the degree of correlation between these activation sequences as a function of distance, we have been able to construct spatial correlation functions for atrial activation. We have found that atrial activation remains well-correlated, independent of distance during normal sinus rhythm and atrial flutter. During atrial fibrillation, correlation decays monotonically with distance and the space-constant for this decay may be used to describe the relative spatial organization of atrial fibrillation. We provide examples of the impact of antiarrhythmic agents on the space-constant and suggest that assessment of the relative spatial organization of atrial activation using this methodology may potentially provide an objective framework to guide therapy in patients with AF.

Adenosine↗

Long-term prevention of vagal atrial arrhythmias by atrial pacing at 90/minute: experience with 6 cases.

Six patients (5 men, 1 woman) with a history ranging from 3-16 years of resistant vagal atrial arrhythmias were treated by atrial pacing at a rate of 90/Min. These patients have been followed up for an average of 5.5 years (range 2-11 years) with favorable results. The arrhythmias were characterized by daily or weekly attacks of typical atrial flutter and atrial fibrillation occurring mainly or exclusively at night, at rest, or in the digestive periods in otherwise normal hearts of middle-aged patients (first attack between 25 and 54, mean 40). The arrhythmias were resistant to quinidine, and were usually aggravated by digitalis, beta-blockers and verapamil. Amiodarone is usually the only effective drug in this syndrome, but was not used before pacing in the 2 first cases, and was ineffective in the other 4 cases. Electrophysiologic studies confirmed the absence of sick sinus syndrome, and the close relationship between relative bradycardia and the onset of the arrhythmia. Atrial pacing alone totally controlled the arrhythmia in 1 patient; amiodarone was used in conjunction with pacing in 3 patients. In 1 patient the improvement was clear but incomplete, and in 1 patient permanent atrial fibrillation occurred shortly after pacemaker implantation.

Adult↗

Mechanisms determining the ventricular rate in wolff-parkinson-white arrhythmias.

In patients with WPW syndrome the maximal ventricular rate attained during ectopic rapid supraventricular thythms depended on the type of arrhythmia as well as on the physiological properties of the AP. During reciprocating tachycardias the impulse is almost invariably conducted to the ventricles through the AV node. Therefore, the maxiaml ventricular rate is a function of the AV nodal ERP. On the other hand, when atrial flutter or atrial fibrillation were present the ventricular rate could be moderately elevated (when the ERP of the AP was longer than that of the AV node) or very rapid where the ERP of the AP was significantly short. Therefore, from the electrophysiological viewpoint, the AP appears to behave as His-Purkinje tissue in some cases and as ordinary artrial muscle in other patients. These assumptions await further documentation.

Adult↗

[Radiofrequency ablation of supraventricular tachycardias].

Radiofrequency catheter ablation has been established as a non-surgical curative treatment modality for the management of patients with paroxismal supraventricular tachycardia. Success rates for atrioventricular node reentrant tachycardia and accessory pathway-mediated macroreentrant tachycardia exceed 95%. Results in patients with atrial flutter and atrial tachycardia are encouraging, with success rates exceeding 75%.

Atrial Fibrillation↗

[Antiarrhythmic effects of verapamil].

The effect of verapamil were studied on 50 episodes of supraventricular and ventricular tachycardia in 44 patients. An i.v. dose of 0.10 to 0.15 mg/kg. was used. In 5 cases His bundle electrograms were obtained while maximal dp/dt was determined in 7 others. Sinus rhythm was obtained in 21 (81%) of 26 cases of PSVT. In all cases of rapid atrial fibrillation (n-11), an important decrease in the ventricular response was elicited. Of 7 cases of atrial flutter, verapamil induced sinus rhythm in 3 and a significant decrease in the ventricular rate in 3 others. In 2 out of 6 cases ventricular tachycardia reverted to sinus rhythm. The latency time between the injection and the manifestation of the effect ranged from 2 to 4 minutes. A slight and short-lasting depression of dp/dt was observed in all cases studied. Verapamil produced an increase in the A-H interval in 4 of the 5 cases studied with His bundle recordings. Verapamil was found to be a useful drug to suppress PSVT, to decrease the ventricular response in flutter or atrial fibrillation and to convert some ventricular tachycardias to sinus rhythm. Verapamil should be used with caution in previously digitalized patients and is contraindicated when there is S-A node dysfunction as in the tachycardia-bradycardia syndrome.

Adult↗

Surgical therapy for patients with supraventricular tachycardia.

Surgical techniques have now been developed to treat a variety of supraventricular arrhythmias, including the Wolff-Parkinson-White syndrome, arrhythmias associated with other atrioventricular accessory connections, AV nodal reentrant tachycardia, and automatic (ectopic) atrial tachycardias. In addition, atrial flutter and atrial fibrillation are not potentially curable with surgical intervention. This article will discuss the current surgical techniques used to treat these supraventricular tachyarrhythmias.

