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Europace Advance Access originally published online on February 7, 2008
Europace 2008 10(3):284-288; doi:10.1093/europace/eun012
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

ELECTROPHYSIOLOGY

Clinical and electrophysiological characteristics of patients having atrial flutter with 1:1 atrioventricular conduction

Mihoko Kawabata*, Kenzo Hirao, Kouji Higuchi, Takeshi Sasaki, Toshiyuki Furukawa, Hiroyuki Okada, Hitoshi Hachiya and Mitsuaki Isobe

Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan

Manuscript submitted 15 October 2007. Accepted after revision 7 January 2008.

* Corresponding author. Tel: +81 358035231; fax: +81 358030131.E-mail address: mihoko_kawabata.cvm{at}tmd.ac.jp


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Limitations
 Clinical implications
 Conclusions
 References
 
Aims: The purpose of this retrospective study was to assess characteristics of patients who had suffered atrial flutter (AFL) with 1:1 atrioventricular (AV) conduction (1:1 AFL).

Methods and results: Subjects were 8 patients (61 ± 14 years) with documented 1:1 AFL, and 101 AFL patients without a history of 1:1 AFL (control patients). 1:1 AFL occurred during physical activity with a ventricular rate of 218 ± 18 bpm. Antiarrhythmic agents were administered to all eight 1:1 AFL patients, whereas AV nodal conduction-suppressing agents were administered to four. The maximum ventricular rate at which 1:1 AV conduction occurred was significantly lower than when spontaneous 1:1 AFL occurred (164 vs. 218 bpm, P < 0.05). The 1:1 AFL patients had a significantly longer AFL cycle length (CL) (292 vs. 258 ms, P < 0.05) and more rapid AV nodal conduction time (maximum 1:1 AV conduction: 375 vs. 464 ms, P < 0.05) than did control. Arrhythmia had occurred in patients with an AFL CL ≥ 250 ms and a CL of maximum 1:1 AV conduction ≤400 ms.

Conclusion: Clinicians should be aware of the potential for 1:1 AV conduction in AFL patients, especially in those with remarkable prolongation of the CL in addition to enhanced AV conduction.

Key Words: Atrial flutter, 1:1 AV conduction, Syncope, Exercise, Sympathetic tone


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Limitations
 Clinical implications
 Conclusions
 References
 
Atrial flutter (AFL) with 1:1 atrioventricular (AV) conduction (1:1 AFL) can be associated with haemodynamic compromise and require emergency treatment. Treatment with antiarrhythmic agents (AAs) can provoke this disorder by decreasing the atrial rate. Therefore, use of an AA in combination with a drug that slows conduction through the AV node is recommended. Beta-blockers have been proposed as candidate drugs.1Go,2Go However, negative dromotropic medication is not always effective.3Go–7Go

The purposes of this retrospective study were to identify clinical and electrophysiological characteristics of patients who had suffered 1:1 AFL and to identify risk factors for this hazardous arrhythmia.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Limitations
 Clinical implications
 Conclusions
 References
 
Study population
Eight patients with clinically documented 1:1 AFL were included in the study: seven men (87%) and one woman, with a mean age of 61 ± 14 years (range 39–78 years). The mean duration of AFL was 44 months (range 1–110 months). Two patients had underlying cardiovascular disease, old myocardial infarction in one, and tachycardia-induced cardiomyopathy in the other.

Characteristics of these patients were compared with those of 101 consecutive patients (control group) who were referred to our institution for RF ablation of AFL between March 1997 and October 2006 but who had no history of 1:1 AV conduction during AFL [89 men (88%) and 12 women; mean age 64 ± 14 years, range 15–89 years). Fifty-four of these patients had cardiovascular disease: ischaemic heart disease (n = 14), hypertrophic cardiomyopathy (n = 6), post-cardiac surgery state (n = 8), dilated cardiomyopathy (n = 2), pericarditis (n = 2), tachycardia-induced cardiomyopathy (n = 2), and cor pulmonae (n = 1). Ten patients had sick sinus syndrome (three with a pacemaker). Primary hypertension was diagnosed in 30 patients. The mean duration of AFL in the control group was 37 months (range 3 days–420 months).

