Intra-atrial Conduction Research Articles

Mechanism of Double Ventricular Response to a Single Atrial Extrastimulus in Patients with Wolff‐Parkinson‐White Syndrome

The purpose of this study is to elucidate electrophysiological determinants of double ventricular response (DVR) to a single atrial extrastimulus in Wolff-Parkinson-White (WPW) syndrome. DVR was observed in 5 (3.4%) out of 146 consecutive patients with WPW syndrome. The site of accessory pathway was located in left lateral free wall in four patients and posterior septum in one. DVR was induced by extrastimulus from coronary sinus in four patients with left-sided accessory pathway, and from both coronary sinus and high right atrium in a patient with septal accessory pathway. However, it was not possible to induce DVR from high right atrium in patients with left-sided accessory pathway, because 50 to 80 ms are needed for intra-atrial conduction from high right atrium to coronary sinus. Critical prolongation of normal AV conduction allowing DVR was seen in the slow pathway of AV node in four patients. In the remaining patients requisite conduction delay occurred in both AV node and His-Purkinje system. Single right ventricular extrastimulus could easily elicit orthodromic AV reciprocating tachycardia or echo beat in four out of five patients and incremental ventricular stimulation induced it in the remaining patient, indicating the presence of retrograde block in the normal AV pathway. As requisites of DVR to a single atrial extrastimulus in WPW syndrome: (1) slow antegrade conduction and retrograde block in the normal AV pathway; and (2) stimulation site in the vicinity of accessory pathway, are needed.

Electrophysiologic effects and efficacy of cibenzoline on stimulation-induced atrial fibrillation and flutter and implications for treatment of paroxysmal atrial fibrillation

The effects of intravenous cibenzoline (1.5 mg/kg) on atrial vulnerability and electrophysiology were assessed in 25 patients with documented paroxysmal atrial fibrillation (AF), in whom sustained (> 30 seconds) AF was induced by atrial stimulation with up to 2 extrastimuli and paced rates between 100 and 180 beats/min. In 7 patients AF persisted despite the application of cibenzoline, and in 8 patients induction of AF was not prevented. In 10 patients the induction of sustained AF was prevented by cibenzoline. Intraatrial conduction time, flutter cycle length and shortest ventricular cycle length during AF were increased by cibenzoline (p ≤ 0.01). Sinus cycle length was decreased (p ≤ 0.05), whereas sinus node recovery time remained unchanged. The effective refractory period of the right atrium was not significantly affected. Eight patients with frequent episodes of paroxysmal AF received oral cibenzoline for control of paroxysmal AF irrespective of the efficacy of intravenous cibenzoline. Prevention of stimulation-induced AF predicted successful treatment of paroxysmal AF (p = 0.018). Cibenzoline could be effective in the treatment of atrial arrhythmias, and selection of an antiarrhythmic therapy for recurrent AF seems to be useful.

Modulation of electrophysiological properties of neonatal canine heart by tonic parasympathetic stimulation

The effects of tonic right and left vagal stimulation (RVS and LVS) on electrophysiological properties of the immature myocardium and specialized conduction system were evaluated in 11 neonatal canines pretreated with propranolol (1 mg/kg iv). Electrophysiological studies were performed by recording intracardiac electrograms from multiple endocardial catheters during programmed electrical stimulation. Assessments were made of sinus node function, intra-atrial, atrioventricular (AV) nodal and His-Purkinje conduction, and atrial and ventricular refractoriness in the control state and during RVS and LVS at 4-12 Hz. Vagal stimulation prolonged the sinus cycle length; RVS produced a 38% increase and LVS a 25% increase at 8 Hz (P less than 0.01). There were no changes in the intra-atrial or His-Purkinje conduction times. Comparable increases occurred during RVS and LVS in the paced cycle length resulting in AV nodal Wenckebach, the AV nodal conduction time at a paced cycle length of 340 ms, and the effective and functional refractory periods of the AV node, suggesting symmetrical influences of the right and left vagus on neonatal AV nodal function. Right atrial effective and functional refractory periods shortened significantly during vagal stimulation (ERP, 36% RVS and 23% LVS; FRP, 27% RVS and 15% LVS), and in 5 of 11 neonates, a sustained regular atrial tachyarrhythmia was induced during atrial extra-stimulation. Small yet significant increases were observed in the right ventricular ERP and FRP during vagal stimulation. This study provides information regarding the functional integrity of the parasympathetic nervous system and its potential role as a modulator of the electrophysiological properties of the newborn heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic studies of the heart in patients with rheumatoid arthritis

