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PubMed1997

Risk of thromboembolism in chronic atrial flutter.

Anticoagulant therapy is not conventionally used in the treatment of patients with atrial flutter. This recommendation has been based on sparse clinical experience, and recent preliminary reports suggest a significant risk of thromboembolism for these patients. A retrospective study was undertaken to assess the frequency of thromboembolic events as well as potential risk factors for these events in a cohort of patients with atrial flutter referred for radiofrequency ablation treatment. Eighty-six consecutive patients with a primary diagnosis of atrial flutter were evaluated. A history of embolic events was noted in 12 of 86 patients (14%) with atrial flutter, with an annual risk of approximately 3%. There were no differences in the prevalence of coronary artery disease, cardiomyopathy, valvular disease, or atrial fibrillation between the 2 groups of patients having an embolic event and those of patients without embolic events. Left ventricular function and left atrial size were also similar between the 2 groups. The only significant risk factor was hypertension (p < 0.05). However, in a regression model with other clinical variables (i.e., age, gender, left atrial size, presence or absence of any cardiac disease, length of time in flutter, left ventricular function, type of flutter, flutter cycle length, type of secondary arrhythmias) no significant predictors were found. Patients with transient ischemic attacks or pulmonary emboli were then excluded from the analysis in order to compare the thromboembolic risk in the present study to that reported in major atrial fibrillation trials. The overall risk becomes 7% (6 of 86), which over a mean follow-up period of 4.5 years yields an annual risk of approximately 1.6%. Although this risk is only 1/3 of that for patients with atrial fibrillation, this risk is higher than previously recognized for patients with chronic atrial flutter. Anticoagulant therapy should be seriously considered for these patients.

Adult↗
PubMed2005

Clinical comparison of ibutilide and propafenone for converting atrial flutter.

OBJECTIVE: To evaluate the efficacy and safety of intravenous ibutilide and propafenone for immediate treatment of atrial flutter. METHODS: Forty patients with atrial flutter with an arrhythmia duration of three hours to 90 days were randomized to receive up to two 10-minute infusions of ibutilide (1 and 1 mg) or propafenone (70 and 70 mg) with a 10-minute interval. RESULTS: Ibutilide was superior to propafenone for treating atrial flutter (90% vs. 30%, p < 0.01). The median conversion time in the ibutilide group was 11 min (the 25th and 75th percentile was 10 and 45 min), and the median conversion time in the propafenone group was 35 min (range 20-55 min). In all patients, the duration of arrhythmia before treatment was a predictor of arrhythmia termination, although this was more obvious in the group that received ibutilide. Conversion of atrial flutter by ibutilide was characterized mainly by increased cycle length variability. Bradycardia (2/20) and hypotension (4/20) were more common side effects with propafenone. Of 20 patients given ibutilide, 8 (40%) who developed monomorphic ventricular extrasystoles or repetitive atrial flutter with aberrant conduction tachycardia, no one required any specific treatment except for the interruption of ibutilide infusion. CONCLUSION: Ibutilide is highly effective for rapidly terminating atrial flutter. This new class III drug, under monitored conditions, is a potential alternative to currently available cardioversion options.

Adult↗
PubMed1979

Polymorphous ventricular tachycardia: clinical features and treatment.

Thirty-four cases of ventricular tachyarrhythmia characterized by polymorphy of the QRS complexes with changing R-R intervals and a heart rate of 150 to 300 beats/min, termed polymorphous ventricular tachycardia, are described. The factors involved in the appearance of this arrhythmia were the administration of antiarrhythmic drugs (quinidine 22 patients, procainamide 5 patients, ajmaline 1 patient), antianginal drugs (prenylamine [Synadrin] 4 patients) and antidepressant drugs (thioridazine 1 patient). Twenty-one patients were treated for premature ventricular complexes, three for chronic recurrent ventricular tachycardia, six for atrial flutter and fibrillation, three for anginal pain and one patient for mental depression. All patients except one had a drug-induced prolonged corrected Q-T interval before the appearance of polymorphous ventricular tachycardia. Most of the patients with this arrhythmia were considered to have severe myocardial disease. Lidocaine and electric cardioversion were administered to all patients, but were effective only in seven patients whose tachycardia occurred in short, single episodes. The most effective treatment (17 patients) was temporary ventricular pacing at rates ranging from 100 to 140 beats/min. Intravenous isoproterenol proved to be successful in another 10 cases. It is concluded that patients with severe myocardial involvement receiving antiarrhythmic drugs for premature ventricular complexes, especially the multiform variety, are at high risk for the development of polymorphous ventricular tachycardia.

