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Effects of commonly used cardioactive drugs on atrial and sinoatrial conduction in man.

Atrial and sinoatrial conduction intervals were measured in patients before and after the intravenous administration of one of four cardioactive drugs: procainamide, atropine, ouabain, and propranolol. Procainamide uniformly prolonged atrial conduction and shortened sinoatrial conduction. Atropine also shortened sinoatrial conduction but did not significantly alter atrial conduction. Ouabain prolonged sinoatrial conduction in patients with normal control sinoatrial conduction intervals and did not affect atrial conduction. Propranolol did not significantly alter sinoartrial conduction and only prolonged interatrial conduction in patients with normal base line atrial conduction intervals. Of the cardioactive drugs tested, only procainamide and propranolol significantly altered the atrial conduction intervals; furthermore, the effects of these cardioactive drugs on sinoatrial conduction were disparate from their effects on atrial conduction.

Adult↗

Effect of digitalis in patients with paroxysmal atrioventricular nodal tachycardia.

Atrioventricular (A-V) conduction, ventriculo-atrial conduction and mechanism of tachycardia were studied by programmed electrical stimulation before and after the administration of ouabain in 15 patients suffering from paroxysmal supraventricular re-entrant tachycardia. In 13 patients the tachycardia circuit was confined to the A-V node. In two patients the stimulation study showed that an accessory pathway was used in a ventriculo-atrial direction during tachycardia. Ouabain lengthened the effective and functional refractory period of the A-V node and A-V nodal transmission time in all patients in whom this could be studied. Only six patients showed lengthening in ventriculo-atrial conduction time or refractory period of the ventriculo-atrial conduction system. In seven patients no tachycardia could be initiated after ouabain. The width of the zone of atrial premature beats able to initiate tachycardia (the tachycardia zone) narrowed in five patients, showed no change in two patients, and increased in one patient. In these eight patients the tachycardia zone shifted to longer premature beat intervals. Ouabain resulted in slowing of cardiac rate during tachycardia. Both patients who used an accessory pathway during tachycardia showed no change in width of their tachycardia zone following ouabain administration. Seven patients were restudied two weeks after chronic oral administration of digoxin. The results were similar to those obtained following ouabain administration. This indicates that in patients suffering from paroxysmal A-V nodal tachycardia the effect of chronic oral digoxin administration can be predicted from the study of the effect of ouabain during programmed stimulation of the heart.

Adolescent↗

Ventricular tachycardia with alternate ventriculo-atrial Wenckebach conduction due to two-level block.

A 54-year-old patient was studied because of ventricular tachycardia following an inferior myocardial infarction. During one episode of non-sustained ventricular tachycardia a 9:4 alternating ventriculo-atrial Wenckebach block was noted. This was based upon a 2:1 block between the ventricles and the bundle of His and a 5:4 Wenckebach block between the bundle of His and the atria. Our study shows that alternate Wenckebach periods during ventriculo-atrial conduction may be caused by two or more levels of block in the ventriculo-atrial conduction system.

Cardiac Pacing, Artificial↗

Differentiation of the electrophysiological effects on the atrial myocardium between the pure Na channel blocker, pilsicainide, and flecainide.

UNLABELLED: The purpose of this study was to identify the difference between the pure Na channel blocker, pilsicainide and Ic-antiarrhythmic drug, flecainide, on the atrial electrophysiological characteristics. METHODS: The subjects consisted of 24 patients (48 +/- 12 years-old: P-group) in whom pilsicainide was administrated intravenously (1 mg/kg/10 min) and 31 patients (47 +/- 15 years-old: F-group) in whom flecainide was administrated intravenously (2 mg/kg/10 min). The atrial effective refractory period (ERP-A), intra-atrial conduction time (CT), max intra-atrial conduction delay (Max CD), repetitive atrial firing zone (RAFZ), fragmented atrial activity zone (FAZ) and intra-atrial conduction delay zone (CDZ) were measured before and after the drugs. RESULTS: Pilsicainide and flecainide significantly prolonged the ERP-A (211 +/- 27 msec to 246 +/- 39 msec; p < 0.001, 217 +/- 25 msec to 244 +/- 33 msec; p < 0.001, respectively) and CT (121 +/- 33 msec to 149 +/- 43 msec; p < 0.001, 122 +/- 22 msec to 153 +/- 27 msec; p < 0.001, respectively) to the same degree. However, the Max CD was shortened by pilsicainide, but not by flecainide. The RAFZ, FAZ and CDZ decreased in the P-group (21 +/- 25 msec to 4 +/- 10 msec; p < 0.01, 24 +/- 24 msec to 14 +/- 18 msec; p < 0.05, 56 +/- 29 msec to 43 +/- 32 msec, p < 0.05, respectively), but not in the F-group. CONCLUSIONS: The effects of atrial conduction delays may differ between pilsicainide and flecainide. Further examination will be needed to explain this mechanism.

