Intra-atrial Conduction Time Research Articles

Sinus node dysfunction and impairment of global atrial conduction time after high rate atrial and ventricular pacing in dogs.

It has been shown in animals and humans that AF shortens the atrial refractory period and impairs its rate adaptation. The aim of the study was to evaluate the effects of high rate pacing on sinus node function and intraatrial conduction. Eight dogs were subjected to rapid atrial pacing (AP) at a rate of 400 beats/min for 16 days. After a complete recovery of left ventricular function, they underwent rapid ventricular pacing (VP) at 240 beats/min of equal duration. Sinus node recovery time (SNRT) was measured after pacing at 150, 160, and 170 beats/min. P wave duration was measured on a surface ECG recorded at a paper speed of 200 mm/s. Measurements were performed at baseline, immediately after AP or VP, and four weeks after termination of AP or VP. SNRT immediately after AP and VP was significantly prolonged at all three pacing rates (P < 0.03). P wave duration increased significantly after either type of pacing (AP: 74.3 +/- 6.4 ms, VP: 70.0 +/- 3.8 ms) compared with baseline values (60.6 +/- 6.2 ms, P < 0.05). Rapid AP and VP induces sinus node dysfunction and prolongs intraatrial conduction time. The effects of sustained AP and VP on sinus node function and atrial myocardium returned toward control values 4 weeks after cessation of pacing. The authors hypothesize that reversible electrical remodeling occurs both in the sinus node and in the atrial myocardium.

Atrial fibrillation and atrial vulnerability in patients with Brugada syndrome

ObjectivesWe sought to study atrial vulnerability in patients with Brugada syndrome. BackgroundAtrial fibrillation (AF) often occurs in patients with Brugada syndrome, but atrial vulnerability in Brugada syndrome has not been evaluated. MethodsThe 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. ResultsSpontaneous 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. ConclusionsAtrial 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.

Effects of percutaneous mitral balloon valvuloplasty on P-wave dispersion in patients with mitral stenosis

