The contribution of artificial pacemaking to understanding the pathogenesis of arrhythmias

Right atrial or ventricular pacing was performed on 36 occasions in 26 patients in an attempt to terminate a variety of tachyarrhythmias. Of 16 episodes of atrial flutter, 13 were terminated successfully; in 9 of the 13, sinus rhythm or the patient's pre-flutter rhythm was restored immediately, whereas in 4 patients, intervening atrial fibrillation or unstable atrial flutter occurred. Pacing terminated paroxysmal atrioventricular junctional or paroxysmal atrial tachycardia on 3 occasions; in a fourth patient, this tachyarrhythmia terminated during catheter manipulation. Six episodes of pacemaker-induced ventricular tachycardia were abolished by ventricular pacing. In 2 patients, atrial tachycardia was only transiently suppressed, and in 1 of these patients, d-c cardioversion produced a similar effect. Atrial fibrillation, spontaneously converting to atrial flutter, resulted during pacing for atrial tachycardia with block; the latter arrhythmia returned when the atrial flutter was terminated. Atrial fibrillation in 7 patients remained unaffected by atrial pacing. Based on the different electrophysiologic mechanisms responsible for reentrant excitation and automatic pacemaker discharge, an attempt has been made to determine the pathogenesis of the tachyarrhythmia by its response to pacing.     

Antegrade conduction and AV node function in patients with unidirectional retrograde accessory pathways

In 26 patients with unidirectional retrograde accessory pathways (URAP), antegrade conduction properties were evaluated. During electrophysiologic study the interval from the low septal right atrial potential to the His bundle potential (LSRA-H) in sinus rhythm (SR) was found to be less than 60 msec in 7 out of the 18 patients with left-sided URAP and in one out of two patients with septal URAP. Each of the six patients with right-sided URAP had an LSRA-H equal to or greater than 70 msec. During atrial extrastimulus testing, LSRA-H failed to prolong more than 100 msec (LSRA-H increment equal to or less than 100 msec) in four of six patients with left-sided URAP and LSRA-H of less than 60 msec in SR as well as in the one of two patients with septal URAP in whom the LSRA-H in SR was less than 60 msec. During rapid atrial pacing, we found 1:1 AV node conduction at a pacing rate of more than 200 bpm in the one patient with septal URAP and in 7 out of 14 patients with left-sided URAP who could be assessed. Three of these patients had progression from 1:1 AV conduction to 2:1 AV block without intervening Wenckebach. In conclusion, accelerated AV node conduction in SR and reduced AV node function during rapid atrial pacing or extrastimulus testing was found in 44% of our patients with left-sided or septal URAP. Since these patients are at higher risk for faster ventricular response to atrial flutter and fibrillation and for high frequency during supraventricular tachycardia, these findings were of clinical relevance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Flecainide acetate for conversion of acute supraventricular tachycardia to sinus rhythm

The efficacy of intravenous flecainide acetate (maximum 2 mg/kg or 150 mg given at a rate of 15 mg/min) was assessed in patients with acute supraventricular tachycardia (SVT) (within 24 hours). Fifty patients were studied, 46 with spontaneous SVT and 4 with induced SVT at electrophysiologic assessment. Conversion to sinus rhythm was achieved within 45 minutes in 76%: in 25 patients with atrial fibrillation (76% conversion), 15 with atrioventricular (AV) nodal or AV reentrant tachycardia (100% conversion) and 10 with atrial flutter or atrial reentrant tachycardia (40% conversion). Adverse effects were noted in 21 patients (42%): paresthesia in 9, drowsiness in 8, nausea in 2, accelerated ventricular rate in 5, ventricular tachycardia in 1, sinus bradycardia in 1 and hypotension in 5. Adverse effects were associated with larger dosage and atrial flutter or atrial reentrant tachycardia. Thus, flecainide acetate is effective in converting to sinus rhythm acute atrial fibrillation and AV nodal and AV reentrant tachycardias, but not atrial flutter or atrial reentrant tachycardia.     