Adult↗
PubMed2001

Incidence and short-term prognosis of late sustained ventricular tachycardia after myocardial infarction: results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI-3) Data Base.

BACKGROUND: There is little epidemiologic information from large multicenter databases on sustained monomorphic ventricular tachycardia occurring after the initial 48 hours of myocardial infarction. METHODS: We reassessed its incidence and short-term prognosis in 16,842 patients with a definite myocardial infarction enrolled in the Gruppo Italiano per lo Studio della Soprovvivenza nell'Infarto Miocardico (GISSI-3) trial. RESULTS: The incidence rate of late sustained ventricular tachycardia by 6 weeks was around 1%. Older age, a history of hypertension, diabetes, and myocardial infarction, nonadministration of lytic therapy, Killip class > I, > or = 6 leads with ST-segment elevation, higher heart rate, and bundle branch block on admission were significantly more frequent among patients with than without late sustained ventricular tachycardia. Patients with ventricular tachycardia had a more complicated course in-hospital and posthospital to 6 weeks than the reference group did. The arrhythmia was associated with a significant excess of pump failure, atrial flutter-fibrillation, asystole, atrioventricular block, ventricular fibrillation within the first 48 hours of myocardial infarction, and recurrent ischemic events. Larger left ventricular end-systolic volumes and lower ejection fractions were more frequent among ventricular tachycardia patients than in the reference group by 6 weeks. Death rates by 6 weeks were 35% for patients with ventricular tachycardia and 5% for those without the arrhythmia. Irrespective of the stratification of patients by site and type of infarct and presence/absence of bundle branch block, the occurrence of the arrhythmia was associated with reduced 6-week survival. CONCLUSION: In a proportional hazard regression model late sustained ventricular tachycardia was retained as a strong, independent predictor of 6-week mortality after myocardial infarction (hazard ratio 6.13, 95% confidence interval 4.56-8.25).

Aged↗
PubMed2001

[Usefulness of a VDD defibrillation electrode in recording atrial electrograms during atrial flutter and atrial fibrillation].

BACKGROUND: Monitoring of atrial signals improves the accuracy in identifying supraventricular tachyarrhythmias to prevent inappropriate therapies in patients with implantable cardioverter-defibrillators (ICD). Since complications due to the additional atrial lead were found in dual chamber ICD systems with 2 leads, we designed a single-pass VDD-lead for use with dual chamber ICDs. PATIENTS AND METHODS: After promising animal experiments in a German multicenter study a prototype VDD lead (single-coil defibrillation electrode with 2 additional fractally coated rings for bipolar sensing in the atrium) was temporarily used in 20 patients. Atrial and ventricular signals were recorded during sinus rhythm, atrial flutter, atrial fibrillation and ventricular tachycardia or ventricular fibrillation. Terminations of ventricular arrhythmias were performed by internal DC shock. RESULTS: The implantation of the electrode was successful in 18 of 20 patients. Mean atrial pacing threshold was 2.45 +/- 0.9 V/0.5 ms, mean atrial impedance was 215 +/- 31 Ohm. Atrial amplitudes were greater during sinus rhythm (2.7 +/- 1.6 mV) than during atrial flutter (1.36 +/- 0.28 mV, p < 0.05) or atrial fibrillation (0.92 +/- 0.29 mV, p < 0.01). During ventricular fibrillation atrial "sinus"-signals had significantly (p < 0.01) lower amplitudes than during sinus rhythm. Mean ventricular sensing was 13.3 +/- 7.9 mV, mean ventricular impedance was 577 +/- 64 Ohm. Defibrillation was successful with 20 J shock. 99.6% of P waves could be detected in sinus rhythm and 85 +/- 9.9% of flutter waves during atrial flutter. During atrial fibrillation 55% of atrial signals could be detected without modification of the signal amplifier. CONCLUSIONS: A new designed VDD dual chamber electrode provides stable detection of atrial and ventricular signals during sinus rhythm and atrial flutter. For reliable detection of atrial fibrillation modifications of the signal amplifier are necessary.