Patient evaluations
Demographic data, pertinent prior medical history, symptoms, treatment history, and physical findings were obtained from the clinical records of each patient. A 12-lead electrocardiogram (ECG) was recorded, and duration of the PR interval during sinus rhythm and cycle length (CL) during AFL were automatically measured. Two-dimensional echocardiographic parameters [left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter, and left atrial diameter (LAD)] were obtained for each patient.

Electrophysiological study
Written informed consent was obtained from all patients for electrophysiological study (EPS). Electrophysiological study was performed without interruption of AA and AV nodal-blocking drugs to assess AV nodal conduction, including atrial pacing at incremental rates to determine the maximal rate of consistent 1:1 AV conduction and programmed atrial stimulation with one extrastimulus. Measurement of the CL and AH and HL intervals was also performed during sinus rhythm.

Statistical analysis
All data are reported as mean ± SD. Differences in continuous variables were analysed with unpaired Student’s t-test, and the {chi}2 test was used to assess homogeneity in contingency tables. P < 0.05 was considered statistically significant. SPSS version 11.0.1 was used for all statistical analyses.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Limitations
 Clinical implications
 Conclusions
 References
 
Atrial flutter with 1:1 atrioventricular conduction
In all eight 1:1 AFL patients, arrhythmia had occurred during physical activity. The ventricular rate of arrhythmia was 218 ± 18 bpm (range 188–240 bpm). Syncope accompanied arrhythmia in five patients, near syncope in two, and a shock state in one. Both patients with underlying heart disease suffered syncope during 1:1 AFL.

Clinical and electrophysiological characteristics of the patients with 1:1 atrial flutter
The average LVEF was 58 ± 17% (range 28–79%), and LAD was 38 ± 7 mm (range 29–50 mm) (Table 1).


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  		Table 1 Clinical and electrophysiological characteristics of patients with and without 1:1 atrial flutter

 
All eight patients had been treated with an AA. This was to prevent paroxysmal AFL in five patients and paroxysmal atrial fibrillation (AF) in three. A class Ia drug (cibenzoline) was administered to two patients, class Ic drugs were administered to five patients (flecainide to two, pilsicainide to three), and a class III drug (amiodarone) was administered to one patient. Meanwhile, an AV nodal conduction-suppressing agent was given to four of these patients [atenolol (25 mg) to one, verapamil (120 or 320 mg) to two, and digoxin (0.125 mg) to one].

The PR interval of the surface ECG was not short in any of the eight patients (range 133–225 ms, mean 175 ± 34 ms). The AFL CL was 292 ± 28 ms (255–330 ms). During EPS, the AH interval varied from 65 to 100 ms (mean 86 ± 14 ms). There was no AV nodal duality property with a single premature atrial extrastimulus. The maximum pacing rate at which 1:1 AV conduction was maintained was 375 ± 74 ms (range 290–400 ms).

In all eight patients, second-degree AV block developed during atrial pacing at rates lower than those during which 1:1 AV conduction was sustained during spontaneous AFL (164 bpm during atrial pacing vs. 218 bpm during spontaneous 1:1 AFL; P < 0.05, Figure 1).


Figure 1
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  		Figure 1 The rate of maximum 1:1 atrioventricular conduction during spontaneous 1:1 atrial flutter and during atrial pacing in patients with clinically documented 1:1 atrial flutter.

The rate of maximum 1:1 atrioventricular conduction during atrial pacing was less than that during clinical 1:1 atrial flutter in all patients (164 ± 30 bpm during atrial pacing vs. 218 ± 18 bpm during spontaneous 1:1 atrial flutter; P < 0.05).

 
The ECG of a 44-year-old man without any underlying heart disease but who suffered 1:1 AFL during exercise under administration of 100 mg/day cibenzoline and 25 mg/day atenolol is shown in Figure 2. This patient’s blood pressure was 60 mmHg during 1:1 AFL. After intravenous injection of 2.5 mg verapamil, the AV conduction was suppressed to 4:1.


Figure 2
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  		Figure 2 Electrocardiograms of a 44-year-old man.