Electrophysiologic study of patients with ventricular dysrhythmias during long-term follow-up after repair of tetralogy of Fallot

We performed an electrophysiologic study (EPS) in 8 patients who had received corrective surgery for tetralogy of Fallot. The mean age was 30 years. An average of 15 years had elapsed after corrective surgery. Two patients had episodes of syncope. ECG showed normal sinus rhythm in 7 patients and atrial fibrillation in 1, and all had complete right bundle branch block. All patients had ventricular premature beats of grade 3 or higher of Lown's classification. Overdrive suppression test was performed in 6 patients. Corrected sinus node recovery time (CSNRT) ranged from 230 msec to 510 msec. Wenckebach block of atrioventricular nodal conduction occurred at rates of 130 to 170 bpm during atrial pacing. The H-V interval was prolonged to 60 msec in 1 patient, but was below 55 msec in the others. Programmed stimulation induced ventricular tachycardia (VT) in 3 patients, nonsustained VT in 2 and sustained VT in 1. In 2 of 3 patients, delayed potential or fragmentations were recorded in the outflow tract of the right ventricle. During the follow-up period of 20 months, 2 patients died suddenly. Their CSNRTs and H-V intervals were normal. Ventricular tachyarrhythmia seems to be important as a cause of late sudden death after repair of tetralogy of Fallot.     

Effects of diltiazem in supraventricular paroxysmal tachyarrhythmias

Diltiazem (0.3 mg/kg body weight intravenous in 2 minutes) was administered to 40 patients (24 males, 16 females, mean age 51.55 years) with paroxysmal supraventricular tachyarrhythmias: 7 patients with atrial fibrillation, 6 patients with atrial flutter, 25 patients with paroxysmal supraventricular tachycardia, 2 patients with uncommon atrioventricular reciprocating tachycardia. In patients with atrial fibrillation intravenous diltiazem produced a significant decrease of ventricular response (from 160 +/- 11 to 113.57 +/- 10.34--p less than 0.01). In patients with atrial flutter intravenous diltiazem produced variable effects: an increase in atrio-ventricular block (from 2:1 to 3:1 atrio-ventricular conduction (2 patients); conversion to sinus rhythm (1 patient); change to atrial fibrillation (1 patient); no appreciable change of the basic rhythm (2 patients). In paroxysmal supraventricular tachycardia patients conversion to sinus rhythm occurred in 20/22 patients (91%) treated with intravenous diltiazem (mean conversion time 4.69 minutes). In the 2 patients with uncommon atrioventricular nodal reciprocating tachycardia diltiazem increased P'-R and R-P' intervals without appreciable change of the basic rhythm. No serious side effects from drug administration were noted. Intravenous diltiazem appears to be as a highly effective medication in conversion or control of paroxysmal supraventricular tachyarrhythmias.     

Utility of the filtered bipolar esophageal lead in the diagnosis of arrhythmias

Electrophysiologic study was performed in 25 patients with tachycardia or bradycardia attacks. The coronary sinus (CS) and filtered bipolar esophageal electrograms were recorded simultaneously to compare the phase of atrial activations. During sinus rhythm and high right atrial pacing, the esophageal and proximal CS atrial activations were nearly simultaneous but earlier by 26 +/- 5 msec on the average than the distal CS atrial activations. During reciprocating tachycardia due to reentry using a left-side accessory atrioventricular pathway for retrograde conduction the esophageal and CS atrial activations occurred earlier than the low septal right atrial activation, so the esophageal lead can be used as a substitute for the CS lead to clarify the eccentric retrograde atrial activation sequence. By using the filtered bipolar esophageal lead, the interval from Q wave on the surface electrocardiogram to the first rapid deflection in the esophageal atrial activation (Q-AESO interval) was measured in 15 patients with supra-ventricular tachycardia. All patients with reciprocating tachycardia due to reentry using a left side accessory atrioventricular pathway had Q-AESO intervals between 100 to 130 msec and four of five patients with a right side accessory atrioventricular pathway for retrograde conduction had Q-AESO intervals between 130 to 150 msec. In contrast, all patients with reentry in the atrioventricular node had Q-AESO intervals between 30 to 60 msec. The esophageal lead is also of value in the prompt diagnosis of atrial flutter and ventricular tachycardia, since the esophageal electrograms readily reveal the relationship between atrial and ventricular activations. In conclusion, the filtered bipolar esophageal lead provides a non-invasive method for the quick diagnosis of various arrhythmias.     