Aged↗
PubMed1975

[Oxprenolol in the treatment and prevention of cardiac arrhythmias].

Authors have analyzed the antiarrhythmic effect of oxprenolol, a beta blocking agent, in the treatment of various types of arrhythmias and in the prophylaxis of recurrences of auricular flutter and fibrillation. The results obtained in a group of 68 cases of different arrhythmias may be summarized in the following way: a) the drug efficiently reduces the ventricular rate in sinus tachycardia and in atrial flutter and fibrillation with high ventricular rate, even if resistant to treatment with digitalis; b) in patients with asynchronous pacemaker oxprenolol leads to disappearance or an important reduction of competitive rhythms; c) in supraventricular paroxysmal tachycardias the results are positive in the majority of cases (while on the contrary in 2 cases of ventricular tachycardias the drug was not effective). A group of 116 cases with auricular flutter or fibrillation (in which sinus rhythm had been restored with quinidine or cardioversion has been analyzed to study the prophylactic activity of oxprenolol in these arrhythmias. The cases have been divided at random into two groups and have been treated with quinidine (g 0.80 p.d.) or with an association of oxprenolol (mg 60 p.d.) and quinidine (g 0,60 p.d.). The observation period varied from a minimum of 1 month to a maximum of 3 years and 3 months. The curves showing the percentage of persistance of sinus rhythm in the two groups were very similar and after 3 years and 3 months 100% of patients observed presented a recurrence of arrhythmias.

Adult↗
PubMed1979

Uncontrolled ventricular rate in atrial fibrillation. A manifestation of dissimilar atrial rhythms.

A patient with coarse atrial fibrillation and a rapid ventricular response developed periods of high grade atrioventricular block interpersed with periods of rapid ventricular conduction after the administration of digitalis and propranolol. Intracardiac atrial recordings showed similar atrial rhythms of high right atrial flutter and left atrial fibrillation. The low right atrial recordings showed flutter during the periods of fast ventricular rates and fibrillation during periods of slower ventricular rates.

Adult↗
PubMed2006

[Treatment for perioperative arrhythmias with nifekalant hydrochloride].

Ventricular tachycardia (VT), ventricular fibrillation (VF), and atrial flutter (AFL) are potentially fatal or serious complications arising after cardiac surgery. Generally, we treat these complications with class I antiarrhythmic agents and/or direct counter shock (DC). However, sometimes these complications do not respond to antiarrhythmic agents and require frequent DC. Moreover, these class I agents induce heart failure due to their negative inotropic effect. Nifekalant hydrochloride (NIF) is a class III antiarrhythmic agent that prolongs the refractory period of the atrial and ventricular myocardium without any negative inotropic action. From July 2003 to September 2004, we treated 11 patients with NIF for perioperative arrhythmias (VT 5, VF 2, and AFL 4). NIF was administered by continuous intravenous infusion (0.3 to 0.4 mg/ kg/h) to prevent the recurrence of VT/VF and AFL. NIF prevented the recurrence of VT in 3 of the 5 cases. No recurrence was observed in 2 cases with VF. Furthermore, NIF prevented the recurrence of AFL in all the 4 patients. None of the patients exhibited changes in heart rate, cardiac output, and QTc interval. Additionally, no occurrence of Torsades de pointes was observed in any of the cases. In conclusion, NIF is an effective and safe antiarrhythmic agent for the treatment of perioperative arrhythmias under continuous monitoring of the QTc interval.

Adult↗
PubMed2002

[Arrhythmias after surgery for congenital heart disease].

The improvement of surgical techniques over the last few years have made postoperative chronotropic insufficiency either by sinus node dysfunction or iatrogenic atrioventricular block less common. However, reentrant tachycardia around lines of incision or a patch may be observed. Persistent dilatation of a cardiac chamber or ventricular dysfunction are predisposing factors. Flutter-like arrhythmias occur mainly after atrial surgery (closure of atrial septal defects, Mustard, Senning or Fontan procedures). Ventricular tachycardias are observed more often after correction of tetralogy of Fallot or in patients with severe ventricular dysfunction. In fact, any type of arrhythmia may arise, especially when the lesion is operated late in childhood or in adulthood with a partial haemodynamic result (residual gradient, valvular regurgitation or ventricular dysfunction...). In this context, regular ECG follow-up should be associated with repeated Holter monitoring and exercise stress testing. From the therapeutic point of view, amiodarone remains the best antiarrhythmic drug. Radiofrequency ablation techniques represent a recent but decisive advance in the management of atrial arrhythmias.