P-wave dispersion (PWD) is a new electrocardiographic marker that has been associated with inhomogeneous and discontinuous propagation of sinus impulses. 1 Dilaveris P.E Gialafos E.J Andrikopoulos G.K Richter D.J Papanikolaou V Poralis K Gialafos J.E Clinical and electrocardiographic predictors of recurrent atrial fibrillation. Pacing Clin Electrophysiol. 2000; 23: 352-358 Crossref PubMed Scopus (201) Google Scholar , 2 Dilaveris P.E Gialafos E.J Sideris S Theopistou A.M Andrikopoulos G.K Kyriakidis M Gialafos J.E Toutouzas P.K Simple electrocardiographic markers for the prediction of paroxysmal idiopathic atrial fibrillation. Am Heart J. 1998; 135: 733-738 Abstract Full Text Full Text PDF PubMed Scopus (570) Google Scholar It can be defined as the difference between maximum and minimum P-wave duration. The prolongation of intra-atrial and interatrial conduction time, and the inhomogeneous propagation of sinus impulses are well known electrophysiologic characteristics of the atrium prone to fibrillate. 1 Dilaveris P.E Gialafos E.J Andrikopoulos G.K Richter D.J Papanikolaou V Poralis K Gialafos J.E Clinical and electrocardiographic predictors of recurrent atrial fibrillation. Pacing Clin Electrophysiol. 2000; 23: 352-358 Crossref PubMed Scopus (201) Google Scholar , 2 Dilaveris P.E Gialafos E.J Sideris S Theopistou A.M Andrikopoulos G.K Kyriakidis M Gialafos J.E Toutouzas P.K Simple electrocardiographic markers for the prediction of paroxysmal idiopathic atrial fibrillation. Am Heart J. 1998; 135: 733-738 Abstract Full Text Full Text PDF PubMed Scopus (570) Google Scholar Furthermore, prolonged P-wave duration and increased PWD have been reported to carry an increased risk for atrial fibrillation (AF). 2 Dilaveris P.E Gialafos E.J Sideris S Theopistou A.M Andrikopoulos G.K Kyriakidis M Gialafos J.E Toutouzas P.K Simple electrocardiographic markers for the prediction of paroxysmal idiopathic atrial fibrillation. Am Heart J. 1998; 135: 733-738 Abstract Full Text Full Text PDF PubMed Scopus (570) Google Scholar , 3 Aytemir K Ozer N Atalar E Sade E Aksoyek S Ovunc K Oto A Ozmen F Kes S P wave dispersion on 12-lead electrocardiography in patients with paroxysmal atrial fibrillation. Pacing Clin Electrophysiol. 2000; 23: 1109-1112 Crossref PubMed Scopus (244) Google Scholar Rheumatic mitral stenosis (MS) is frequently seen in developing countries and causes significant morbidity and mortality. 4 Braunwald E Valvular heart disease. in: Braunwald E Zipes D.P Libby P Heart Disease A Textbook of Cardiovascular Medicine. 6th ed. WB Saunders, Philadelphia2001: 1643-1653 Google Scholar Percutaneous mitral balloon valvuloplasty (PMBV) is the procedure of choice in patients who have symptomatic, hemodynamically severe MS, and are suitable for this procedure. 4 Braunwald E Valvular heart disease. in: Braunwald E Zipes D.P Libby P Heart Disease A Textbook of Cardiovascular Medicine. 6th ed. WB Saunders, Philadelphia2001: 1643-1653 Google Scholar , 5 Inoue K Owaki T Nakamura T Kitamura F Miyamoto N Clinical application of transvenous mitral commissurotomy by a new balloon catheter. J Thorac Cardiovasc Surg. 1984; 87: 394-402 PubMed Google Scholar , 6 Reyes V.P Raju B.S Wynne J Stephenson L.W Raju R Fromm B.S Rajagopal P Mehta P Singh S Rao D.P Percutaneous balloon valvuloplasty compared with open surgical commissurotomy for mitral stenosis. N Engl J Med. 1994; 331: 961-967 Crossref PubMed Scopus (344) Google Scholar This procedure is highly successful with a low complication rate and significant short- and long-term improvement in hemodynamics and symptoms. 7 McKay C.R Kawanishi D.T Kotlewski A Parise K Odom-Maryon T Gonzalez A Reid C.L Rahimtoola S.H Improvement in exercise capacity and exercise hemodynamics 3 months after double-balloon, catheter balloon valvuloplasty treatment of patients with symptomatic mitral stenosis. Circulation. 1988; 77: 1013-1024 Crossref PubMed Scopus (80) Google Scholar , 8 Block P.C Palacios I.F Block E.H Tuzcu E.M Griffin B Late (two-year) follow-up after percutaneous balloon mitral valvotomy. Am J Cardiol. 1992; 69: 537-541 Abstract Full Text PDF PubMed Scopus (50) Google Scholar The objectives of this study were (1) to identify PWD in patients with MS, and (2) to determine the effects of PMBV on PWD. There is currently no study on the effects of MS and PMBV on PWD.

Effects of a novel class III antiarrhythmic agent, NIP-142, on canine atrial fibrillation and flutter.

The effects of a new benzopyran derivative, NIP-142, on atrial fibrillation (AF) and flutter (AFL) and on electrophysiological variables were studied in the dog. NIP-142 (3mg/kg) was administered intravenously to pentobarbital-anesthetized beagles during vagally-induced AF and during AFL induced after placement of an intercaval crush. Isolated canine atrial tissues were studied using standard microelectrode technique. NIP-142 terminated AF in 5 of 6 dogs after an increase in fibrillation cycle length (CL) and prevented reinitiation of AF in all 6 dogs. NIP-142 terminated AFL in all 6 dogs without any appreciable change in flutter CL, and prevented reinitiation of AFL in all 6 dogs. NIP-142 prolonged atrial effective refractory periods (11+/-5%, 3+/-3%, 12+/-3%, and 10+/-5% from the baseline value at basic CLs of 150, 200, 300, and 350ms, respectively) without changes in intraatrial conduction time. The prolongation of the atrial effective refractory period was greater in the presence of vagal stimulation. NIP-142 decreased action potential phase-1 notch and increased phase-2 plateau height without making any changes in the action potential duration, although it did reverse carbachol-induced shortening of the action potential duration. In conclusion, NIP-142 is effective in treating AFL and vagally-induced AF by prolonging atrial refractoriness.