We investigated the electrophysiological properties of the heart in patients with definite or classical rheumatoid arthritis using programmed electrical stimulation techniques. Twelve patients with rheumatoid arthritis and without evidence of organic heart disease or arrhythmia detectable with serial electrocardiograms and 24-hour ambulatory electrocardiographic monitoring were compared with 12 control subjects. Stimulation was performed from the high right atrium and right ventricular apex at a drive cycle length of 600 msec and the recording sites included high right atrium, atrioventricular junction and distal coronary sinus. There was no statistically significant difference in the corrected sinus node recovery time between the study and control group of patients. Similarly, no differences from normal were found in the AH and HV intervals or in the atrial and ventricular refractoriness, whereas the atrioventricular nodal effective refractory period was higher in patients with rheumatoid arthritis, compared with the control group (338 ± 38 vs 286 ± 29, P < 0.02). The atrial conduction time during basic cycle length had a tendency to increase from high right atrium to atrioventricular junction in the study group and reached statistical significance from high right atrium to coronary sinus (92 ± 15 vs 74 ± 14, P < 0.05). Electrophysiologic differences between the study and control patients also included a greater increase in maximal intraatrial (40 ± 13 vs 27 ± 16, P < 0.05) and interatrial conduction delay (54 ± 16 vs 31 ± 12, P < 0.01) of early premature stimuli in patients with rheumatoid arthritis. In addition atrial arrhythmias were induced in 3 patients with rheumatoid arthritis but in no control patient. The clinical importance of these findings is uncertain. Nevertheless, our data suggest that abnormalities in atrial conduction time may be present in patients with rheumatoid arthritis and predispose to the initiation of atrial tachyarrhythmias.

Electrophysiologic effects of intravenous dipyridamole

We evaluated the electrophysiologic effects of dipyridamole given intravenously to 24 patients during intracardiac electrophysiologic study. Electrophysiologic parameters were measured before and 5 minutes following infusion of 0.5 mg/kg of dipyridamole. The drug significantly shortened the sinus cycle length by 26 per cent ( P < 0.001), sinuatrial conduction time by 15 per cent ( P < 0.01), maximal sinus node recovery time by 21 per cent ( P < 0.001), atrial and atrioventricular nodal effective refractory period by 8 and by 11 per cent, respectively (both P < 0.01), ventricular effective refractory period by 4 per cent ( P < 0.001), paced cycle length to atrioventricular nodal Mobitz type II block by 5 per cent ( P = 0.046), and QT interval during sinus rhythm by 10 per cent ( P < 0.01). After dipyridamole, the PA interval increased by 16 per cent ( P < 0.001), the AH interval by 11 per cent ( P < 0.01), and the corrected QT interval by 5 per cent ( P < 0.01). During retrograde conduction we observed a shortening of the ventriculoatrial interval by 6 per cent ( P = 0.036), retrograde atrioventricular nodal effective refractory period by 5 per cent ( P < 0.001), paced cycle length to atrioventricular nodal Wenckebach and atrioventricular nodal Mobitz type II block both by 8 per cent ( P < 0.01). We conclude that intravenous dipyridamole increases sinus node automaticity and reduces atrial, atrioventricular nodal and ventricular refractory periods, prolongs intra-atrial and atrioventricular nodal conduction, but does not produce any changes in His-Purkinje system conduction times. Paced cycle length to atrioventricular nodal Wenckebach and Mobitz type II block decreased after dipyridamole during antegrade as well as retrograde conduction.

Transient Complete AV Block in Lyme Disease: Electrophysiologic Observations

The findings in a patient with complete AV block and intra-atrial conduction disturbances due to Lyme disease are presented. The electrocardiographic follow-up and serial EP findings suggest that complete AV block in Lyme disease may signify a more extensive affection of the AV conduction system (with eventually attendant intra-atrial conduction disturbances) than described in earlier reports. An almost complete resolution of the considerable damage to the conduction system occurred within two weeks.

Intra-atrial conduction delay and fragmented atrial activity in patients with paroxysmal atrial fibrillation.