Intravenous cibenzoline in the management of acute supraventricular tachyarrhythmias

Summary Intravenous cibenzoline was evaluated in 37 patients with acute supraventricular tachyarrhytymias and a ventricular rate >120 beats/min. The presenting arrhythmia was atrial fibrillation in 15 patients, atrial flutter in 5, ectopic atrial tachycardia in 11, and paroxysmal atrioventricular (AV) junctional reentrant tachycardia in 6 patients. Intravenous cibenzoline was administered as a bolus given over 2 minutes, at a dose of 1 mg/kg in the first 26 patients and 1.2 mg/kg in the subsequent 11 patients, 15 minutes following failure of placebo (isotonic glucose). The results were evaluated 15 minutes after the intravenous injection. Restoration of sinus rhythm was obtained in 3 out of 6 patients with paroxysmal AV junctional tachycardia (50%) and in 7 out of 31 patients (23%) with atrial tachyarrhythmias (5 out of 15 patients with atrial fibrillation and 2 out of 16 patients with ectopic atrial tachycardia or atrial flutter). Five additional patients with atrial tachyarrhythmias had slowing of ventricular rate below 100 beats/min. Therefore, a satisfactory result, that is, restoration of sinus rhythm or slowing of ventricular rate, occurred in 15 patients (40.5%). Side effects were transient, including visual disturbance (one patient), asymptomatic widening of QRS complex (three patients), incessant reciprocating tachycardia (one patient), and acceleration of ventricular rate (eight patients), resulting in 1:1 flutter, with poor tolerance in two patients. In conclusion, intravenous cibenzoline may be useful in selected patients with supraventricular tachyarrhythmias. Careful monitoring is recommended during therapy in view of the possible occurrence of 1:1 atrial flutter.     

Functional abnormalities of the conduction system in children with an atrial septal defect

We performed an electrophysiologic study in 40 children with an atrial septal defect and analyzed their pre- and postoperative electrocardiograms and 24-hour Holter recordings. The electrophysiologic study showed a prolonged corrected sinus node recovery time in 83% and an abnormal sinuatrial conduction time in 25% of the children. An early Wenckebach response to atrial pacing was seen in 18%. Sixteen percent had a prolonged atrial conduction time. The atrial functional refractory period was abnormal in 35%. Two children developed nonsustained supraventricular tachycardia during the electrophysiologic study. The preoperative electrocardiogram showed first-degree atrioventricular block in 15% of the children; prolonged periods of accelerated atrial rhythm were found in 35% of the preoperative 24-hour Holter recordings. The incidence of first-degree atrioventricular block and accelerated atrial rhythm decreased postoperatively. We could not find a significant correlation between age or shunt size and the presence of electrophysiologic abnormalities or arrhythmias. These results indicate that the sinus node, atrioventricular node and atrial myocardium show some degree of dysfunction in patients with an atrial septal defect. An early operation may prevent further progression of electrophysiologic abnormalities and the development of symptomatic arrhythmias.     

Spectrum of regular tachycardias with wide QRS complexes in patients with accessory atrioventricular pathways

Reciprocating tachycardia and atrial flutter or fibrillation are the rhythm disorders most frequently documented in patients with accessory atrioventricular (A-V) pathways. Reciprocating tachycardia typically results in a regular tachycardia (140 to 250/min) with a normal QRS pattern, although on occasion bundle branch block aberration occurs. Atrial flutter or fibrillation may result in an irregular ventricular response, with the QRS configuration being normal or exhibiting bundle branch block or various degrees of ventricular preexcitation, or both. Although much less common than either reciprocating tachycardia or atrial flutter/fibrillation, regular tachycardias with a wide QRS complex suggestive of ventricular preexcitation are observed in patients with accessory pathways. Excluding functional or preexisting bundle branch block, several arrhythmias may cause these electrocardiographic findings which may mimic those of ventricular tachycardia.In the present study a variety of arrhythmias that resulted in tachycardias with a wide QRS complex were examined in 163 patients with accessory pathways who underwent clinical electrophysiologic study for evaluation of recurrent tachyarrhythmias. Twenty-six patients (15 percent) manifested a regular tachycardia with a wide QRS complex suggesting ventricular preexcitation. Atrial flutter with 1:1 anterograde conduction over an accessory pathway (15 of 26 patients, 58 percent) was the most frequent arrhythmia and was usually associated with a heart rate of 240/min or greater (12 of 15 patients). Reciprocating tachycardia with conduction in the anterograde direction over an accessory pathway (antidromic reciprocating tachycardia) occurred in 7 of 26 patients (27 percent), and resulted in a slower ventricular rate than atrial flutter (217 ± 22 versus 262 ± 42, P < 0.01). Other arrhythmias included reciprocating tachycardia with reentry utilizing a fasciculoventricular or nodoventricular connection (two patients, 8 percent), reciprocating tachycardia with reentry in the atrium or A-V node and anterograde accessory pathway conduction (one patient, 4 percent) and ventricular tachycardia (one patient, 4 percent).In this study the clinical electrophysiologic diagnostic features of several arrhythmias which cause tachycardias with a wide QRS compex suggesting ventricular preexcitation are outlined. It is apparent that definitive arrhythmia diagnosis during these tachycardias is often complex and usually requires careful study using intracardiac electrode catheter techniques.     