Amiodarone↗
PubMed1982

His bundle recordings in double tachycardias not due to digitalis intoxication.

Electrophysiological studies were performed in a patient with chronic chagasic cardiomyopathy, recurrent sustained ventricular tachycardia, and a history (without electrocardiographic documentation) of paroxysmal atrial flutter. Ventriculoauricular conduction occurred during short bursts of ventricular pacing. Moreover, the retrograde P of ectopic ventricular beats which appeared after pacing was stopped precipitated an atrial tachyarrhythmia with an irregular atrial rate. In addition, burst ventricular pacing, performed while this atrial tachyarrhythmia was present, initiated and subsequently terminated a ventricular tachycardia with similar characteristics to the one occurring spontaneously. The double (atrial and ventricular) tachycardias described in this communication were different from those previously reported in that the arrhythmias were not due to digitalis toxicity, but resulted from the modality of ventricular stimulation performed in a patient who had the specific type of cardiomyopathy seen in the chronic stage of Chagas' disease.

Atrial Flutter↗
PubMed1995

Intravenous administration of diltiazem in the treatment of supraventricular tachyarrhythmias.

UNLABELLED: The aim of the study was to investigate the efficacy of diltiazem bolus intravenous administration, compared to disopyramide, in the treatment of various types of paroxysmal supraventricular tachyarrhythmias. METHOD: Fifty patients (23 males, 27 females, mean age 47.7 +/- 15.2 years) with paroxysmal supraventricular tachyarrhythmia (20 with paroxysmal atrial tachycardia, 23 with paroxysmal atrial fibrillation and rapid ventricular response and 7 with atrial fluttering) were studied. Diltiazem at a dose of 0.25-0.30 mg/kg BW or disopyramide at a dose of 50 mg were given bolus IV. If conversion of the arrhythmia to sinus rhythm could not be achieved with the initial drug, the alternate was given. The order of administration of the drugs was random, independent of the type of the arrhythmia. Before and during drug administration detailed clinical examination and frequent blood pressure (BP) measurements were performed. Twenty-four hour Holter monitoring was done in all patients, starting with the administration of the antiarrhythmic drug. RESULTS: 1) Paroxysmal atrial tachycardia: diltiazem administration converted the arrhythmia to sinus rhythm in all patients while disopyramide in only 1 of 9 patients who received this drug. 2) Paroxysmal atrial fibrillation: disopyramide converted the arrhythmia in 5 patients without significant change in ventricular response in the others. Diltiazem did not convert the arrhythmia though it caused significant decrease in ventricular response (< 100 bpm) and in 1 patient an important bradycardia (45 bpm). 3) Atrial fluttering: disopyramide converted the arrhythmia to sinus rhythm in 1 patient without significant change in the ventricular response in the others. Diltiazem caused significant decrease in the ventricular response without conversion to sinus rhythm. During conversion to sinus rhythm an AV junctional rhythm of short duration (< 1 min) was noticed in 5 patients and a short pause (< 2 sec) with or without an initial premature contraction in the remaining 21. Disopyramide administration was not associated with side effects. Diltiazem administration cause small (< 20 mm Hg), transient (< 30 min) decrease of BP without symptoms with the exception of the patient with bradycardia in whom the BP decrease was significant (90/60 from 160/80 mm Hg) followed by intense symptoms which lasted for six hours. CONCLUSIONS: Diltiazem administration is extremely effective in conversion of paroxysmal atrial tachycardia to sinus rhythm. In addition it retards ventricular response in patients with atrial fibrillation and fluttering. Compared to disopyramide these effects of diltiazem are more pronounced and clinically pertinent.

Adult↗
PubMed1994

Clinical experience with propafenone for cardiac arrhythmias in the young.