Atrial Fibrillation↗

Short- and intermediate-term efficacy of amiodarone in infants and children with cardiac arrhythmia.

The antiarrhythmic effect of amiodarone was examined in this retrospective study in a group of 20 patients with a mean age of 8.5 +/- 6.7 years (range 42 days to 20 years, median 9 years). Five patients with atrial flutter, one patient with atrial fibrillation, two patients with an intermediate rhythm between atrial flutter and atrial fibrillation, four patients with chaotic atrial tachycardia, three patients with atrioventricular reentry tachycardia, two patients with junctional ectopic tachycardia, and three patients with ventricular arrhythmias were treated with amiodarone. The mean duration of therapy was 9.1 +/- 12.3 months (range 1 month to 4 years). Before amiodarone treatment, 18 patients had been unresponsive to various antiarrhythmic drugs (range 1-8, median 2). Two patients received amiodarone as an initial therapy. It was administered orally at a dose of 10 mg/kg once per day for 10 days and then decreased to 5 mg/kg once per day. Amiodarone was effective in 16 patients (80%). Side effects occurred in three patients, including thyroid dysfunction, elevation of liver enzymes, and keratopathy. All side effects disappeared upon cessation of the therapy. We recommend amiodarone for the treatment of childhood arrhythmias, especially for the refractory types.

Administration, Oral↗

Bystander cavo-tricuspid isthmus activation during post-incisional intra-atrial reentrant tachycardia.

We describe a case of post-incisional atrial tachycardia resembling typical atrial flutter on the surface ECG. Typical atrial flutter reentry was ruled out by the results of activation and entrainment mapping. Nevertheless, overdrive pacing from the lateral edge of the cavo-tricuspid isthmus produced tachycardia entrainment with concealed fusion associated with post-pacing and stimulus-to-P wave onset intervals exactly matching the tachycardia cycle length duration and the electrogram-to-P wave onset interval, respectively. Therefore, that site was firstly severed by sequential radiofrequency pulses. However, a transformation of the tachycardia P wave morphology and endocardial activation sequence, not associated with tachycardia termination or cycle length modification occurred. After additional mapping manoeuvres, a relatively small reentrant circuit was identified in the low and mid aspect of the lateral right atrium with the critical isthmus located between the lower border of a cannulation atriotomy and the crista terminalis, close to the inferior vena cava orifice. A single radiofrequency pulse at that site terminated the tachycardia. Both the electrocardiographic pattern and the endocardial mapping data obtained in our case might be explained by a split of the reentrant wavefront into a secondary wavelet which freely propagated through the cavo-tricuspid isthmus without completing the peritricuspid loop. In conclusion, bystander cavo-tricuspid isthmus activation during atrial tachycardia may simulate a typical atrial flutter pattern on the surface ECG. Further studies should evaluate the prevalence of this propagation pattern in post-incisional atrial reentry and atypical atrial flutters, and identify its implications for ablation strategy.

Atrial Flutter↗

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↗

Flecainide acetate in the treatment of tachycardias associated with Mahaim fibres.

Patients with Mahaim fibres are susceptible to tachycardias which can be refractory to conventional drug therapy, leading to treatment with surgery and catheter ablation. The effects of flecainide acetate were studied in 3 patients (61, 21 and 35 years of age) with Mahaim fibres presenting with tachycardias refractory to beta-blockers, quinidine and verapamil. One also had ophthalmic side-effects from amiodarone. Three types of tachycardias were induced: a reentrant tachycardia with left bundle branch block morphology (LBBBM) in all 3 patients, atrial flutter in one and atrial fibrillation in another. Intravenous flecainide acetate (2 mg kg-1) terminated reentrant tachycardia and abolished duality of atrioventricular conduction in patient 1. In patient 2, it abolished preexcitation during atrial flutter prior to termination. Atrial fibrillation could not be induced in patient 3 after flecainide acetate. In all patients, retrograde conduction was blocked, preexcitation was not present with atrial pacing and no tachycardia was induced after flecainide. All have remained asymptomatic on oral flecainide acetate (100 mg bd) for a mean follow-up period of 9 months. We conclude that (1) flecainide acetate is effective for the treatment of various tachycardias associated with Mahaim fibres; (2) since different mechanisms responsible for the tachycardia with LBBBM may be present in the same patient and difficult to determine in some, treatment with flecainide acetate which affects both the atrioventricular node and Mahaim fibre conduction may be appropriate for the condition and; (3) its use should be considered before more aggressive therapies.

Adult↗