Left: atrial flutter (cycle length, 255 ms) with 1:1 atrioventricular conduction exhibiting right bundle branch block during exercise under administration of 100 mg/day cibenzoline and 25 mg/day atenolol. Blood pressure was 60 mmHg. Right: after intravenous injection of 2.5 mg verapamil, atrioventricular conduction was suppressed to 4:1.

 
Clinical and electrophysiological characteristics of the control group
At least 1 AA had been administered to 77 of the control patients (76%) (Table 1). This was to prevent paroxysmal AFL in 21, paroxysmal AF in 54, ventricular tachycardia in 1, and atrial tachycardia in 1. Class Ia drugs were administered to 22 of these patients (cibenzoline to 17, disopyramide to 4, procainamide to 1). A class Ib drug (aprindine) was administered to five patients; class Ic drugs were administered to 36 patients (flecainide to 11, pilsicainide to 23, propafenone to 2); class III drugs were administered to seven patients (amiodarone to four, sotalol to two, sematilide to one); and a class IV drug (bepridil) was administered to one patient. The remaining six patients were given two different AAs in combination (bepridil + flecainide to three patients, cibenzoline + pilsicainide to one, disopyramide + cibenzoline to one, pilsicainide + bepridil to one). To depress AV nodal conduction, beta-blockers were given to 28 patients, verapamil to 31, diltiazem to 3, and digoxin to 12.

The PR interval of the surface ECG was 183 ± 42 ms, and the CL during AFL was 258 ± 44 ms. During EPS, the AH interval was 110 ± 32 ms, the rate of maximum 1:1 AV conduction was 464 ± 106 ms.

Comparison of 1:1 atrial flutter patients and control patients
There were no significant differences in clinical characteristics between the two study groups (Table 1). The patients with 1:1 AFL had a significantly longer AFL CL (292 vs. 258 ms, P < 0.05) and more rapid AV nodal conduction time (maximum 1:1 AV conduction: 375 vs. 464 ms, P < 0.05) than did the control patients. All 1:1 AFL patients except one had a longer AFL CL than the average CL of the control patients. 1:1 AFL had occurred in patients with a CL during AFL ≥ 250 ms and a CL of maximum 1:1 AV conduction ≤400 ms (Figure 3).


Figure 3
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  		Figure 3 Scatter plot of the cycle length during atrial flutter and cycle length of maximum 1:1 atrioventricular conduction. Atrial flutter with 1:1 atrioventricular conduction was observed in patients with a cycle length during atrial flutter ≥250 ms and a cycle length of maximum 1:1 atrioventricular conduction ≤400 ms.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Limitations
 Clinical implications
 Conclusions
 References
 
Major findings
The present study revealed that in all eight 1:1 AFL patients, arrhythmia had occurred during physical activity and caused a potentially life-threatening haemodynamic state. Five patients suffered syncope, two suffered near syncope, and one suffered a shock state. Two patients had underlying heart disease. In all eight patients, the maximum rate at which 1:1 AV conduction occurred was significantly lower during atrial pacing than when the 1:1 AFL was spontaneous. These patients had a significantly prolonged AFL CL and a significantly shorter CL of maximum 1:1 AV conduction than did the control patients despite the fact that AA administration did not differ between them. Atrial flutter with 1:1 AV conduction occurred in patients with a CL during AFL ≥ 250 ms and a CL of maximum 1:1 AV conduction ≤400 ms.

Pro-arrhythmic effects of antiarrhythmic agents: prolongation of the atrial cycle length during atrial flutter
AFL with 1:1 AV conduction is recognized as a pro-arrhythmic complication of antiarrhythmic therapy.1Go,2Go The mechanism of the 1:1 ventricular response in AFL during administration of AA is two-fold: (i) a prolongation in the AFL CL occurs due to drug-induced depression of atrial conduction velocity; (ii) if the atrial rate is slowed sufficiently, the AV node may permit 1:1 AV conduction under weak action of the AA on the AV node.

All eight patients with 1:1 AFL had been treated with an AA. The AA attributed to the significant slowing of the atrial rate enough to allow acceleration of the ventricular response during AFL; however, there was no significant difference in the percentage of patients given an AA between the 1:1 AFL group and the control group (100 vs. 76%).