Seventy-two children were treated with propafenone between 1980 and 1990. The mean age was 34 months (range 0-192). Arrhythmias included atrioventricular re-entry tachycardia in 32 patients (44%), atrial flutter in 16 (22%), atrial or junctional ectopic tachycardia in 10 (14%), atrial re-entry tachycardias in three (4%) and ventricular arrhythmias in 11 patients (16%). The efficacy of oral treatment was good in patients with atrio-ventricular re-entry tachycardia (80%), atrial flutter (71%) and atrial ectopic tachycardia (83%); it was poor in ventricular arrhythmias (40%). The mean oral dose was 13.5 mg.kg-1. day-1. Dosage and serum levels of propafenone did not differ whether the patients were treated successfully or not. No correlation between dosage and serum level was observed. Intravenous propafenone administration was only partially successful in suppressing supraventricular tachycardias (6 of 11 patients). The presence of a congenital heart defect and the time of onset of the arrhythmias had a significant influence on the efficacy of propafenone. Better results were observed in patients with normal hearts and in whom onset of arrhythmia was pre-natal (success 80%) as well as in patients with arrhythmias seen early after surgery for congenital heart defects (success 87%). Success (65%) was also observed in patients without congenital heart defects and postnatal onset of supraventricular arrhythmias. Patients with ventricular or supraventricular arrhythmias late after corrective surgery showed the poorest response (31%).

Administration, Oral↗
PubMed1996

Control of heart rate during transition from intravenous to oral diltiazem in atrial fibrillation or flutter.

We tested whether patients presenting with atrial fibrillation (AF) or flutter (AFl) with a rapid ventricular response could maintain control of heart rate while transferring from a bolus and continuous infusion of intravenous diltiazem to oral diltiazem. Forty patients with AF or AFI and sustained ventricular rate > or = 120 beats/min received intravenous diltiazem "bolus" (20 to 25 mg for 2 minutes) and "infusion" (5 to 15 mg/hour for 6 to 20 hours). Oral long-acting diltiazem (diltiazem CD 180, 300, or 360 mg/24 hours) was administered in patients in whom stable heart rate control was attained during constant infusion. Intravenous diltiazem infusion was discontinued 4 hours after the first oral dose, and patients were monitored during 48 subsequent hours of "transition" to oral therapy. Response to diltiazem was defined as heart rate <100 beats/min, > or = 20% decrease in heart rate from baseline, or conversion to sinus rhythm. Other rate control or antiarrhythmic medications were not allowed during the study period. Thirty-seven of 40 patients maintained heart rate control during the bolus, and 35 of the remaining 37 maintained control during the infusion of intravenous diltiazem. Of the 35 patients achieving heart rate control with intravenous diltiazem who entered the transition to oral therapy, 27 maintained heart rate control (response rate of 77%/, 95% confidence interval 63% to 91%). The median infusion rate of intravenous diltiazem was 10 mg/hour, and the median dose of oral diltiazem CD was 300 mg/day. Oral long-acting diltiazem was 77% effective in controlling ventricular response over 48 hours in patients with AF or AFl in whom ventricular response was initially controlled with intravenous diltiazem.

Administration, Oral↗
PubMedDate not supplied

Class III antiarrhythmic action in experimental atrial fibrillation and flutter in dogs.

Progress in the pharmacological treatment of atrial fibrillation and flutter has been achieved by the introduction of the class III antiarrhythmic drug amiodarone. In the present study we tested amiodarone and a new class III antiarrhythmic drug, melperone, in experimentally induced atrial fibrillation and flutter in pentobarbital-anesthetized dogs. By high-rate stimulation in the right atrium, atrial fibrillation was induced in 4, and atrial flutter in 10 out of 22 dogs. Atrial flutter rate was 496 +/- 13 min-1 (median +/- 95% confidence interval). Both drugs converted the arrhythmias at doses from 2.5 to 10 mg . kg-1 and reduced that atrial flutter rate before conversion. Average ventricular rate during arrhythmias (261 +/- 16 min-1) decreased after amiodarone, and was unchanged or, in three out of nine dogs, increased after melperone. The doses of amiodarone converting the arrhythmias increased atrial refractoriness, whereas the effects on AV nodal conduction and refractoriness were variable. The results support the concept that atrial flutter is due to circus movement where the flutter rate is dependent upon atrial refractoriness. The class III antiarrhythmic drugs amiodarone and melperone seem to be equally potent in converting atrial arrhythmias.

Amiodarone↗
PubMedDate not supplied

[The use of endocavitary fulguration in the treatment of common auricular flutter].