Adult↗

[A-V conduction in atrial fibrillation and flutter].

The assessment of A-V conduction in the presence of atrial fibrillation is based upon analysis of the R-R intervals. This is because in atrial fibrillation it is impossible both to identify the impulse that has been conducted to the ventricles, and to measure the A-V conduction time. The first step is, therefore, to evaluate whether the QRS complexes are the expression of conducted atrial impulses, or they are A-V junctional or ventricular in origin. In other words, it is necessary to distinguish between A-V conduction and A-V dissociation. Conduction in atrial fibrillation commonly results in irregular R-R cycles, whereas in the presence of dissociation the R-R cycles are mainly regular. This differentiation can be difficult in the presence of: aberrant conduction; A-V conduction disturbances; or A-V junctional tachycardia with anterograde 2nd degree exit block. The problem occurs both with tachycardia-dependent (or phase 3), and with bradycardia-dependent (or phase 4) aberrant conduction. Distinction between aberration and ectopy is helped by: the sequence long cycle-short cycle; the pause that follows the wide QRS complex; the configuration of the wide QRS complex. Since aberrant conduction may be sustained, due to the linking phenomenon, the pattern may mimick ventricular tachycardia. In atrial flutter the atrial electrical activity is far less chaotic than in atrial fibrillation, so that assessment of A-V conduction is less difficult. Nevertheless, it is impossible to determine exactly which out of the atrial impulses has been conducted, due to the extremely fast atrial rate: the conducted impulse, indeed, is not always the one that immediately precedes the QRS complex. Furthermore, it is also difficult to measure the A-V conduction time, because the F waves follow to each other without any interruption, so that it is impossible to define exactly the beginning of atrial activation. In atrial flutter, thus, as well as in atrial fibrillation, A-V conduction may be assessed by analysis of the R-R intervals, apart from measurement of F-R intervals. In the absence of drugs, atrial flutter is usually associated with 2:1 (or, less frequently, 4:1) conduction ratio, being the odd ratios (3:1, 5:1) far more rare. Due to concealed penetration of non-conducted impulses, A-V conduction intervals are often variable, so that the R-R cycles are irregular even in the presence of a constant A-V conduction ratio. The most common mechanisms leading to irregularity are the alternation of A-V conduction times, and the alternating Wenckebach phenomenon.(ABSTRACT TRUNCATED AT 400 WORDS)

Atrial Fibrillation↗

Donor-to-recipient decremental conduction of atrial fibrillation following orthotopic heart transplantation: insights into the mechanism of atrioatrial conduction.

We describe the unique case of a heart transplant patient with type I atrial fibrillation that arose in the donor atrium during a late acute rejection episode and conducted to the recipient atrium with second-degree type I local block. After internal cardioversion, programmed stimulation showed bidirectional decremental conduction across the suture line with nearly equal atrioatrial interval, whereas the recipient atrium showed progressively delayed intra-atrial conduction. These findings strongly suggest that the mechanism of atrioatrial conduction may be electrical propagation along viable myocardium bridging the surgical scar and that the electrophysiologic characteristics of the recipient atrium are involved in decremental conduction across the suture line.

Atrial Fibrillation↗

Improvement of atrial signal-averaged electrocardiographic abnormalities after radiofrequency catheter ablation in persistent atrial flutter.

