Role of autonomic reflexes in syncope associated with paroxysmal atrial fibrillation.

OBJECTIVES: The purpose of this study was to evaluate the role of autonomic reflexes in the genesis of syncope associated with the onset of paroxysmal atrial fibrillation. BACKGROUND: Syncope associated with paroxysmal atrial fibrillation has been interpreted as an ominous finding predictive of rapid ventricular rates. However, various mechanisms may be involved when heart rate is not particularly high. METHODS: Forty patients (age 60 +/- 14 years, 20 men, 20 women) with syncope and atrial fibrillation were compared with atrial fibrillation without syncope. Carotid sinus massage and head-up tilt testing (at 60 degrees for 60 min at baseline and during isoproterenol infusion) were performed during sinus rhythm. A positive response was defined as the induction of syncope. Atrial fibrillation was also induced on a tilt table at 60 degrees by means of short bursts of atrial pacing. RESULTS: Results of carotid sinus massage were positive in 15 (37%) of 40 patients but in no control subjects (p = 0.002). Head-up tilt test findings were positive in 25 (66%) of 38 patients and in 2 (12%) of 16 control subjects (p = 0.0004). The induction of atrial fibrillation in the upright position elicited syncope in 16 (42%) of 38 patients but in none of 16 control subjects (p = 0.001). At the beginning of atrial fibrillation, systolic blood pressure was lower in patients than in control subjects (88 +/- 32 vs. 127 +/- 32 mm Hg), whereas mean heart rate was similar (142 +/- 35 vs. 134 +/- 25 beats/min). The correlation between heart rate and systolic blood pressure was weak (r = 0.35), and in five patients syncope occurred at a heart rate < or = 130 beats/min. At the time of syncope, heart rate decreased (-12 +/- 21 beats/min) in patients with induced syncope, whereas it remained unchanged in patients without induced syncope (+1 +/- 17 beats/min, p = 0.04) or slightly increased in control subjects (+9 +/- 21 beats/min, p = 0.009). CONCLUSIONS: Patients with syncope associated with paroxysmal atrial fibrillation are predisposed to an abnormal neural response during both sinus rhythm and arrhythmia. In some patients the onset of atrial fibrillation triggers vasovagal syncope.

Progression of permanent atrial fibrillation after atrioventricular junction ablation and dual-chamber pacemaker implantation in patients with paroxysmal atrial tachyarrhythmias.

Among 63 patients affected by symptomatic drug refractory paroxysmal atrial fibrillation who had undergone atrioventricular junction ablation and dual-chamber pacemaker implantation, the actuarial estimate of progression of permanent atrial fibrillation was 22%, 40%, and 56% respectively, 1, 2, and 3 years after ablation. A stratification of the risk of development of permanent atrial fibrillation was obtained on the basis of several clinical variables.

A controlled trial of acute and long-term medical therapy in tilt-induced neurally mediated syncope.

To study the efficacy of medical treatment for preventing syncopal recurrences in patients affected by tilt-induced neurally mediated syncope, a randomized placebo-treatment prospective study was performed in 30 patients (10 men and 20 women, mean age 42 +/- 21 years) who had syncope reproduced in 2 consecutive head-up tilt-table tests without pharmacologic intervention (n = 20) or during isoproterenol infusion (n = 10). Patients were randomly assigned to 2 groups: 15 to placebo, and 15 to drug therapy (determined on the basis of serial pharmacologic tilting tests). Therapy was either atenolol (n = 7), dihydroergotamine (n = 2), domperidone (n = 2), cafedrine (n = 1), or elastic compression stockings, alone or in association with drugs (n = 3). During a mean of 10 +/- 7 months of follow-up, syncope recurred in 3 patients (20%) in the treatment group and in 4 (27%) in the placebo group; actuarial rates of absence of syncopal recurrences after 20 months were 70 and 67%, respectively. Thus, the outcome of either treated or untreated patients was favorable (with a low recurrence rate of syncope), and the usefulness of tilting-guided medical therapy remains uncertain.