Effects of intravenous verapamil on cardiac arrhythmias and on the electrocardiogram.

The effects of intravenous verapamil on the electrocardiogram in 15 patients with heart disease in sinus rhythm and in 44 patients with supraventricular and ventricular tachyarrhythmias were evaluated. Verapamil prolonged the P-R interval without effect on the QRS duration or the Q-Tc interval. In patients with atrial flutter and fibrillation, A-V block was increased, with slowing of the ventricular rate, in almost all cases but sinus rhythm was restored in only 1 of 12 patients in atrial fibrillation and in 2 of the 11 patients with flutter. Verapamil had no effect in 3 patients with atrial fibrillation complicating WPW syndrome; in 1 of 5 patients with ventricular tachycardia it caused reversion to sinus rhythm. Sinus rhythm was restored promptly by verapamil in 13 of 17 patients with paroxysmal supraventricular tachycardias; in 2 others, sinus rhythm became established 1 to 2 hours after administration of the drug. Transient hypotension, not requiring treatment, was the only side effect noted but not in the patients with supraventricular tachycardias, in whom blood pressure generally increased after reversion to sinus rhythm by verapamil.     

Surgical management of tachyarrhythmias

In this study of surgical procedures for various tachyarrfiythmias, Wolff-Parkinson-White syndrome comprised most of the cases. An endocardial approach was used to ablate accessory pathways. Additional use of cryocoagulation after surgical incision of the atrium, previously routinely performed, is at present only done occasionally for septal accessory pathways.

Ventricular tachycardia (VT) was the next most frequent condition. The surgical procedures for ischemic and nonischemic VTs are completely different, although both are based on the principle of complete electrophysiologic mapping. For ischemic VT, surgery consists of resection of the left ventricular aneurysm and excision or cryocoagulation of the endocardium, or both. For nonischemic VT, either excision of the entire thickness of the myocardium (2.0 × 2.5 cm on average) at the earliest excitation site of the right ventricle and cryocoagulation of the area of delayed potential or only incision and cyrocoagulation of the left ventricle were performed to avoid reduction of the left ventricular cavity.

Ectopic atrial tachycardia was cured by excision of the earliest excitation site without use of a heart-lung machine, when the focus was located in the atrial free wall. Other successful treatments were of reentrant atrial tachycaroia by cryocoagulation, atrial flutter by cryocoagulation of impulse pathways at the coronary sinus and around the atrioventricular node, and a new surgery for atrial fibrillation and flutter, which retained sinus rhythm. Johnson's procedure was used for surgical ablation of atrioventricular nodal reentrant tachycardia.     

Provocation of supraventricular tachycardias by an intravenous class I antiarrhythmic drug.