It has been reported that abnormalities of atrial conduction are present in patients with atrial flutter (AFL). We analyzed the P wave signal-averaged ECG (PSE) in patients after cardioversion of chronic AFL by radiofrequency catheter ablation (RFCA) to determine whether abnormalities of atrial conduction exist in patients with AFL and whether they recover. We studied 11 patients undergoing ablation of persistent AFL (AFL group), 11 patients with paroxysmal AFL (PAFL group), and 14 patients without any evidence of arrhythmias (control group). The PSEs were recorded 1 day, 7 days, and 1 month after RFCA. The filtered P wave duration (FPD) was calculated from the PSE recording. The FPD correlated with interatrial conduction time (r = 0.644) and left atrial dimension (r = 0.675) in combined assessment of the AFL and PAFL groups. The FPD was longer in the AFL group 1 day (165 +/- 14 ms, P < 0.001) and 1 month (150 +/- 18 ms, P < 0.05) after RFCA than in the control group (134 +/- 10 ms). Our findings suggest that atrial conduction abnormalities detected by PSE are present in patients with persistent AFL and improve 1 month after cardioversion.

Adult↗

Atrial fibrillation and atrial vulnerability in patients with Brugada syndrome.

OBJECTIVES: We sought to study atrial vulnerability in patients with Brugada syndrome. BACKGROUND: Atrial fibrillation (AF) often occurs in patients with Brugada syndrome, but atrial vulnerability in Brugada syndrome has not been evaluated. METHODS: The patient group consisted of 18 patients with Brugada syndrome. The control group consisted of 12 age- and gender-matched subjects who had neither organic heart disease nor AF episodes. The incidence and clinical characteristics of AF were evaluated in all 18 patients with Brugada syndrome, and an electrophysiologic study was performed in all 12 control subjects and in 14 of the 18 patients with Brugada syndrome. The atrial effective refractory period of the right atrium (RA-ERP), intra-atrial conduction time (conduction time from the stimulus at the right atrium to atrial deflection at the distal portion of the coronary sinus), duration of local atrial potential, and repetitive atrial firing (occurrence of two or more premature atrial complexes after atrial stimulation) were studied. RESULTS: Spontaneous AF occurred in 7 of the 18 patients with Brugada syndrome but in none of the control subjects. The RA-ERP was not different between the two groups. The intra-atrial conduction time was increased in the Brugada syndrome group versus the control group (168.4 +/- 17.5 vs. 131.8 +/- 13.0 ms, p < 0.001). The duration of atrial potential at the RA-ERP was prolonged in the Brugada syndrome group versus the control group (80.3 +/- 18.0 vs. 59.3 +/- 9.2 ms, p < 0.001). Repetitive atrial firing was induced in nine patients with Brugada syndrome and in six control subjects. Atrial fibrillation was induced in eight patients with Brugada syndrome but in none of the control subjects. In patients with Brugada syndrome without spontaneous AF, the intra-atrial conduction time and duration of atrial potential were also increased. CONCLUSIONS: Atrial vulnerability is increased in patients with Brugada syndrome. Abnormal atrial conduction may be an electrophysiologic basis for induction of AF in patients with Brugada syndrome.

Adult↗

[A-V conduction in atrial flutter. Electrocardiographic study].

One hundred and twenty-nine cases of atrial flutter were analyzed to assess the A-V conduction. The R-R intervals, the A-V conduction ratio, and the F-R intervals were measured in each case. Conduction in atrial flutter was defined either as constant or as variable depending on whether the A-V conduction ratio was fixed or variable. Furthermore, atrial flutter was defined as regular whenever the R-R intervals were mathematically related to each other, any interval being a multiple of the F-F cycle. On the other hand, atrial flutter was defined as irregular when the R-R cycles did not reflect a precise mathematical relationship. The R-R intervals in irregular atrial flutter were not exactly multiples of the F-F cycle. This was because the F-R intervals were variable. Sixty-five cases of atrial flutter had constant A-V conduction, whereas 64 cases were associated with variable A-V conduction. Eighty-eight per cent of cases with constant conduction were regular. On the contrary, 91% of cases with variable A-V conduction were irregular. These data reflect a relationship between the constancy of the A-V conduction ratio and the regularity of the R-R intervals. Several mechanisms were identified as being responsible for atrial flutter irregularity. Alternation of the F-R intervals was the most frequent mechanism leading to irregularity of atrial flutter with constant A-V conduction. Alternating Wenckebach periodicity was the most common cause of irregularity in atrial flutter with variable conduction ratio. Concealed conduction of blocked impulses was also frequently involved in determining atrial flutter irregularity.