To examine the electrophysiologic characteristics of paroxysmal atrial fibrillation (PAF), we studied intra-atrial conduction delay and fragmented atrial activity during premature stimulation of high right atrium in the following four groups: Group I (n = 25), patients without PAF and without sick sinus syndrome (SSS); Group II (n = 22), patients with PAF but without SSS; Group III (n = 10), patients without PAF and with SSS; Group IV (n = 6), patients with PAF and SSS. Intra-atrial conduction delay was the increase in the interval (from the stimuli to the coronary sinus electrogram) observed with early premature beats greater than or equal to 20 ms compared with that of basic rhythm. Fragmented atrial activity was defined as disorganized atrial activity greater than or equal to 150% of the duration of high atrial activity of basic beats recorded. The conduction delay zone (CDZ) and fragmented atrial activity zone (FAZ) were significantly wider in Groups II, III and IV than in Group I. There were no significant differences in either CDZs or FAZs among Groups II, III and IV. Thus, the widening of CDZs and/or FAZs are characteristic of PAF and SSS. CDZ and FAZ may be good indices of development of PAF in patients without SSS.

DDD Pacing: An Effective Treatment Modality for Recurrent Atrial Arrhythmias

We performed atrial EP studies (atrial substrate evaluation) on 10 patients. These patients had evidence of paroxysmal, sustained, recurrent atrial arrhythmias (7 men and 3 women with a mean age of 64 +/- 15 years). All patients combined a brady-tachy syndrome; 7 patients had a sick sinus syndrome (SSS) and 3 patients a typical vagally induced atrial arrhythmia. No anti-arrhythmic drug was allowed in 3 patients with SSS, 1 drug failed in 4 patients and the combination of 2 drugs failed in 3 patients during the first to eighth years prior to pacemaker implantation. Atrial substrate evaluation was feasible in all these patients off anti-arrhythmic therapy and showed important abnormalities of atrial loco-regional conduction parameters and long refractory periods (RP). The remarkable point was, in 7 patients, a paradoxical improvement in intra-atrial conduction delay at rapid pacing rate. The DDD pacing mode was chosen in all patients. No technical problem occurred during implantation. Atrial pacing rate was programmed to be slightly higher than the mean diurnal heart rate calculated on Holter monitoring. After implantation, the mean follow-up period was 18 +/- 25 months with an average of one Holter every 4 months during the first 2 years. The 7 patients who improved intra-atrial conduction at rapid pacing rate were controlled without drugs, 2 patients were controlled with 1 drug, and 1 patient with 2 drugs. Atrial pacing in the DDD mode in a selected group of patients prevents paroxysmal and drug-resistant atrial arrhythmias. Atrial substrate evaluation is a sensitive tool for assuring the long-term benefit of atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Thresholds, refractory periods, and conduction times of the normal and diseased human atrium

In order to better understand the electrophysiology of the diseased human atrium, we measured high right atrial refractory periods, threshold, and conduction times of 61 patients undergoing routine electrophysiologic study. Refractory periods and conduction times of patients with apparently normal atria were compared to those of patients with a history of persistent sinus bradycardia, atrial fibrillation, or other forms of primary atrial tachyarrhythmia. Refractory periods and thresholds were derived from strength-interval curves. Conduction times were measured for all premature beats induced. Threshold, refractory periods, and conduction times of premature beats induced late in the cardiac cycle did not distinguish patients with normal atria from patients with bradycardia or tachycardia. In contrast, increases in conduction time of early cycle premature beats separated patients with these abnormalities from patients with normal atria. The increases in interatrial and intraatrial conduction time of early cycle premature beats were the strongest correlates of primary atrial tachyarrhythmia ( r = 0.52, p = 0.0065 and r = 0.274, p = 0.041, respectively) and induction of repetitive atrial firing ( r = 0.65, p = 0.002, and r = 0.59, p = 0.0001, respectively). This increase in conduction time of early cycle premature beats may predispose these patients to primary atrial tachyarrhythmias.