Antiarrhythmic drugs may aggravate or induce ventricular arrhythmia. The induction of a supraventricular tachycardia or its facilitation has rarely been reported. The purpose of the study was to know whether the potential for supraventricular proarrhythmic effect of a class Ia intravenous antiarrhythmic drug can be exposed during electrophysiologic study. Ajmaline was chosen because of its short duration of action. The protocol of the study consisted of an electrophysiological study and programmed atrial stimulation using 1 and 2 extrastimuli on driven rhythm and atrial pacing up to second-degree atrioventricular block. Then 1 mg/kg of ajmaline was injected and atrial pacing was performed 3 minutes after its injection. Supraventricular proarrhythmic effect of ajmaline was defined as the spontaneous occurrence of a supraventricular tachycardia or the facilitation of its induction. Seventy patients among 1955 presented a proarrhythmic effect: 63 developed a supraventricular tachyarrhythmia (atrial flutter, fibrillation, tachycardia) and 7 an atrioventricular reentrant tachycardia, either spontaneously (n = 23) or during atrial pacing (n = 47). Risk factors were identified in most patients: old age, underlying heart disease, history of spontaneous supraventricular tachycardia and/or induction of a supraventricular tachycardia by 2 extrastimuli on driven rhythm in the control state (34 patients), sinus node dysfunction (22 patients). Compared with patients without proarrhythmic supraventricular effect only the history of spontaneous supraventricular tachycardia and the existence of a sinus node dysfunction were significantly more frequent (P less than 0.05) in patients with proarrhythmic effect of ajmaline. In conclusion, the supraventricular proarrhythmic effect of intravenous ajmaline exists and is related both to the electrophysiologic characteristics of the drug and to the arrhythmia substrate. The results indicate that a supraventricular tachyarrhythmia may be induced by a class I antiarrhythmic drug.     

Intravenous flecainide acetate for supraventricular tachycardias

Flecainide acetate, 2 mg/kg body weight, given intravenously at 10 mg/min was administered to 128 (74 male and 54 female) patients whose ages ranged from 11 to 86 years (mean 44). All patients had supraventricular tachycardias (SVT) that developed spontaneously or were induced during electrophysiologic study. There were 26 patients with atrial flutter, 34 with atrial fibrillation, 7 with ectopic atrial tachycardia, 41 with atrioventricular (AV) reentrant tachycardia and 40 with AV nodal reentrant tachycardia. Twenty patients had more than 1 variety of SVT. Flecainide was administered during SVT to 9 patients with atrial flutter, 11 with atrial fibrillation, 7 with atrial tachycardia, 38 with AV reentrant tachycardia and 34 with AV nodal reentrant tachycardia. In the remaining 31 patients with inducible SVT at electrophysiologic study, flecainide was administered during sinus rhythm. Reinitiation of SVT was attempted in these patients after completion of flecainide administration. Flecainide successfully terminated atrial flutter in 2 patients (22%), atrial fibrillation in 9 (82%), atrial tachycardia in 5 (71%), AV reentrant tachycardia in 32 (84%) and AV nodal reentrant tachycardia in 30 (88%). Reinitiation of SVT was possible in 10 of 26 patients with atrial flutter (38%), 5 of 34 with atrial fibrillation (15%), 3 of 7 with atrial tachycardia (43%), 14 of 41 with AV reentrant tachycardia (34%) and 11 of 40 with AV nodal reentrant tachycardia (27%). In patients with AV reentrant tachycardia and AV nodal reentrant tachycardia, reinitiation occurred when retrograde anomalous pathway refractoriness was not significantly prolonged by intravenous flecainide.(ABSTRACT TRUNCATED AT 250 WORDS)     

Value of diazepam ('Valium') in treatment of cardiac arrhythmias.

Diazepam did not alter the rate or rhythm in III patients with atrial fibrillation. In 3 out of 38 patients with atrial flutter the use of diazepam was followed by an increase in atrioventricular block. Diazepam restored sinus rhythm in I patient with atrial tachycardia (total 7 patients) and in I patient with ventricular tachycardia (total 8 patients). Experimentally in the dog diazepam raised the electrically-induced ventricular tachycardia threshold significantly. Pretreatment with diazepam did not alter significantly the dose of strophanthidin K required to induce ventricular tachycardia in the dog. The value of diazepam as a cardiac anti-arrhythmic agent should be further assessed in a controlled clinical trial, especially in patients with acute myocardial infarction.     

Short-term rapid atrial pacing produces electrical remodeling of sinus node function in humans