Follow-up of asystolic episodes in patients with cardioinhibitory, neurally mediated syncope and VVI pacemaker.

The occurrence rate of spontaneous asystolic episodes during long-term follow-up in patients with abnormal asystolic responses induced by means of vasovagal maneuvers was evaluated. The heart rate of 23 patients (mean age 64 +/- 12 years; 6 women and 17 men) affected by neurally mediated syncope (mean 4.3 +/- 4.9 episodes) was continuously monitored by a specially designed implanted pacemaker able to detect and store in its memory all asystolic episodes lasting 3 to 6 or > 6 seconds. Asystolic, neurally mediated syncope was diagnosed when a reflex asystole of > 3 seconds was induced during carotid sinus massage (n = 22), eyeball compression test (n = 3) or head-up tilt test (n = 2). During a total of 357 months (mean 15 +/- 7) of monitoring, asystolic episodes occurred in 17 patients (74%): 1,765 episodes of 3- to 6-second (median 3) duration occurred in 14 patients, and 47 episodes of > 6-second (median 2) duration occurred in 11. The actuarial estimates of occurrence of asystolic episodes of > 3 and > 6 seconds were 82 and 53%, respectively, after 2 years of follow-up. Only 12 episodes of 3 to 6 seconds (0.7%), and 20 episodes of > 6 seconds (43%) resulted in presyncopal or syncopal symptoms. Thus, an asystolic response to vasovagal maneuvers predicts the occurrence of spontaneous asystolic episodes during follow-up. With few exceptions, spontaneous episodes are asymptomatic and their incidence is low.

Neurally mediated syncope detected by carotid sinus massage and head-up tilt test in sick sinus syndrome.

It is generally accepted that a positive response to carotid sinus massage (CSM) or head-up tilt (HUT) in patients affected by syncope suggests a reflex cause of the syncope. To study the role of the autonomic nervous system in causing syncope in the sick sinus syndrome (SSS), CSM and HUT were performed in 35 consecutive patients (20 men, mean age 70 +/- 9 years) with syncope and SSS. Results were compared with those in 35 patients affected by syncope that, despite careful cardiovascular and neurologic examination, were of uncertain origin (21 men; mean age 68 +/- 9 years) and with those of 35 subjects without syncope (20 men; mean age 69 +/- 10). All patients underwent CSM in the supine and standing positions for 10 seconds and HUT to 60 degrees for 60 minutes. In the patients with SSS, the full reproduction of spontaneous symptoms by CSM occurred in 21 (60%) and by HUT, in 19 (54%). At least 1 test was positive in 28 patients (80%): cardioinhibitory or mixed responses in 69%, vasodepressor responses in 11%. The percentages of positive tests in the patients with syncope of uncertain origin were similar to or slightly less than those of patients with SSS (CSM 63%, HUT 26%, overall 74%) with cardioinhibitory or mixed responses in 54% and vasodepressor in 20% (p less than 0.05). In control subjects, syncope was induced by CSM in 1 (3%) and by HUT in 2 (6%); overall positivity was 9%. In conclusion, in most patients affected by syncope and SSS, an abnormal neural reflex probably plays a major role in causing syncope.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of atrioventricular junction radiofrequency ablation in patients with chronic atrial fibrillation and flutter on quality of life and cardiac performance.