Recovery of electrophysiological parameters after conversion of atrial fibrillation

We investigated the recovery of electrophysiological parameters from electrical remodeling after conversion of chronic lone atrial fibrillation in humans. Clinical studies have shown that the longer atrial fibrillation lasts, the more difficult it becomes to maintain the sinus rhythm after cardioversion. To explore the effects of the duration of atrial fibrillation on changes of electrophysiological parameters after conversion, we determined the atrial effective refractory period and P wave duration during right atrial pacing at 1 and 24 h after electrical cardioversion in 15 patients with chronic lone atrial fibrillation (median duration, 6 months). By 24 h after cardioversion, the effective refractory period at a pacing cycle length of 600 ms increased from 225±19 to 254±27 ms. However, the P wave duration did not decrease significantly 24 h after conversion. As the duration of atrial fibrillation became longer, the prolongation of effective refractory period was more delayed ( P<0. 001, r=0.82), and the shortening of P wave duration was significantly smaller within 24 h after cardioversion ( P<0. 001, r=0.67). After cardioversion of chronic lone atrial fibrillation, the recovery of shortened atrial refractoriness and prolonged intraatrial conduction time is dependent on the duration of preexisting atrial fibrillation.

P-wave dispersion: a novel predictor of paroxysmal atrial fibrillation.

The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiologic characteristics in patients with paroxysmal atrial fibrillation (AF). Previous studies have demonstrated that individuals with a clinical history of paroxysmal AF show a significantly increased P-wave duration in 12-lead surface electrocardiograms (ECG) and signal-averaged ECG recordings. The inhomogeneous and discontinuous atrial conduction in patients with paroxysmal AF has recently been studied with a new ECG index, P-wave dispersion. P-wave dispersion is defined as the difference between the longest and the shortest P-wave duration recorded from multiple different surface ECG leads. Up to now the most extensive clinical evaluation of P-wave dispersion has been performed in the assessment of the risk for AF in patients without apparent heart disease, in hypertensives, in patients with coronary artery disease and in patients undergoing coronary artery bypass surgery. P-wave dispersion has proven to be a sensitive and specific ECG predictor of AF in the various clinical settings. However, no electrophysiologic study has proven up to now the suspected relationship between the dispersion in the atrial conduction times and P-wave dispersion. The methodology used for the calculation of P-wave dispersion is not standardized and more efforts to improve the reliability and reproducibility of P-wave dispersion measurements are needed. P-wave dispersion constitutes a recent contribution to the field of noninvasive electrocardiology and seems to be quite promising in the field of AF prediction.

Lengthening of intraatrial conduction time in atrial fibrillation and its relation with early recurrence of atrial fibrillation.

Intraatrial conduction delay in atrial fibrillation (AF) that is considered a component of atrial electrical remodeling has been demonstrated previously in experimental models and it is considered an important factor for the induction or stabilization of AF. However, it is not known if this phenomenon exists in human AF. The present study aimed to compare intraatrial conduction time (IACT) in patients with chronic atrial fibrillation who were converted to sinus rhythm and a matched control group, and to investigate its relation with early AF recurrence. Seventeen patients with chronic AF (mean duration of 20.71+/-16.35 months) were enrolled in the study (7 males, 10 females, 63+/-8 years). An age and sex matched control group (n=12) consisted of patients with sinus rhythm who underwent electrophysiological study (EPS). None of the patients were on any antiarrhythmic treatment during the procedures. Cardioversion was performed via external DC cardioversion. Eight patients in the control group were delivered a DC shock because of induced ventricular tachycardia during EPS. IACT was defined as the interval between the onset of P wave surface ECG and the beginning of A wave at high right atrium (IACT 1) and low right atrium (IACT 2). Additionally, the interval between A wave at high right atrium and low right atrium was measured (IACT 3). Patient characteristics such as age, sex and echocardiographic variables were not different between the AF group and the control group. Heart rate after cardioversion was found to be similar between the two groups. Total delivered energy was significantly higher in the AF group than in the control group (464.47+/-165.82 joules vs. 315.00+/-27.77 joules, p<0.001). IACT 1 (15.30+/-7.61 msec vs 8.50+/-5.29 msec, p<0.02 ), IACT 2 (45.25+/-836 msec vs 26.44+/-10.45 msec, p<0.001) and IACT 3 (26.9+/-8.26 msec vs. 18.67+/-10.05, p<0.05) significantly lengthened in the AF group after maintenance of sinus rhythm compared to the control group. There were 6 early AF recurrences during the 1 week follow-up period. Multivariate analysis, revealed IACT 2 and IACT 3 were significantly different between the control group, the patient with recurred AF and the patients with maintained sinus rhythm. Post-hoc analysis revealed that IACT 2 and IACT 3 significantly lengthened in the patients with recurred AF compared to both the control group and patients with maintained sinus rhythm. On the other hand, only IACT 2 patients with maintained sinus rhythm were found to be higher than those of the control group. The present study indicated that intraatrial conduction was disturbed in patients with AF, a finding which is consistent with those of previous experimental studies. Additionally, such a phenomenon may be a risk factor for the early recurrence of AF after cardioversion to sinus rhythm.