Atrial Flutter↗

Mechanism of atrial fibrillation: decremental conduction, fragmentation, and ectopic activity in patients with drug resistance paroxysmal atrial fibrillation and structurally normal heart.

Atrial fibrillation (AF) has been associated with premature beats and decreased atrial conduction velocity. This study examined a new index of dynamic inter-atrial conduction time (iaCT) in patients with paroxysmal AF (PAF). We compared 42 consecutive patients with paroxysmal AF (mean age = 52 +/- 16 years) without structural heart disease with 39 age-matched patients (mean age = 49 +/- 15 years) who underwent ablation of junctional tachycardias. Prior to investigation, all antiarrhythmic drugs were discontinued for an appropriate period of time. The following measurements were made: baseline iaCT (iaCTb) between high right atrium (HRA) and distal coronary sinus, iaCT during HRA pacing S1S1 600 ms (iaCTS1), maximum prolongation of iaCT during S2 and S3 delivery (iaCTS2, iaCTS3). We then derived the decremental index (DI), the maximum percent prolongation of iaCT = iaCT S3-iaCTS1/iaCTS1%. In patients with PAF, iaCTb was 81.3 +/- 24 ms versus 59.5 +/- 14 ms in controls (P = 0.0001). Atrial fibrillation was reproducibly and easily induced with a prominent increase in iaCT in 11 patients with AF. In this subgroup DI was 92 +/- 17%, compared to 45 +/- 21% in the other patients with AF (P = 0.0001) and 21 +/- 15% in the control group (P = 0.0001). Spontaneous isolated or repetitive ectopic activity was observed in 11 patients with AF (26%), and decremental atrial conduction was observed in 76% of patients with AF. This study supports the role of dynamic inter-atrial conduction disturbances in patients with lone PAF. The DI may be a new index of vulnerability to paroxysmal AF.

Atrial Fibrillation↗

In vivo validation of the origin of the esophageal electrocardiogram.

Esophageal electrocardiography is a clinical and investigational technique that is useful for determining atrial conduction intervals, analyzing atrial rhythms and mapping conduction pathways. Although the left atrial origin of the esophageal electrocardiogram has long been implied, recently that origin has been questioned. In the present study, the origin of the esophageal deflection is defined by direct right and left atrial mapping studies performed with simultaneous esophageal electrograms obtained from three positions (high, mid and low). Seven patients with normal left atrial dimensions (group I) and five patients with left atrial enlargement (group II) underwent transseptal catheterization during the course of electrophysiologic study. In group I (normal left atrial dimensions), conduction time from the high right atrium to each of the three esophageal positions corresponded to conduction times to left atrial sites ranging from 1 to 3 cm lateral to the left interatrial septum. The mid- and low esophageal conduction times were all significantly longer than conduction time to the left side of the septum (p less than 0.05). In group II (enlarged left atrium), conduction times to each of the esophageal sites corresponded to conduction times to left atrial sites lying between the mid-left atrium and a point 1 cm lateral to the left side of the septum. A significant trend toward longer conduction time to the mid-esophageal position than to the left septum was noted (p less than 0.1). In both groups, conduction times measured with the esophageal catheter were significantly longer than conduction time to the right interatrial septum (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Pronounced effect of procainamide on clockwise right atrial isthmus conduction compared with counterclockwise conduction: possible mechanism of the greater incidence of common atrial flutter during antiarrhythmic therapy.