The purpose of this study was to evaluate the effects of atrioventricular junction radiofrequency ablation on the quality of life, exercise performance, and echocardiographic parameters in 23 patients with chronic, severely symptomatic, drug-refractory atrial fibrillation or flutter. Initially, patients were randomized to receive ablation plus pacemaker therapy (n = 12) or pacemaker therapy alone (n = 11). After 15 days, palpitations decreased by 92% and 37% (p = 0.004), rest dyspnea by 79% and 40% (p = NS), effort dyspnea by 65% and 30% (p = 0.03), exercise intolerance by 54% and 17% (p = 0.005), and asthenia by 67% and 31% (p = 0.02) in the 2 groups, respectively. At the end of this short-term study, control patients also underwent ablation therapy, and a 3-month intrapatient follow-up study was performed in 22 patients. New York Heart Association functional class > or = 3 was present in 14 patients (64%) before, but in only 3 patients (14%) after ablation therapy (p = 0.002); specific activity scale functional class > or = 3 was present in 9 patients (41%) before, but in only 5 (23%) after ablation therapy (p = NS). Exercise duration during standardized stress testing increased by a mean of 63 +/- 93 seconds (15% increase) (p = 0.001). In the 9 patients with depressed left ventricular systolic function, echocardiographic fractional shortening increased by 34% (from 23 +/- 5% to 31 +/- 9%) (p = 0.003). In the remaining 13 patients with normal systolic function, fractional shortening decreased by 10% (from 40 +/- 5% to 36 +/- 6%) (p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of syncope caused by transient bradycardia and the diagnostic value of electrophysiologic testing and cardiovascular reflexivity maneuvers.

Transient bradycardia may be intrinsic because of sinus node or atrioventricular (AV) conduction abnormalities, or extrinsic because of abnormal vagal reflex. Twenty-five consecutive patients, referred to us for study of unexplained syncope, who, during electrocardiographic monitoring, had a documented episode of intermittent bradycardia that caused syncope, underwent a full electrophysiologic study, carotid sinus massage, and the head-up tilt test. A prolonged ventricular asystole (5 to 20 seconds) was documented during syncope in all patients: sinus arrest in 13, AV block in 7, sinus arrest plus AV block in 3, and asystolic pause during atrial fibrillation in 2. Abnormal electrophysiologic findings suggested the correct diagnosis in 6 patients (24%): block within the bundle of His in 5 and sick sinus syndrome in 1. An abnormal response to carotid sinus massage or to the head-up tilt test suggested a neurally mediated mechanism in 17 patients (68%). Overall, electrophysiologic study and vasovagal maneuvers were able to identify the mechanism of spontaneous syncope in 23 patients (92%). Thus, in patients affected by syncope due to transient bradycardia, the most likely mechanism of syncope is neurogenic, whereas it is cardiogenic only in a few instances. Electrophysiologic testing, carotid sinus massage, and the head-up tilt test can identify most of these patients. Conversely, when all these tests are negative, it is unlikely that transient bradycardia is the cause of syncope. Because of the different mechanisms involved, electrophysiologic study and vasovagal maneuvers are complementary diagnostic tools.

Clinical usefulness of slow pathway ablation in patients with both paroxysmal atrioventricular nodal reentrant tachycardia and atrial fibrillation.

Some patients with atrioventricular (AV) node reentrant tachycardia (AVN RT) also presented with atrial fibrillation (AF). In this study we demonstrate that slow pathway ablation is able to suppress both AVN RT and AF in subjects without structural heart abnormalities, whereas in patients with structural heart abnormalities after ablation AF frequently recurs.

Carotid sinus syncope: the most frequent neurally mediated syncope in the elderly.

The present work reviews current literature and the authors' experience of carotid sinus syndrome (CSS), which is considered to be the most common cause of neurally mediated acute disorders of consciousness in the elderly. Although no definitive consensus about its nosology has yet been reached, most groups agree that three features fulfill the diagnosis: anamnestic presence of syncope or its minor equivalents, and their reproduction by carotid sinus massage associated with defined values of cardioinhibition or vasodepression or both. The technique for performing carotid sinus massage used by the authors is described; this manoeuvre seems very safe and reproducible as long as simple rules are followed, and it allows the classification of CSS types. The treatment of CSS is varied, according to several factors. No pharmacological therapy has yet been demonstrated to be effective. While severe cardioinhibitory forms require an appropriate pacing, vasodepressive ones and types with only minor symptoms show a more favourable natural history. Pacing is advised in mixed CSS with either frequent and invalidating relapses, or 'high risk' attacks (severe, abrupt, with major traumas, etc.). Finally, the protocol for choosing the adequate mode of pacing is illustrated. In most cases VVI is sufficient, but the decision requires a careful individual examination.