Frequency-dependent electrophysiological effect of ibutilide on human atrium and ventricle.

Most of the class III antiarrhythmic agents developed in recent years blocks the rapid component of delayed rectifier potassium current (IKr). IKr blocker shows reverse use-dependency and also may cause torsades de pointes at slower heart rate. Ibutilide fumarate, a novel class III antiarrhythmic agent, increases window Na(+) current at the action potential plateau phase. We studied the rate-dependent effect of ibutilide on the electrophysiological parameters of human atrium and ventricle. Franz catheter and a pacing catheter were placed closely in the high right atrium and right ventricular apex to record monophasic action potentials (MAP) during pacing at cycle length (PCL) of 600 ms and 350 ms in eight patients who underwent electrophysiological study. MAP duration of right atrium (RA-MAPD) and right ventricle (RV-MAPD), effective refractory period of RA and RV (RA-ERP and RV-ERP), intra-atrial conduction time (IACT) and intra-ventricular conduction time (IVCT) were measured before and after intravenous administration of ibutilide (0.01 mg/kg up to 1mg). A conduction time from RA pacing spike to distal coronary sinus potential was used to measure IACT, while QRS duration of surface ECG during RV pacing was used to measure IVCT. Ibutilide prolonged RA-MAPD by 60 ms at PCL 600 ms and by 53 ms at PCL 350 ms; RV-MAPD by 48 ms at PCL 600 ms and by 55 ms at PCL 350 ms. Ibutilide did not affected RA and RV-ERP/MAPD ratio, IACT, and IVCT. Ibutilide prolongs MAPD and ERP of human atrium and ventricle without reverse use-dependency.

Frequency-dependent electrophysiological effects of flecainide, nifekalant and d,l-sotalol on the human atrium.

To compare the effects of class Ic and III antiarrhythmic agents on the termination and prevention of atrial fibrillation, the present study investigated the use-dependent electrophysiological effects of flecainide, nifekalant and d,l-sotalol on the human atrium. Flecainide significantly prolonged effective refractory period (ERP), intra-atrial conduction time (IACT) and monophasic action potential duration (MAPD), and its effects on ERP and IACT were use-dependent. Nifekalalant significantly prolonged ERP and MAPD, and these effects were reverse use-dependent; however, there was no significant change in IACT. d,l-Sotalol significantly prolonged MAPD and the effect was reverse use-dependent. It significantly prolonged ERP, but the effect was not reverse use-dependent. d,l-Sotalol increased IACT in a use-dependent manner. Thus, for atrial fibrillation, class Ic antiarrhythmic agents might be more effective in termination and class III antiarrhythmic agents might be more effective in prevention.