INTRODUCTION: Depression of sinus node function occurs in dogs and in patients after cessation of atrial flutter and fibrillation. We tested whether transient atrial pacing might produce similar changes in humans. METHODS AND RESULTS: We studied the impact of short-term rapid atrial pacing, simulating atrial tachyarrhythmias, on sinoatrial conduction time (SACT) and corrected sinus node recovery time (CS-NRT) in 10 patients undergoing electrophysiologic study. None had recognizable structural heart disease, history of atrial fibrillation or flutter, autonomic dysfunction, or any tachycardia for at least 24 hours before study. All cardiac drugs were discontinued >5 half-lives prior to study. No patient had significant hypotension during atrial stimulation. SACT and CSNRT were measured at baseline, and sinus node reset zone was determined. Right atrial pacing was performed for 10 to 15 minutes, after which SACT and CSNRT were measured again. Both parameters increased significantly, from 423+/-208 msec to 491+/-214 msec and from 80+/-50 msec to 96+/-53 msec, respectively (P = 0.02 and P < 0.001, respectively). CONCLUSION: Rapid atrial pacing for only 10 to 15 minutes, simulating transient atrial tachyarrhythmias, alters sinus node function in humans. Additional studies are needed to evaluate the mechanism, but the clinical implication is that even transient episodes of atrial tachyarrhythmias can cause sinus node remodeling in patients.     

Use of intravenous adenosine in sinus rhythm as a diagnostic test for latent preexcitation

In a proportion of patients with left free wall accessory connections, preexcitation is apparent only during atrial arrhythmias or atrial pacing (latent preexcitation). These patients may be at risk of a rapid ventricular response to atrial fibrillation despite the absence of preexcitation in sinus rhythm. The ability of intravenous adenosine to unmask latent preexcitation was evaluated in 22 patients with a history of documented supraventricular tachycardia and a normal electrocardiogram during sinus rhythm. Preexcitation was unmasked in response to adenosine in 4 patients: all 4 were shown to have latent preexcitation at electrophysiologic study. In 12 patients atrioventricular (AV) nodal conduction delay or block was induced without preexcitation after adenosine (first-degree AV block in 8, second-degree block in 4): at subsequent electrophysiologic study none of these patients was found to have latent preexcitation. Five patients had little or no PR prolongation in response to adenosine: of these, 2 were shown to have latent preexcitation at electrophysiologic study. Atrial fibrillation was induced in 1 patient and a narrow complex regular tachycardia in another after intravenous adenosine. Intravenous adenosine during sinus rhythm is capable of producing AV nodal conduction delay or block in 73% of patients with a history of supraventricular tachycardia: in these patients adenosine provides a diagnostic test that is both 100% sensitive and 100% specific for latent preexcitation. In those patients in whom adenosine does not produce AV conduction delay or block, further investigation is required to establish or refute the diagnosis of latent preexcitation.     

Intravenous flecainide acetate for the clinical management of paroxysmal tachycardias

Intravenous flecainide acetate (2 mg/kg) was administered to 40 patients undergoing routine electrophysiological evaluation for the investigation of recurrent paroxysmal tachycardias. Ten patients had recurrent atrial flutter, 11 patients had recurrent atrial fibrillation, one of whom also had paroxysmal left atrial tachycardia, and 19 patients had recurrent ventricular tachyarrhythmias (17 with recurrent ventricular tachycardia and 2 with recurrent fascicular tachycardia). Flecainide was administered during tachycardia (over 5 to 10 minutes) to all patients with atrial flutter, to 10 patients with atrial fibrillation, and to 17 patients with ventricular tachyarrhythmias. In the remaining 3 patients with ill-sustained arrhythmias flecainide was administered during sinus rhythm and reinitiation of tachycardia was then attempted. Flecainide restored sinus rhythm in only 2 patients with atrial flutter (20%), in 9 patients with atrial fibrillation (90%), in 12 patients with ventricular tachycardia (80%), and in one of the 2 patients with fasicular tachycardia. Flecainide also successfully terminated the left atrial tachycardia. Two patients experienced proarrhythmic side effects during flecainide administration, one of whom required intervention by cardioversion. Minor dose effects included oral paresthesia, transient drowsiness or dizziness, and occasional visual blurring. Flecainide acetate is an effective antiarrhythmic agent for the acute termination of recent onset paroxysmal atrial and ventricular tachyarrhythmias.     