Effects of beta-adrenergic stimulation on atrial latency and atrial vulnerability in patients with paroxysmal supraventricular tachycardia

To assess the effects of β-adrenergic stimulation on atrial latency and atrial vulnerability, the electrophysiologic properties of the atrium were studied before and during intravenous infusion of isoproterenol at 2 to 5 μg/min in 11 patients with paroxysmal supraventricular tachycardia exhibiting atrial latency during programmed atrial extrastimulation. In all patients, the isoproterenol infusion reduced the extent of maximum atrial latency (from 86 ± 19 to 62 ± 16 ms, p < 0.001). This was accompanied by a significant shortening of both effective and functional refractory periods of the atrium (from 213 ± 31 to 174 ± 40 ms, p < 0.005 and from 259 ± 31 to 215 ± 29 ms, p < 0.001, respectively). The intraatrial and interatrial conduction times were also significantly reduced (from 24 ± 15 and 63 ± 17 to 15 ± 10 and 48 ± 15 ms, p < 0.005, respectively). In 3 patients with demonstrable atrial vulnerability, the isoproterenol infusion abolished the inducibility of repetitive atrial responses or atrial flutter, or both. Although the clinical significance of the suppressive action of β-adrenergic stimulation on atrial vulnerability remains to be determined, the present study has demonstrated that β-adrenergic stimulation significantly reduces atrial latency.

Effects of halothane with and without histamine and/or epinephrine on automaticity, intracardiac conduction times, and development of dysrhythmias in the isolated guinea pig heart.

Histamine is released during allergic reactions, and is known to produce cardiac dysrhythmias. The authors compared the cardiac effects of histamine and epinephrine during exposure to halothane in the isolated perfused guinea pig heart. Responses studied were spontaneous sinus rate, intra-atrial conduction time, atrial-septal conduction time (ASCT), intraventricular conduction time (IVCT), and left ventricular pressure (LVP). The incidence and type of dysrhythmias with histamine and halothane and with epinephrine and halothane were analyzed from electrograms. The authors found that halothane alone (0.7 to 2.1 vol%) causes dose-dependent depressions of sinus rate and LVP, prolongs ASCT and IVCT, and produces atrioventricular (AV) block with junctional bradycardia. Histamine alone (.01-10 microM) increases sinus rate and LVP but, like halothane, prolongs ASCT. Halothane antagonizes the inotropic and chronotropic effects of histamine, but enhances ASCT compared with histamine alone. Histamine with halothane greatly increases the incidence of junctional tachycardia with AV dissociation from 0% with histamine alone up to 48%. Epinephrine alone (0.1-5 microM), like histamine, increases sinus rate and LVP, but does not cause a relative increase in ASCT. Halothane antagonizes the inotropic and chronotropic effects of epinephrine, but increases the incidence of ventricular tachycardia from 6% to 28%, and the incidence of premature ventricular excitations from 0% to 40%, compared with epinephrine alone. The authors' in vitro findings show that histamine and halothane, like epinephrine and halothane, can cause dysrhythmias, but that the genesis and type of dysrhythmias induced by these agents are dissimilar. Consequently, the release of histamine with an anaphylactoid reaction during halothane anesthesia, and the treatment of the reaction with epinephrine, could result in dangerous ventricular tachydysrhythmias.

The effects of the novel anti-anginal compound RS 43285 on myocardial conduction in the anaesthetized dog.

1. A pentobarbitone-anaesthetized canine model of myocardial conduction was developed to evaluate drug effects on intra-atrial (I-A), intra-ventricular (I-V) and atrioventricular (A-V) conduction parameters, both at rest and during electrical pacing of the right atrium or ventricle. Drug effects on the ability of the sino-atrial (SA) node to re-establish sinus rhythm on switching off electrical pacing were also considered. The effects of the novel anti-anginal compound RS 43285-193 ((+/-)-N-(2,6-dimethyl-phenyl)-4[2-hydroxy-3-(2-methoxyphenoxy)propyl] -1-piperazine acetamide dihydrochloride) were compared to those of the standard anti-anginal compounds nicardipine, nifedipine and verapamil. 2. In the dose range 15-7000 micrograms kg-1, RS 43285 had no significant effects on I-A, I-V or A-V conduction either at rest or during electrical pacing and did not affect the re-establishment of sinus rhythm. 3. Nicardipine had no effects on conduction parameters at resting heart rate. There were no effects on I-A or I-V conduction on electrical pacing but A-V conduction was increased at 200-500 micrograms kg-1 (with a 2:1 A-V conduction block in two out of six dogs); this was accompanied by a prolongation of the interval to reversion of sinus rhythm. 4. Nifedipine had no significant effects on I-A or I-V conduction but significantly prolonged A-V conduction at 1000 micrograms kg-1 and this dose also increased the interval to SA node recovery. 5. Verapamil did not effect I-A or I-V conduction. However, A-V conduction was affected with a significant prolongation occurring at resting heart rate at 100-400 Atg kg-' and a 2:1 A-V block in one dog at rest. During right atrial pacing verapamil significantly increased A-V conduction at 50- 400 fig kg-'. All dogs exhibited a 2:1 A-V conduction block at the highest frequency at 400 jig kg-'.