INTRODUCTION: It has been shown that the induction rates of common and reversed common atrial flutter are comparable during baseline control study, whereas the rate is significantly greater for common flutter than reversed common flutter during administration of antiarrhythmic agents. The mechanism of this discrepancy is not known. METHODS AND RESULTS: The study consisted of 15 patients (group 1) with clinically documented common atrial flutter either with (n = 10) or without (n = 5) Class I antiarrhythmic therapy, and 15 patients with paroxysmal supraventricular tachycardia (group 2). Bidirectional conduction velocity and minimal pacing cycle length of 1:1 conduction during incremental pacing from both the low lateral right atrium and coronary sinus were assessed. The response of these variables to procainamide was analyzed in correlation with the induction rate of each type of flutter during the pacing protocol. Conduction velocity in the clockwise (CW) direction was significantly slower for all pacing cycle lengths than conduction velocity in the counterclockwise (CCW) direction in group 1 but was similar in group 2. Minimal pacing cycle length of 1:1 conduction did not differ between CW and CCW conduction in either group. However, in group 1, minimal pacing cycle length of 1:1 conduction of CW conduction was prolonged to a greater degree after procainamide than that of CCW conduction. There also was a significant increase in the induction rate of common flutter. This preferential effect of procainamide on CW conduction was not observed in group 2. CONCLUSION: CW conduction over the isthmus is preferentially influenced by procainamide compared with CCW conduction, which may explain the greater incidence and induction probability of common flutter during antiarrhythmic therapy.

Adult↗

Prevalence and significance of ventriculoatrial conduction.

Because retrograde atrioventricular conduction may predispose to pacemaker-induced tachycardia when DDD pacing is employed, we assessed ventriculo-atrial conduction in 117 patients undergoing electrophysiologic studies. Ventriculo-atrial conduction was present in 40% with a mean (+/- sem) conduction time of 205 +/- 12 ms. The maximum VA conduction time following minimum extrastimulus intervals averaged 258 +/- 14 ms. Antegrade AV nodal properties predicted VA conduction in only 67% by using stepwise discriminant analysis. Only the PR interval, AH interval, and AV nodal effective refractory periods were helpful in predicting ventriculo-atrial conduction. Although ventriculo-atrial conduction time increased on most antiarrhythmic drugs, it was infrequently eliminated.

Aged↗

AV conduction with atrial rate adaptive pacing in the bradycardia tachycardia syndrome.

AV conduction with atrial rate adaptive pacing (AAIR) during exercise was investigated in 43 patients (28 men, 15 female, mean age 68 +/- 7 years) who were paced and medicated with antiarrhythmic drugs for the bradycardia tachycardia syndrome (BTS). Patients were included if they had no second- or third-degree AV block, no complete bundle branch or bifascicular block, and a PQ interval < or = 240 ms during sinus rhythm at rest. The interval between the atrial spike and the following Q wave (SQ) was measured in the supine position at rest (R) with maximum AAI pacing rate (Fmax) achieved below the Wenckebach point (SQ-R-Fmax). Bicycle ergometry was performed using the Chronotropic Assessment Exercise Protocol, and AAI pacing rate was increased stepwise by programming load-adapted increments. Seven patients showed intrinsic rhythm during exercise. In those 36 patients who were atrially paced throughout ergometry (E), SQ was measured with 70 beats/min on the lowest CAEP stage (SQ-E-70) and with Fmax at maximum work load (SQ-E-Fmax). During exercise, no second-degree AV block was observed, but 28 of 36 patients (78%) showed a nonphysiological increase of the SQ interval, and the average SQ-E-Fmax was significantly longer than SQ-E-70 (250 +/- 31 versus 228 +/- 32 ms, P < 0.01). There was only a weak correlation between SQ-R-Fmax and SQ-E-Fmax (r = 0.35824, P < 0.05). When Fmax obtained during exercise was kept during recovery, 14 patients (39%) developed a second-degree AV block between 15 and 240 seconds after ergometry, 8 patients within 90 seconds. Patients who had exhibited a P on T wave in the ECG with Fmax at the end of exercise (11 of 36 patients) were reevaluated by Doppler echocardiography. Using the same exercise protocol and identical, load-adapted rate increments, only 3 of 11 patients showed premature mitral valve closure. It is concluded that patients paced and medicated for BTS are prone to a nonphysiological prolongation of AV conduction with AAIR pacing during and after exercise. As this risk can hardly be predicted by rapid atrial pacing at rest, the pacing system should be dual chamber in this subset of patients. This especially applies to the patients in whom mechanical AV timing is affected by the conduction delay.