Long-term outcome in symptomatic carotid sinus hypersensitivity.

Between 1982 and 1988, we observed 312 patients who were affected by syncope or presyncope and whose spontaneous symptoms could be reproduced by means of carotid sinus massage (CSH); no other definite cause of syncope could be identified. The clinical outcome during a 2- to 8-year follow-up period (mean 44 +/- 24 months) was assessed in 262 of them (mean age, 71 +/- 11 years; 183 men) and was compared with that of a group of 55 patients who were affected by unexplained syncope (control patients) who were matched 4:1 for age and sex with CSH patients. CSH patients had an overall mortality rate of 7.3 per 100 person-years (cardiovascular, 66%; sudden death, 9%); overall predicted cumulative survival rates at 1, 3, 5, and 7 years were 92%, 80%, 66% and 53%. Survival was similar in control patients; mortality rate was 5.8 per 100 person-years (cardiovascular, 82%; sudden death, 18%); cumulative survival rates at 1, 3, 5, and 7 years were 85%, 80%, 73%, and 69%. Standardized mortality rate of the general population with similar age and sex distribution, as calculated by means of Italian Istituto Centrale di Statistica death-rate data (1987 edition) was 8 per 100 person-years. Of 13 clinical variables, age, sex, abnormal electrocardiogram, and heart failure (but not CSH type or related arrhythmias) were independently linked to mortality in CSH patients (Cox model). In the vasodepressor form of CSH, patients were younger than those with other forms of CSH and the percentage of women was higher.(ABSTRACT TRUNCATED AT 250 WORDS)

[Carotid sinus syndrome and sick sinus syndrome: 2 frequent and distinct indications for pacemaker implantation]. / Sindrome del seno carotideo e malattia del nodo del seno: due cause frequenti e distinte di indicazione all'impianto di pacemaker definitivo.

UNLABELLED: At present, patients affected by carotid sinus syndrome and, more general by speaking, by vasovagal syncopes, are being considered more and more for pacemaker implant. However, neither the real incidence of the carotid sinus syndrome or its relation with the sick sinus syndrome with which it is often associated or even confused is precisely known. Of a total of 298 consecutive pacemaker implants, 36 (12%) were executed for carotid sinus syndrome, 33 (11%) for sick sinus syndrome and 24 (8%) for both. The annual incidence was respectively of 40, 37 and 26 implants per year/million of inhabitants. Patients affected by carotid sinus syndrome, when compared with those affected by sick sinus syndrome, showed: a higher prevalence of syncopes (97 vs 42%) more syncopal episodes per patient (2.9 +/- 2 vs 1.8 +/- 0.9), a lower prevalence of associated cardiac diseases (53 vs 100%), cardiac enlargement (36 vs 88%), heart failure (6 vs 36%) and paroxysmal atrial fibrillation (0 vs 97%), a more frequent indication to VVI pacing (75 vs 3%). Generally, when both syndromes were present, the patients showed intermediate characteristics. IN CONCLUSION: carotid sinus syndrome is a frequent indication of cardiac pacing as sick sinus syndrome; even if an association is present in about one third of patients, a distinction between carotid sinus syndrome and sick sinus syndrome is justified by theoretical and practical considerations.

Validation of a method for choice of pacing mode in carotid sinus syndrome with or without sinus bradycardia.