Electrophysiologic effects of intravenous magnesium in patients with normal conduction systems and no clinical evidence of significant cardiac disease

Parenteral magnesium has been used for several decades in the empiric treatment of various arrhythmias, but the data on its electrophysiologic effects in man are limited. We evaluated the electrophysiologic effects of magnesium sulfate (MgSO 4) administration in eight normomagnesemic patients with normal mononuclear cell magnesium content, who had no clinically significant heart disease and had normal baseline electrophysiologic properties. After administration of intravenous MgSO 4, serum magnesium rose significantly from 1.9 ± 0.1 to 4.4 ± 1.7 mg/dl ( p < 0.02). During a maintenance magnesium infusion, we observed significant prolongation of the ECG PR interval (145 ± 18 to 155 ± 26 msec, p < 0.05), AH interval (77 ± 27 to 83 ± 26 msec, p < 0.002), antegrade atrioventricular (AV) nodal effective refractory period (278 ± 67 to 293 ± 67 msec, p < 0.05), and sinoatrial conduction time (60 ± 34 to 76 ± 32 msec, p < 0.02). No significant effect was observed on sinus cycle length, sinus node recovery time, intra-atrial or intraventricular conduction times, QRS duration (during both sinus rhythm and ventricular pacing), QT interval, HV interval, paced cycle length resulting in AV nodal Wenckebach block, AV nodal functional refractory period, retrograde ventriculoatrial (VA) effective refractory period, or atrial and ventricular refractory periods. These findings, in conjunction with the demonstrated ability of magnesium to block slow channels for sodium movement, may provide an explanation of the mechanism by which magnesium exerts its effect in the treatment of atrial and junctional arrhythmias.

Inducible atrial flutter after the Mustard repair of complete transposition of the great arteries

Atrial flutter is a common postoperative arrhythmia in patients with complete transposition of the great arteries (d-TGA) after the Mustard repair. Sixty patients with d-TGA who had the Mustard repair were evaluated by electrophysiologic studies. Thirty-three (55%) had inducible sustained atrial flutter; 17 of them developed spontaneous clinical episodes of atrial flutter (clinical atrial flutter group) and 16 did not (nonclinical atrial flutter group). In 6 of the 17 patients (35%) with clinical inducible atrial flutter, the condition was first documented in the electrophysiologic laboratory with subsequent development of spontaneous clinical episodes. Catheter endocardial mapping, used to determine atrial activation sequences and conduction intervals, revealed intraatrial conduction delays with late activation of the low atrial sites in all patients. Abnormalities of atrial refractoriness were present, with a greater dispersion of atrial refractoriness found in the clinical atrial flutter group. Severe abnormalities of sinus nodal function appeared to a significantly greater degree among patients who had clinical episodes of atrial flutter. These electrophysiologic abnormalities and associated arrhythmias may predispose patients with d-TGA to sudden death.

Electrophysiologic consequences of the mustard repair of d-transposition of the great arteries