Structural heart disease is known to increase the risk of ventricular pro-arrhythmia.8Go–12Go However, it was not a risk factor for pro-arrhythmias in the AFL patients.

Enhanced atrioventricular conduction with increasing sympathetic tone
The ventricular response during AFL is determined by the refractory period of the AV node, the degree of concealed conduction within the node, and the level of autonomic tone. Pre-existing rapid AV nodal conduction can also be a predisposing factor for the occurrence of 1:1 AFL.

Although 1:1 AV conduction during AFL is thought to be unusual in the absence of AA therapy, there have been a few reports of this phenomenon.13Go–15Go None of the reported patients had electrocardiographic evidence of pre-excitation, such as an abnormally short PR interval or delta waves during sinus rhythm. However, EPS suggested that some patients may have had either partial AV nodal bypass tracts with a shorter refractory period than the AV node or an AV node with unusual capacity for rapid conduction.14Go,15Go In our patients, the normal PR and AH intervals excluded total AV nodal bypass. Although EPS showed AV conduction to be within normal range, all the eight of our patients had 1:1 AFL during physical activity, which might have heightened sympathetic tone. The association of 1:1 AFL with high catecholamine states, such as exercise, is well documented.3Go Like other reported patients,13Go,14Go,16Go our patients showed that the maximum rate at which 1:1 AV conduction occurred was significantly lower during atrial pacing than when spontaneous 1:1 AFL was present. Sympathetic tone might play an important role in the occurrence of 1:1 AFL, making it more difficult to detect patients at risk of 1:1 AFL and to forecast sufficient amounts of negative dromotropic agents needed for prevention on the basis of basal characteristics.

Previous reports
Brembilla-Perrot et al.17Go reported that rapid AV nodal conduction indicated by a short PR interval on the surface EGG and continuity between the P wave and QRS complex on the signal-averaged ECG is a predisposing factor for the development of 1:1 AFL under administration of class I AAs. Like us, they showed that age and the presence of underlying heart disease do not predict the occurrence of 1:1 AFL. Although they did not mention the AFL CL, our results revealed the importance of two factors underlying 1:1 AFL: CL during AFL and a property of enhanced AV nodal conduction particularly under heightened sympathetic tone.


   Limitations
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
Clinical implications
 Conclusions
 References
 
Our study was limited by the fact that a stress test was not performed. Isoproterenol (ISP) was injected during evaluation of the AV conduction property in only one patient. Maximum 1:1 AV conduction improved in this patient from 340 to 270 ms with infusion of ISP. In contrast, the atrial CL during spontaneous 1:1 AFL was 316 ms. Because it is more likely that enhanced AV conduction occurred secondarily to heightened adrenergic tone and circulating catecholamines during 1:1 AFL under physical activity, the existence of an AV node with an unusual capacity for rapid AV conduction in an increasing sympathetic state could not be completely ruled out without the infusion of ISP. The study was also limited by its retrospective design and the small size of the 1:1 AFL group.


   Clinical implications
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Clinical implications
Conclusions
 References
 
We consider it mandatory to use drugs capable of slowing AV nodal conduction in addition to AA treatment to prevent 1:1 AFL. Although beta-blockers have been proposed as the best candidate drugs, use of these drugs does not guarantee protection against arrhythmia. The dosage must be adequate to surely suppress the AV conduction. To the best of our knowledge, this is the first reported study to assess the risk factors for 1:1 AFL on the basis of multiple clinical data, such as patient characteristics, ECG and EPS findings, and medical treatment including AA and AV node blockers. Results of the study show the limitations of classifying patients as ‘high risk’ or ‘low risk’ for 1:1 AFL.

Atrial fibrillation often converts to AFL under pharmacological therapy; therefore, AAs must be administered cautiously along with AV nodal conduction-suppressing agents at adequate doses in patients with AF.