A new method for selection of the pacing mode in 60 consecutive patients with severe cardioinhibitory or mixed carotid sinus syndrome was prospectively validated. DDD pacing was preferred for 26 patients with: (1) the cardioinhibitory form and who had symptomatic pacemaker effect; (2) mixed type I form, (cardioinhibitory and vasodepressor) with symptomatic pacemaker effect, ventriculoatrial conduction or orthostatic hypotension; (3) mixed type II; or (4) severe bradycardia. VVI pacing was selected in the remaining 34 patients without these symptoms. During a 32 +/- 10 month follow-up period syncope and severe dizziness persisted in five patients in the VVI group (15%) and in three patients in the DDD group (12%). Symptomatic relief occurred in 87% (52/60) of patients. Minor symptoms persisted in 47% of the VVI group and 42% of the DDD group. No patient developed cardiac insufficiency or intolerance to pacing. During a 2-month duration a single-blind, randomized, cross-over study compared VVI and DDD pacing, 69% of the patients programmed from DDD to VVI suffered more frequent, severe, and intolerable symptoms. (1) Thirty four of 60 patients (57% of the entire group) in whom VVI pacing was satisfactory were identified prior to pacemaker implant. In the remainder, VVI pacing was contraindicated as it produced frequent side effects. (2) The preimplant predictive value that VVI pacing would be successful was 85% for those eventually receiving VVI pacemakers and the preimplant predictive value that VVI pacing would fail was 69% for those who underwent DDD implant.

Spontaneous occurrence of the induced cardioinhibitory vasovagal reflex.

ECG recording of spontaneous, neurally-mediated syncope is rare. We have observed ten patients who sustained 70 syncopal episodes in whom: (1) ECG monitoring recorded syncope caused by ventricular asystole (AV block, three patients; sinus arrest; seven patients); (2) syncope and the spontaneously observed arrhythmias were reproducible by carotid sinus massage, upright tilt test, or eyeball pressure; and (3) no discernable cause of precipitating factors were detected. Two patients had a history of cardiac disease and four patients had only mild nonclinical ECG or echocardiographic abnormalities. Syncopal episodes recorded during Holter monitoring were of sudden onset in four patients and preceded by prodromal symptoms in six patients. The maximum RR pause was 9.4 +/- 3.7 seconds (range 4.5-15). Electrophysiological evaluation was normal in seven patients. Slight sinus node dysfunction or atrioventricular conduction abnormalities were noted in three others. The clinical characteristics of spontaneous and induced episodes strongly suggest that increased vagal tone played a role in causing the spontaneous events. Vagal stimulation tests are useful for the diagnosis of syncope of unknown origin.

Carotid sinus massage, eyeball compression, and head-up tilt test in patients with syncope of uncertain origin and in healthy control subjects.

To verify the role of abnormal neural mechanisms in unexplained syncopes, we evaluated the results of carotid sinus massage (CSM), eyeball compression (EBC), and head-up tilt test (HUT) in the basal state (B) and during isoproterenol infusion (ISO) in: (1) 100 consecutive patients affected by syncope which, despite careful cardiovascular and neurologic examination, was of uncertain origin (age 60 +/- 18 years; 54 men) and (2) 25 healthy subjects matched 4:1 with the patients of the previous group. All the patients underwent CSM and EBC in the supine and standing position for 10 seconds and HUT at 60 degrees for 60 minutes; if HUT-B was negative (68 cases), it was repeated during ISO (1 to 5 micrograms/min) infusion. In the patients with uncertain syncope, spontaneous symptoms were fully reproduced in 49%, 16%, 32%, and 16% of cases respectively by means of CSM, EBC, HUT, and HUT-ISO; overall positivity for at least one test was observed in 79% of cases. The results of CSM, EBC, or HUT-ISO were linked to age, sex, and underlying heart disease. In the healthy subjects, syncope was induced by CSM, EBC, HUT, and HUT-ISO in one case each; overall positivity was 16%. In conclusion, neural reflex induction tests reproduced spontaneous symptoms in most patients affected by uncertain syncope, while they evoked normal responses in most healthy subjects. Therefore on the basis of results of induction tests, the diagnosis of neurally mediated syncope can be ascribed to most patients affected by syncope of uncertain origin.