Aged↗

Role of the low amplitude potential in the initial P wave signal-averaged electrocardiogram [corrected] in sick sinus syndrome.

BACKGROUND: The cause of abnormally low amplitude of the initial P wave signal-averaged electrocardiogram (P-SAECG) in patients with sick sinus syndrome (SSS) is unknown. METHODS AND RESULTS: Thirteen normal patients (Group C) and 33 with SSS (Group S) were examined. The root mean square amplitude for the initial 30 ms (EP30) and the duration of below-4 microV signals of the filtered P waves (ED4) were measured using the P-SAECG. The interval from an atrial potential on the sinus-node electrogram (SNE) to P wave onset (AS-P), and the interval from the P wave to the atrial potential on the His-bundle-electrogram (P-AH) were measured in the electrophysiological study. The sino-atrial conduction time was measured by a conventional method (indirect sino-atrial conduction time (SACTi)) and using SNE (direct sino-atrial conduction time (SACTd)). The EP30 was significantly lower and the ED4 significantly longer in Group S. The AS-P was significantly longer in Group S (p<0.01), but the P-AH was not different. In Group S, the AS-P was significantly correlated with EP30 and ED4 (p<0.01), but the P-AH was uncorrelated. The SACTi was significantly correlated with EP30 and ED4 (p<0.05), but the SACTd was uncorrelated. CONCLUSION: The abnormality of the initial portion of the P-SAECG observed in SSS appears to be due to disturbed conduction through the atrial myocardium around the sino-atrial node.

Adult↗

Electrophysiologic assessment in selecting patients for multisite atrial pacing.

Electrophysiologic mechanisms of atrial fibrillation (AF) initiation are being actively studied. Multisite atrial pacing has shown, in acute studies, significant potential for prevention of AF. Dual site pacing reduces of intra and inter-atrial conduction time, atrial refractoriness dispersion, and to a limited extent atrial premature beats which modify the atrial remodelling induced by AF. Recently, two clinical trials have shown long term efficacy of multisite atrial pacing. At 3 years of follow-up, 56% of patients are free of AF recurrence with dual site right atrial pacing. Rhythm control was achieved in 86 of patients. Similar results are observed with biatrial resynchronization. In both studies, primary indication for multisite atrial pacing was AF prevention in more than 50% of patients. Selection of patients based solely on long P wave duration and prolonged interatrial conduction is not necessary as clinical outcome and comparable. These patients are comparable to patients who did not have these characteristics. Ongoing multicenter trials will likely definitively answer this question. However, preexcitation of diseased atrial regions or site of ectopic activity previously selected by high density atrial mapping or suppression of inducible AF may offer an interesting future development of multisite atrial pacing.

Atrial Fibrillation↗

Electrophysiology of atrial fibrillation and its prevention by coronary sinus pacing.

Atrial fibrillation (AF) is a re-entrant rhythm, and patients with AF have intra-atrial conduction abnormalities as evidenced by prolonged P-wave duration, abnormal SAECG of P wave, fragmented atrial electrograms and greater intra-atrial conduction delays in response to APDs. Our previous work has proposed that intra-atrial conduction delays and dispersion of refractoriness during extrastimulus testing are site dependent; high right atrial (HRA) stimulation results in marked prolongation of intra-atrial conduction times and AF, whereas distal coronary sinus (CS) stimulation is associated with minimal conduction delays and absence of AF inducibility. Patients with AF induction during HRA stimulation also manifest non-uniform anisotropic conduction in the region of the posterior triangle of Koch. We postulated that if the posterior triangle of Koch is a critical area for re-entry that initiates AF, then prevention of early activation of the posterior triangle may prohibit AF induction by HRA APDs. Distal CS pacing pre-excites the posterior triangle in relation to HRA activation, therefore a subsequent HRA APD will activate the posterior triangle with a longer coupling interval. AF induction by HRA APDs following HRA pacing is prevented when same HRA APDs follow distal CS pacing. We propose that distal CS pacing eliminates the propensity of HRA extrasystoles to induce AF. This observation may have further clinical applicability in AF prevention.

Atrial Fibrillation↗