   Conclusions
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Clinical implications
 Conclusions
References
 
Clinicians should be aware of the risk of 1:1 AV conduction in AFL patients, particularly in those with remarkable prolongation of the CL in addition to essentially enhanced AV conduction properties. It is better to avoid administration of AAs in such patients and to treat them with catheter ablation of the cavo-tricuspid isthmus.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Clinical implications
 Conclusions
 References
 
[1] Marcus FI. The hazards of using type Ic antiarrhythmic drugs for the treatment of paroxysmal atrial fibrillation. Am J Cardiol (1990) 66:366–7.[CrossRef][Web of Science][Medline]

[2] Friedman PL, Stevenson WG. Proarrhythmia. Am J Cardiol (1998) 82:50N–58N.[CrossRef][Web of Science][Medline]

[3] Kawabata M, Hirao K, Horikawa T, Suzuki K, Motokawa K, Suzuki F, et al. Syncope in patients with atrial flutter during treatment with class Ic antiarrhythmic drugs. J Electrocardiol (2001) 34:65–72.[Medline]

[4] Wiesfeld AC, Ansink JM, van Veldhuisen DJ, van Gelder IC. Broad complex tachycardia during treatment of atrial fibrillation with a 1c antiarrhythmic drug: ventricular or supraventricular proarrhythmia? Int J Cardiol (2006) 107:140–1.[CrossRef][Medline]

[5] Feld GK, Chen PS, Nicod P, Fleck P, Meyer D. Possible atrial proarrhythmic effects of class Ic antiarrhythmic drugs. Am J Cardiol (1990) 66:378–83.[CrossRef][Web of Science][Medline]

[6] Aouate P, Elbaz N, Klug D, Lacotte J, Raguin D, Frank R, et al. Atrial flutter with 1/1 nodo-ventricular conduction with amiodarone from physiopathology to diagnosis. Arch Mal Coeur Vaiss (2002) 95:1181–7. (in French).[Medline]

[7] Brembilla-Perrot B, Houriez P, Claudon O, Yassine M, Suty-Selton C, Vancon AC, et al. Can the supraventricular proarrhythmic effects of class 1C antiarrhythmic drugs be prevented with the association of beta blockers? Ann Cardiol Angeiol (Paris) (2000) 49:439–42. (in French).[Medline]

[8] Velebit V, Podrid P, Lown B, Cohen BH, Graboys TB. Aggravation and provocation of ventricular arrhythmias by antiarrhythmic drugs. Circulation (1982) 65:886–94.[Abstract/Free Full Text]

[9] Torres V, Flowers D, Somberg JC. The arrhythmogenicity of antiarrhythmic agents. Am Heart J (1985) 109:1090–4.[CrossRef][Medline]

[10] Creamer JE, Nathan AW, Camm AJ. The proarrhythmic effects of antiarrhythmic drugs. Am Heart J (1987) 114:397–406.[CrossRef][Medline]

[11] Kerin NZ, Somberg S. Proarrhythmia: definition, risk factors, causes, treatment and controversies. Am Heart J (1994) 126:575–85.

[12] The Cardiac Arrhythmia Suppression Trial (CAST) Investigators Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. New Engl J Med (1989) 321:406–12.[Abstract]

[13] Kennelly BM, Lane GK. Electrophysiological studies in four patients with atrial flutter with 1:1 atrioventricular conduction. Am Heart J (1978) 96:723–30.[CrossRef][Medline]

[14] Aranda JM, Moleiro F, Castellanos A, Befeler B. Electrophysiologic studies in a patient with atrial flutter and 1:1 atrioventricular conduction. Chest (1975) 68:200–4.[CrossRef][Medline]

[15] Castellanos A, Vagueiro MC, Befeler B, Myerburg RJ. Syndrome of short P-R, narrow QRS and repetitive supraventricular tachyarrhythmias: the possible occurrence of the R-on-T phenomenon and the limits of this syndrome. Eur J Cardiol (1975) 2:337–42.[Medline]

[16] Lister JW, Stein E, Kosowsky BD, Lau SH, Damato AN. Atrioventricular conduction in man. Effect of rate, exercise, isoproterenol and atropine on the P-R interval. Am J Cardiol (1965) 16:516–23.[CrossRef][Web of Science][Medline]

[17] Brembilla-Perrot B, Houriez P, Beurrier D, Claudon O, Terrier de la Chaise A, Louis P. Predictors of atrial flutter with 1:1 conduction in patients treated with class I antiarrhythmic drugs for atrial tachyarrhythmias. Int J Cardiol (2001) 80:7–15.[CrossRef][Web of Science][Medline]


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