This study describes the electrophysiologic effects of the Mustard repair of d-transposition of the great arteries on the sinus node and on conduction and refractoriness in the atrium, atrioventricular (AV) node and ventricle. Seventy-two electrophysiologic studies were performed on 64 patients after the Mustard operation. Standard rest and 24 hour ambulatory electrocardiograms were evaluated. Catheter endocardial atrial mapping, available in 67 of the 72 studies, revealed that sinus rhythm was present in the atria in 33 patients, ectopic atrial rhythm in 26 and junctional rhythm in 8. Intraatrial conduction delays with very late activation of the low medial, low lateral or low right atrium at the AV junction were present in 53 of 59 patients with atrial or sinus rhythm. Sinus node function was normal in only nine patients. Prolonged refractory periods were found in the right atrial portion of the new right atrium when compared with the left atrial portion of the new right atrium. Forty-one percent of the patients had prolongation of atrial refractoriness with shortening of the paced cycle lengths. Fifty-one percent developed sustained intraatrial reentry with programmed atrial stimulation. Forty-eight percent of these patients with inducible atrial tachycardia have since developed clinical episodes of atrial flutter. In summary, electrophysiologic studies revealed significant abnormalities of sinus node function and atrial conduction and refractoriness. Alone or in combination, these abnormalities, which result in severe bradycardia or rapid atrial arrhythmias, may lead to sudden death. The Jatene or arterial switch procedure may provide an appropriate alternative operation in this group of patients.

Transesophageal Versus Intracardiac Atrial Stimulation in Assessing Electrophysiologic Parameters of the Sinus and AV Nodes and of the Atrial Myocardium

Electrophysiological parameters of the sinus and AV nodes and of the atrial myocardium were assessed with both transesophageal atrial stimulation (TAS) and intracardiac atrial stimulation (ICS) in the same patient during the same study. The study group was comprised of nine men and seven women, aged 45 to 79 years, referred for the evaluation of syncope of possible arrhythmogenic origin. Twelve patients were included for analysis. Autonomic inhibition (AI) was obtained in five patients. The most striking result was the significantly longer AERP with TAS (mean 286 +/- 9 ms) than with ICS (mean 244 +/- 12 ms; p than 0.02). After AI, the AERP was even more prolonged with TAS (mean 332 +/- 20 ms) than with ICS (mean 237 +/- 8 ms; p less than 0.01). Intraatrial and AV nodal conduction times assessed at multiple paced cycle lengths were significantly shorter with TAS than with ICS. There was no difference between TAS and ICS with regard to AVERP, Wenckebach periodicity and H-V intervals. Although a tendency towards shorter sinus node recovery time (SNRT) and sinoatrial conduction time (SACT) was observed with TAS, the difference was not statistically significant. Possible mechanisms of the differences are discussed. It seemed clear that the site of origin of an atrial impulse can have definite effects upon excitability and conduction properties of atrial and AV nodal fibers. Enhanced sympathetic activity during TAS was also suggested. The electrophysiological properties inherent in the TAS technique warrant further elucidation.

Effects of N-acetylprocainamide on experimental atrial flutter and atrial electrophysiologic properties in conscious dogs with sterile pericarditis: Comparison with the effects of quinidine

N-acetylprocainamide (NAPA) is said to have class III antiarrhythmic drug properties. The effects of NAPA (25 mg/kg intravenously) on sustained, stable, reentrant atrial flutter induced in 12 conscious dogs using a sterile pericarditis model were studied and compared with the effects of quinidine (5 mg/kg intravenously) given on a different day in 10 of the same 12 dogs. The effects of these drugs on atrial excitability, the atrial effective refractory period and intraatrial conduction time measured during rapid atrial pacing performed during sinus rhythm were also compared. The mean NAPA and quinidine serum levels were 17.7 and 7.1 micrograms/ml, respectively. Both NAPA and quinidine immediately prolonged the atrial flutter cycle length in all dogs, from 118 +/- 15 to 141 +/- 18 ms and from 119 +/- 17 to 153 +/- 21 ms, respectively (both p less than 0.001), and then terminated atrial flutter in 11 of the 12 NAPA studies and in 6 of the 10 quinidine studies. Neither drug affected atrial excitability. Both NAPA and quinidine increased the atrial effective refractory period significantly, from 138 +/- 17 to 168 +/- 20 ms (p less than 0.001) and from 136 +/- 14 to 148 +/- 16 ms (p less than 0.01), respectively. NAPA did not change intraatrial conduction time measured during atrial pacing at 150 beats/min, but during atrial pacing at 300 beats/min, it prolonged it from 51 +/- 9 to 54 +/- 10 ms (p less than 0.05), and at 400 beats/min, from 52 +/- 10 to 64 +/- 13 ms (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiological studies in thyrotoxicosis with and without associated sick sinus syndrome.