P Wave Dispersion on 12‐Lead Electrocardiography in Patients with Paroxysmal Atrial Fibrillation

The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses have been shown in patients with atrial fibrillation. Recently P wave dispersion (PWD), which is believed to reflect inhomogeneous atrial conduction, has been proposed as being useful for the prediction of paroxysmal atrial fibrillation (PAF). Ninety consecutive patients (46 men, 44 women; aged 55 +/- 13 years) with a history of idiopathic PAF and 70 healthy subjects (42 men, 28 women; mean age 53 +/- 14 years) were studied. The P wave duration was calculated in all 12 leads of the surface ECG. The difference between the maximum and minimum P wave duration was calculated and this difference was defined as P wave dispersion (PWD = Pmax-Pmin). All patients and controls were also evaluated by echocardiography to measure the left atrial diameter and left ventricular ejection fraction (LVEF). There was no difference between patients and controls in gender (P = 0.26), age (P = 0.12), LVEF (66 +/- 4% vs 67 +/- 5%, P = 0.8) and left atrial diameter (36 +/- 4 mm vs 34 +/- 6 mm, P = 0.13). P maximum duration was found to be significantly higher in patients with a history of PAF (116 +/- 17 ms) than controls (101 +/- 11 ms, P < 0.001). P wave dispersion was also significantly higher in patients than in controls (44 +/- 15 ms vs 27 +/- 10 ms, P < 0.001). There was a weak correlation between age and P wave dispersion (r = 0.27, P < 0.001). A P maximum value of 106 ms separated patients with PAF from control subjects with a sensitivity of 83%, a specificity of 72%, and a positive predictive accuracy of 79%. A P wave dispersion value of 36 ms separated patients from control subjects with a sensitivity of 77%, a specificity of 82%, and a positive predictive accuracy of 85%. In conclusion, P maximum duration and P wave dispersion calculated on a standard surface ECG are simple ECG markers that could be used to identify the patients with idiopathic paroxysmal atrial fibrillation.

Electrophysiologic Properties of the Atrium in Patients with Chronic and Paroxysmal Atrial Fibrillation

Background:Atrial fibrillation (AF) causes electrical remodeling of the atrium that plays an important role in increasing atrial vulnerability and the perpetuation of AF. The regional variation and heterogeneities of AFinduced electrical remodeling in patients with AF remain unclear. The purpose of present study was to test the hypothesis that regional heterogeneity of the atrial electrical properties including sinus node dysfunction is more apparent in patients with chronic AF than in patients with paroxysmal AF. Methods:The study group consisted of chronic AF (CAF, n=19), paroxysmal AF (PAF, n=19) and control group (CON, n=13). Monophasic action potential duration 90% (MAPD90) and atrial effective refractory period (AERP) were measured at 9 different sites in the right atrium using MAP catheter. Dispersion of MAPD90 and AERP were calculated from the difference between the maximum and minimum value at 9 sites, respectively. Intra-atrial conduction time (IACT) was calculated from the distance between the earliest activation and the latest one of the electrograms by 20-pole steerable catheter with 2-mm interelectrode distance which was positioned along the tricuspid annulus anterior to the crista terminalis. To evaluate sinus node function, post shock sinus node recovery time (PSRT) was measured. A rate corrected PSRT (PSRTc) was calculated from the difference between PSRT and basic sinus cycle length. Results:MAPD90 significantly shortened in patients with CAF (227.0±32.6 ms) compared with PAF (246.8±38.3 ms, p<0.05) and CON (239.1±39.3 ms, p<0.05), but AERP was not significantly different among 3 groups. The regional changes and dispersion of MAPD90 and AERP in patients with CAF did not differ from those of PAF and CON. IACT was prolonged in CAF group (73.8±22.5 ms) compared with PAF (58.2±8.0 ms, p<0.05) and CON groups (51.6±12.3 ms, p<0.05). IACT in CAF group (73.8±22.5 ms) was significantly prolonged compared with CON groups (51.6±12.3 ms, p<0.05) and was longer than that of PAF groups (58.2±8.0 ms) without statistical significance. PSRTc was longer in CAF group (758.3±525.8 ms) than in PAF group (209.5±125.0 ms, p<0.05). Conclusion: Electrical changes defined as shortened MAPD 90, prolonged IACT and PSRTc were more apparent in 논문접수일:1999년 11월 22일 심사완료일:2000년 2월 17일 교신저자:김영훈, 136-705 서울 성북구 안암동 5가 126-1 고려대학교 의과대학 내과학교실 전화:(02) 920-5445·전송:(02) 927-1478 E-mail:yhkmd@unitel.co.kr

The importance of right atrial pacing electrode position and pacing configuration for intra-atrial and inter-atrial conduction times.