Radiofrequency catheter ablation and modulation of atrioventricular conduction in patients with atrial fibrillation.

We attempted radiofrequency ablation of the AV junction with a sequential right- and left-sided approach in 78 patients affected by severely symptomatic, drug refractory atrial fibrillation. Stable third-degree AV block was obtained in 99% of cases and, after 3 months, persisted in 92% of cases. Single session, stepwise, radiofrequency modulation of the AV node was attempted in 13 patients with paroxysmal atrial fibrillation. During sinus rhythm, ablation of the slow and fast AV node pathways was performed in order to increase the nodal refractory period or to slow conduction. Clinically successful modulation of AV conduction was achieved in 15% of cases and persisted during a 3-month follow-up. In conclusion, AV junction ablation is a well-established means of treating atrial fibrillation, but implies the implant of a permanent pacemaker. AV node modulation avoids the pacemaker implant, but is efficacious only in a minority of patients. Thus, in patients affected by paroxysmal atrial fibrillation, AV modulation should be attempted first; if this is ineffective, AV ablation can be performed during the same session.

[Progression to 2d and 3d grade atrioventricular block in patients after electrostimulation for bundle-branch block and syncope: a long-term study]. / La progressione a blocco atrioventricolare di II e III grado nei pazienti elettrostimolati per blocco di branca e sincope: uno studio a lungo termine.

BACKGROUND: Patients with bundle branch block and syncope, especially those with abnormal electrophysiologic study, are at high risk of progression to second-or third-degree atrioventricular block and therefore they often receive a permanent back-up pacemaker. The aim of this study was to evaluate of the incidence of bundle branch block progression to second or third-degree atrioventricular block during long-term follow-up. METHODS: A retrospective study was performed on 60 patients (49 males, age 77 +/- 9 years) with bundle branch block and permanent back-up pacemaker. The patients were subdivided into 3 groups: 13 patients, at pre-implant electrophysiologic study had HV interval > or = 100 msec and/or second- or third-degree atrioventricular block induced by ajmaline i.v. administration (Group 1); 20 patients with HV interval of 70-100 msec and/or HV > or = 120 msec after ajmaline administration (Group 2); 27 patients who had received a permanent pacemaker because of carotid sinus syndrome or sick sinus syndrome (22 patients) or because of recurrent syncopes and negative electrophysiologic study (5 patients) (Group 3). RESULTS: During a mean follow-up of 62 +/- 41 months, 17/60 patients (28%) had progression to second- (n = 4) or third-degree (n = 13) atrioventricular block: atrioventricular block occurred in 54% of Group 1 patients in 25% of Group 2 patients and in 19% of Group 3 patients. The actuarial rate of progression to atrioventricular block for the overall population was, at 5 and 10 years, 25% and 58% respectively; in Group 1 it was 46% and 62%; in Group 2 it was 22% and 55% and in Group 3 it was 21% and 59% (p = 0.06). The patients with right bundle branch block and left anterior hemiblock were at higher risk of progression to atrioventricular block than those with right bundle branch block or left bundle branch block (risk 42% vs 14%, p = 0.06). The presence of an abnormal electrophysiologic study did not increase the progression rate either in the patients with right bundle branch block and left anterior hemiblock (risk of 43%), nor did it in those patients with other types of bundle branch block (risk of 18%). Moreover, the induction of second- or third-degree atrioventricular block during ajmaline administration was associated with a higher risk of block during the follow-up (60% vs 25%, p = 0.06). CONCLUSIONS: Patients treated with pacemaker because of symptomatic bundle branch block have a high risk of progression to second- or third-degree atrioventricular block in the long-term follow-up. The results argue against the practical usefulness of electrophysiological study since a risk stratification could be obtained by the simpler surface electrocardiogram; moreover, risk of block was also present in the patients affected by carotid sinus syndrome or sick sinus syndrome, and in those affected by unexplained syncope with negative electrophysiologic study.