Electrophysiological studies in 13 patients with thyrotoxicosis (5 men and 8 women, aged 17 to 76 years) are reported. Five patients presented with features of sick sinus syndrome (SSS) (Group A) while the remaining 8 patients (Group B) had no detectable cardiovascular abnormality. Sinus node function (corrected sinus node recovery and sinoatrial conduction time) was abnormal in all Group A but normal in Group B patients. Intra-atrial, artioventricular (AV) nodal, and infranodal conduction time and effective refractory period of atrium were normal in all patients in both groups. Effective refractory period of AV node was decreased in 6 patients (3 in each group). All Group A patients received radioiodine with complete clinical remission of sick sinus state in 4 subjects. Repeat electrophysiological studies in two of these patients, 6 and 12 months after treatment, showed complete normalization of sinus node function. This is the first reported electrophysiological study documenting the occurrence of SSS in thyrotoxicosis reversed by effective antithyroid treatment. We suggest that attempts should be made to identify underlying thyrotoxicosis in all patients with SSS, especially in the older age group. Appropriate medical treatment may prevent unnecessary implantation of permanent pacemakers in such patients.

First degree atrioventricular block.

Prolongation of the PR interval is a nonspecific condition. Etiologies include normal physiologic variance, idiopathic bundle branch fibrosis, calcific valvular heart disease, ischemic heart disease, cardiomyopathies, infections resulting in myocarditis, drugs (especially type I antidysrhythmic medications), collagen vascular diseases, tumors, trauma, electrolyte imbalances, and many other miscellaneous causes. Isolated first degrees atrioventricular block is generally not associated with an increased risk of sudden death, syncope, or progression to higher degrees of atrioventricular block. Exceptions include patients with intra-atrial conduction delays prone to atrial fibrillation, acute myocardial infarction, or bundle branch disease where higher degrees of atrioventricular block may develop. Treatment consists of correction of the underlying disorder or discontinuation of the offending medication.

Susceptibility to atrial fibrillation and ventricular tachyarrhythmia in the Wolff-Parkinson-White syndrome: Role of the accessory pathway

Clinical and electrophysiologic characteristics associated with spontaneous and inducible atrial fibrillation and ventricular tachyarrhythmia were assessed in 20 consecutive patients with Wolff-Parkinson-White (WPW) syndrome undergoing surgical division (n = 12) or transcatheter electrical ablation (n = 8) of accessory pathways. Patients with spontaneous atrial fibrillation were characterized by the trend (not significant) of a shorter antegrade accessory pathway effective refractory period (256 ± 26 vs 303 ± 109 msec). However, patients with and without spontaneous atrial fibrillation did not differ with respect to prevalence of structural heart disease (3 of 11 vs 2 of 9), intra-atrial conduction time (34 ± 10 vs 32 ± 10 msec), or interatrial conduction time (86 ± 21 vs 88 ± 17 msec). Thus, atrial and accessory pathway electrophysiologic properties (per se) were not clear determinants of susceptibility to atrial fibrillation. Among the 20 patients, 10 to 35 beats of nonsustained ventricular tachycardia (seven patients) or ventricular fibrillation (three patients) were induced at electrophysiologic study with one to three programmed extrastimull. Clinically, a ventricular arrhythmia (ventricular fibrillation during atrial fibrillation) had occurred in only one of these patients. The discordance of these observations was significant ( p < 0.01). Patients with and without inducible ventricular arrhythmias were not distinguished by clinical factors or by electrophysiologic properties of the accessory pathway or ventricles. Accessory pathway conduction was completely or partially eliminated by ablation procedures in 14 of 20 patients. During a mean follow-up of 27 months, atrial fibrillation recurred in two patients with failed ablation procedures and in one patient with left atrial enlargement (despite accessory pathway division) ( p = 0.019 vs pre-ablation). Ventricular arrhythmias remained inducible in two patients in whom accessory pathway ablation failed ( p = 0.01 vs initial study). However, spontaneous ventricular tachyarrhythmias did not occur during follow-up. We conclude that susceptibility to spontaneous or inducible atrial fibrillation and ventricular tachyarrhythmia in patients with WPW syndrome and no organic heart disease depends primarlly on the existence of a functional accessory pathway. These susceptibllities are eliminated by interruption of accessory pathway conduction. Ventricular tachyarrhythmias remain infrequent spontaneous events in the WPW syndrome. Their more frequent induction at electrophysiologic study is not predictive of clinical occurrence.