Pace prevention of atrial tachyarrhythmias is based in part on the reduction of intra-atrial (IAA) and/or inter-atrial (IEA) conduction. We previously introduced a novel pacing mode using floating atrial ring electrodes on a VDD-lead (BIdirectional MO nophasic impulSe: BIMOS). The effects of BIMOS pacing on IAA and IEA conduction times has not been studied. In nine Merino sheep electrode catheters were placed at the His-Bundle (HBE), high right atrium (HRA), coronary sinus ostium (Cs-Os), and left lateral atrium (LLA). A VDD-lead was introduced with floating electrodes in the high and mid right atrium (Floating). IAA (S/P-HRA, S/P-Cs-Os, S/P-HBE, S/P-Floating), IEA conduction times (S/P-LLA), and P-wave duration (PD) were measured during sinus rhythm (S), during bipolar cathodal pacing (P) in the HRA, in the Cs-Os position, as well as during BIMOS floating pacing. The mean PD during S was significantly shorter than during HRA- (66. 6+/-12.8ms; vs. 116.2+/-11.1ms; p<0.05) and Cs-Os-P (66.6+/-12.8ms vs. 94.4+/-9.0ms; p<0.05). In comparison to HRA-P, BIMOS configuration lead to a significant reduction of the P-wave duration (116.2+/-11.1ms vs. 85. 4+/-8.8ms; p<0.05). During BIMOS pacing, the global atrial conduction time was significantly shorter than during pacing in the HRA and Cs-Os position. The results of this study demonstrate a clear reduction of IAA and IEA conduction times using BIMOS configurations compared to conventional HRA-P. Furthermore, BIMOS pacing produced a more homogeneous atrial activation when compared with conventional HRA- and Cs-Os-P.

Electrophysiologic characteristics of the atrium in sinus node dysfunction: atrial refractoriness and conduction.

Clinical electrophysiology (EP) has focused attention on the EP properties of atrial muscle in patients with atrial fibrillation (AF). Patients with sinus node dysfunction (SND) sometimes are included in these studies, but the characteristics of these patients with SND alone appear less well investigated. We reviewed EP data of 46 patients (mean age 70 +/- 8 years) with SND, who underwent EP study for evaluation of the atrial substrate. In 16 patients, a history of paroxysmal AF was documented, but not in the remaining 30 patients who had SND alone. We considered as control a group of 25 subjects (mean age 63 +/- 14 years), who were referred to our EP laboratory for unexplained syncope or AV conduction disturbances. Following pharmacologic washout and at a drive cycle of 600 msec, effective (ERP) and functional refractory periods (FRP), S1-A1 and S2-A2 latency, A1 and A2 width, latent vulnerability index (ERP/A2), and P wave duration on the surface ECG were measured. Intra-atrial conduction times were measured from the stimulus artifact by pacing the high right atrium (HRA), to the corresponding atriograms at the AV node (HRA-AVN), low lateral atrium (HRA-LLA), and low interatrial septum close to the coronary sinus ostium (HRA-CSO). Compared with the control group, SND patients did not show differences in ERP (238 +/- 26 msec vs 250 +/- 29 msec), FRP (274 +/- 25 msec vs 280 +/- 32 msec), S1-A1 (38 +/- 15 msec vs 33 +/- 11 msec) and S2-A2 latency (67 +/- 24 msec vs 63 +/- 25 msec), or HRA-AVN (81 +/- 24 msec vs 65 +/- 19 msec), HRA-LLA (36 +/- 30 msec vs 40 +/- 27 msec), and HRA-CSO (77 +/- 17 msec vs 80 +/- 15 msec) conduction times. In contrast, we observed strong differences in atriogram durations A1 (59 +/- 19 msec vs 39 +/- 13 msec; P < 0.001) and A2 (92 +/- 28 msec vs 57 +/- 18 msec; P < 0.001), as well as in the latent vulnerability index ERP/A2 (2.8 +/- 1.2 msec vs 4.8 +/- 1.7; P < 0.001). Also, the P wave was slightly longer (104 +/- 18 msec vs 94 +/- 45 msec; P < 0.05). No significant statistical difference in EP parameters was found between SND patients with or without documented AF. In patients with SND, atrial refractoriness appears similar to that of control subjects. The most important EP abnormality appears to be local conduction slowing disturbances, with prolonged basal and postextrastimuli atriograms, responsible for a lower vulnerability index. This could explain, at least in part, the tendency of patients with SND to develop AF during their natural history. Normality of atrial refractoriness, in contrast to atrial conduction disorders, might explain why atrial pacing shows a preventative effect on the development of AF and why antiarrhythmic drugs often are ineffective.