Assessment of atrioventricular junction ablation and VVIR pacemaker versus pharmacological treatment in patients with heart failure and chronic atrial fibrillation: a randomized, controlled study.

BACKGROUND: Uncontrolled studies have suggested that atrioventricular junction ablation and pacemaker implantation have beneficial effects on quality of life in patients with chronic atrial fibrillation (AF). METHODS AND RESULTS: We performed a multicenter, controlled, randomized, 12-month evaluation of the clinical effects of atrioventricular junction ablation and VVIR pacemaker (Abl+Pm) versus pharmacological (drug) treatment in 66 patients with chronic (lasting >6 months) AF who had clinically manifest heart failure and heart rate >90 bpm on 3 standard ECGs recorded at rest during stable clinical conditions on different days. Before completion of the study, withdrawals occurred in 8 patients of the drug group and in 4 patients of the Abl+Pm group. At the end of the 12 months, the 28 Abl+Pm patients who completed the study showed lower scores in palpitations (-78%; P=0.000) and effort dyspnea (-22%; P=0.05) than the 26 of the drug group. Lower scores, although not significant, were also observed for exercise intolerance (-20%), easy fatigue (-17%), chest discomfort (-50%), Living with Heart Failure Questionnaire (-14%), New York Heart Association functional classification (-4%), and Activity scale (-12%). The intrapatient comparison between enrollment and month 12 showed that in the Abl+Pm group, all variables except easy fatigue improved significantly from 14% to 82%. However, because an improvement was also observed in the drug group, the difference between the 2 groups was significant only for palpitations (P=0.000), effort dyspnea (P=0.01), exercise intolerance (P=0.005), easy fatigue (P=0.02), and chest discomfort (P=0.02). Cardiac performance, evaluated by means of standard echocardiogram and exercise test, did not differ significantly between the 2 groups and remained stable over time. CONCLUSIONS: In patients with heart failure and chronic AF, Abl+Pm treatment is effective and superior to drug therapy in controlling symptoms, although its efficacy appears to be less than that observed in uncontrolled studies because some improvement can also be expected in medically treated patients. Cardiac performance is not modified by the treatment.

Determinants of development of permanent atrial fibrillation and its treatment.

We evaluated the rate of progression of permanent atrial fibrillation (AF) and identified clinical factors that predict this event in 63 consecutive patients who had undergone AV junctional ablation and DDDR pacemaker implantation for drug-refractory paroxysmal atrial fibrillation/ flutter. Immediately after ablation, anti-arrhythmic drugs were discontinued in all cases. Permanent AF was considered to have developed if AF was present on two consecutive 6-monthly examinations with no interim documented sinus rhythm. During a mean follow-up of 23 +/- 16 months, 22 (35%) of the 63 patients developed permanent AF. The actuarial estimate of progression of permanent AF was 22%, 40% and 56%, respectively, 1, 2 and 3 years after ablation. Age and underlying heart disease were independent predictors of progression of permanent AF. Only one (6%) of 16 patients with idiopathic AF had permanent AF (low risk group). Among the 47 patients with structural heart disease, permanent AF developed in 18 (62%) of the 29 who were aged >75 years or had >12 arrhythmic episodes per year and a symptom duration >4 years (high risk group), but only in three (17%) of the remaining 18 patients who did not (intermediate risk group). In conclusion, during a 3-year follow-up period, about half of the patients with a history of drug-refractory paroxysmal AF did not develop permanent AF after AV junctional ablation and dual-chamber pacemaker implantation, even in the absence of anti-arrhythmic drug therapy. Moreover, subgroups of patients whose risk of permanent AF progression differed were identified on the basis of simple baseline clinical variables. The results of this study form the necessary background for the correct management of patients after AV junction ablation and for the planning of future trials in this field.