Utility of transesophageal atrial pacing in the diagnostic evaluation of patients with unexplained syncope associated or not with palpitations

BACKGROUND: Noninvasive studies are often negative in patients with syncope, normal surface ECG and without heart disease. The purpose of the study was to determine the diagnostic impact of an esophageal electrophysiological study performed during a consultation. METHODS: A total of 154 patients aged from 16 to 87 years were consecutively recruited for unexplained syncope; they had a normal ECG in sinus rhythm, no documented arrhythmia and no patent heart disease. Half of them complained of palpitations. Electrophysiologic study was performed during a consultation by transesophageal route: rate of 2nd d AV block occurrence during atrial pacing and sinus node recovery time were determined; programmed atrial stimulation using one and two atrial extrastimuli were delivered in control state and then after infusion of 0.02-1 microg/min of isoproterenol; arterial blood pressure was monitored. RESULTS: (1) Electrophysiologic study was positive in 107 patients (69%); (2) sinus node dysfunction was noted in 9 patients (6%); (3) atrioventricular conduction disturbances were noted in 2 patients (1%); (4) vasovagal reaction which associated a junctional bradycardia and a fall of arterial blood pressure and which reproduced spontaneous symptoms was provoked by isoproterenol infusion in 21 patients (14%); (5) sustained atrial fibrillation was induced in 23 patients (15%); and (6) paroxysmal junctional tachycardia was induced in 52 patients (34%). Patients with negative study were younger (44+/-21.5 years) than those with sinus node dysfunction or atrial fibrillation (71+/-9 and 63+/-14 years, respectively). The treatment was guided by these data: patients with inducible atrial fibrillation were treated by antiarrhythmic drugs and those with inducible paroxysmal junctional tachycardia by the radiofrequency ablation of reentrant circuit. Syncope disappeared in all patients but 2. CONCLUSION: Esophageal electrophysiologic study performed during a consultation was a safe, rapid and economic means to detect an arrhythmia (sinus node dysfunction or supraventricular tachycardia) in patients with dizziness/syncope and palpitations in half cases. Supraventricular tachycardia was clearly an underestimated cause of syncope in this population.     

Radiofrequency catheter ablation of common atrial flutter--acute and follow-up results

Atrial flutter with a structurally well-defined macro-reentrant circuit in the right atrium has recently become amenable to radiofrequency ablation with the recognition of isthmus as a narrow zone of slow conduction. This study describes 20 consecutive and symptomatic patients with atrial flutter (15 males, 5 females; mean age 38.5 +/- 10.2 years) who underwent radiofrequency ablation in our institute in the last 18 months. Fourteen patients had structurally normal hearts, while the remaining six patients had specific disorders (prior surgery for closure of atrial septal defect-2, idiopathic restrictive cardiomyopathy-1, primary sinus node dysfunction-2, tachycardiomyopathy-1). The endpoints of a complete isthmus block and conversion to sinus rhythm were achieved in 19 of the 20 patients. Total number of pulses needed to attain the endpoints was a mean of 4.2 (range 1-5), each pulse being delivered for 90 seconds. At a mean follow up of 9.4 +/- 3.2 months (range 6-12 months), recurrence of atrial flutter was seen in one patient, atrial fibrillation in two and sinus node reentrant tachycardia in one. These results are comparable to those reported in the literature. Achievement of a complete isthmus block appears to be an important endpoint in obtaining optimal results. The issues of alternative sites of ablation, long-term results and advantages of an 8 mm tip catheter need to be examined further. In conclusion, radiofrequency ablation appears to be the preferred mode of treatment for patients with atrial flutter with excellent short-term and mid-term results.     

迷宫手术对二尖瓣病合并的慢性心房颤动电生理的影响

对21例二尖瓣疾患伴心房颤动（简称房颤）施行了迷宫手术和二尖辩手术的患者，采用12导联心电图、心内电生理、动态心电图、踏车运动试验方法进行检查，探讨迷宫手术对慢性房颤患者心脏围手术期和远期电生理的影响。平均随访17．9±7．9个月。结果如下：①术后3个月90％（18／20）恢复窦性心律，随访1年以上者（14例）房颤均未见复发。②术后除1例窦房结恢复时间延长外余均正常，无窦性起搏或房室给传导功能障碍。③术后都有正常的心房激动和房室同步激动顺序。④术后在各标测部位猝发刺激和程控刺激均不能诱发心房扑动和颤动，心房各部位有效不应期均显著长于高位右房有效不应期。⑤动态心电图和运动试验证明有良好的心率变时性反应和运动耐力。⑥1例术后4个半月死于急性坏死性肝炎。以上表明通过电生理检查手段证实了迷宫手术治疗房颤能达到：①消除房颤恢复窦性心律，②重建和（或）维持房室同步活动，③恢复心房传输功能。提出对二尖瓣疾患合并的慢性房颤病人在施行二尖瓣手术时应作迷宫手术。