Between April 1990 and July 1991, 10 patients, were fulgurated after right atrial endocardial mapping with the purpose of destroying or modifying the site of origin of atrial flutter. Mean age, 47 years old (23-61), 9 males. All patients suffered "common" atrial flutter episodes with very rapid ventricular response (greater than or equal to 150 beats per minute) refractory to pharmacological therapy. All patients had pathologic potentials with prolonged duration between 90 and 160 ms (m = 109) which preceded other reference electrodes in the high right atrium and His position. Electrical stimulation from that zone provoked the capture entrainment and termination of the flutter; the same configuration of the arrhythmia was obtained with electrical stimulation from the suspected zone. With the catheter in that situation one or two direct current cathodic, unipolar shocks were given with energy of 60-150 Joules (m = 117). In the follow up (16-73 weeks), 8 patients are free of symptoms without drugs, one suffered a new episode after 7 weeks, His fulguration was performed and a permanent pacemaker implanted. The other patient has failed two session and is still on treatment.

Atrial Flutter↗
PubMed1992

Dofetilide, a novel class III antiarrhythmic agent.

Dofetilide is a potent and selective class III antiarrhythmic agent that is under development for the treatment of re-entrant tachyarrhythmias (ventricular tachycardia/ventricular fibrillation, atrial fibrillation/atrial flutter, and paraoxysmal supraventricular tachycardia). In animal studies, dofetilide selectively inhibits the rapid component of the time-dependent outward potassium current (IKr) and therefore increases the effective refractory period and action potential duration without affecting the fast inward sodium current. Studies in dogs have shown that dofetilide (a) prolongs the effective refractory period in a dose-dependent manner, (b) elevates ventricular fibrillation threshold, (c) facilitates conversion of electrically induced ventricular fibrillation or fibrilloflutter to sinus rhythm, (d) does not influence conduction within the His-Purkinje system or within the myocardium, (e) does not impair cardiac contractility, and (f) reduces dispersion of ventricular repolarization. Dofetilide has been administered to healthy volunteers as well as to patients with ischemic heart disease or with supraventricular arrhythmias; the compound has generally been well tolerated. Side effects have occasionally been reported, but have generally been transient and mild and occur in placebo-treated subjects as well. No clinically significant changes in laboratory safety tests have been detected. The pharmacokinetic profile of dofetilide both in healthy volunteers and patients includes a linear dose-plasma concentration relationship and also a linear plasma concentration-QTc relationship. The terminal plasma elimination half-life is approximately 9-10 h and systemic bioavailability in the region of 100%. The elimination pattern is balanced, with 50% being excreted unchanged via the kidney, the remaining 50% being metabolized in the liver to inactive metabolites, with greater than 90% of circulating drug-related material being unchanged dofetilide. After intravenous administration of the compound, a slight hysteresis in the plasma drug level-QTc relationship has been detected. Pharmacodynamic data demonstrate dose- and concentration-dependent effects on myocardial repolarization as evidenced by prolongations of the QTc interval. This is reflected in significant prolongations in the effective and functional refractory periods and monophasic action potential duration throughout the myocardium. No effects on sinus node function, conduction parameters, or cardiac contractility have been detected in any of the clinical studies, supporting the contention that dofetilide is a highly selective class III antiarrhythmic agent.

Action Potentials↗
PubMed1978

Radiofrequency-triggered pacemakers: uses and limitations. A long-term study.

Seven patients with either recurrent paroxysmal supraventricular tachycardia (five), alternatinng bradycardiatachycardia (one), or ventricular tachycardia (one) underwent insertion of permanent radiofrequency-triggered pacemakers. Follow-up evaluation (36 +/- 24 months, mean +/- SD) revealed that arrhythmias were well controlled in five of seven patients, although three of the five required medication to decrease frequency of arrhythmias. Overdrive pacing was ineffective in one patient with Wolff-Parkinson-White syndrome who had recurrent bouts of atrial fibrillation or atrial flutter. One additional patient with ventricular tachycardia became refractory to overdrive atrial pacing. These studies document the long-term effectiveness of radiofrequency pacemakers in some patients with recurrent refractory arrhythmias. Careful patient selection and electrophysiologic studies are mandatory before implantation of a permanent radiofrequency pacemaker. Physicians must be aware of both the benefits and possible limitations of radiofrequency pacemakers in order to choose between pacemaker versus surgical intervention in patients with cardiac arrhythmias refractory to standard drug therapy.

Adult↗