Conduction disturbances and increased atrial vulnerability in Connexin40-deficient mice analyzed by transesophageal stimulation.

Recently, it has been reported that connexin40 (Cx40) deficiency in targeted mouse mutants is associated with a prolongation of P-wave and QRS complex duration on surface electrograms. The specific effects of Cx40 deficiency on sinus node function, sinoatrial, and atrioventricular conduction properties as well as on atrial vulnerability have not yet been investigated systematically by electrophysiological analysis. Fifty-two mice (18 Cx40(+/+), 15 Cx40(+/-), and 19 Cx40(-/-) mice) were subjected to rapid atrial transesophageal stimulation after anesthesia with avertin. A significant prolongation of sinus node recovery time was noticed in Cx40(-/-) mice compared with Cx40(+/-) and Cx40(+/+) mice (287.8+/-109.0 vs 211.1+/-61.8 vs 204.4+/-60.9 ms; P<0.05). In addition, Wenckebach periodicity occurred at significantly longer atrial pacing cycle lengths in Cx40(-/-) mice than in Cx40(+/-) or Cx40(+/+) mice (93. 3+/-11.8 vs 83.9+/-9.7 vs 82.8+/-8.0 ms, P<0.05). Analysis of 27 Cx40(-/-) mice showed a significant increase in intra-atrial conduction time and atrioventricular conduction time compared with 52 Cx40(+/-) and 31 wild-type (Cx40(+/+)) mice. Furthermore, in Cx40(-/-) mice, atrial tachyarrhythmias could be induced frequently by atrial burst pacing, whereas no atrial arrhythmias were inducible in heterozygous or wild-type mice. This study demonstrates that Cx40 deficiency is associated with sinoatrial, intra-atrial, and atrioventricular conduction disturbances. In atrial myocardium of the mouse, Cx40 deficiency results in increased atrial vulnerability and might contribute to arrhythmogenesis.

Propofol does not affect the canine cardiac conduction system under autonomic blockade.

To determine the effects of propofol on the cardiac conduction system in dogs with pharmacological autonomic blockade. In eight mongrel dogs receiving 6 mg.kg-1.hr-1 propofol and vecuronium under pharmacological autonomic blockade with atropine and propranolol the infusion rates of propofol were increased from 6, (baseline), to 12, 18 and 24 mg.kg-1.hr-1 at 60-min intervals. An electrophysiological study assessed sinus rate, sinus node recovery time, corrected sinus node recovery time, intraatrial conduction time, AV nodal effective refractory period, Wenckebach cycle length and AV conduction times. Electrocardiographical variables and arterial pressures were also measured. All measurements were repeated at 30 min after the beginning of each infusion of propofol. Propofol did not produce direct effects on the electrophysiological or electrocardiographical variables at any infusion rates. Heart rates did not change at higher infusion rates in the presence of decreases in arterial pressures. Propofol did not affect the cardiac conduction system in the presence of autonomic blockade. Thus, the direct cardiac effects of propofol do not play a causative role in the genesis of propofol-associated bradyarrhythmias.

Atrial vulnerability in patients with paroxysmal "lone" atrial fibrillation.

Little is known about the electrophysiological properties of the atrium predisposing to paroxysmal atrial fibrillation (AF), especially in patients without structural heart disease. This study was conducted to analyze intraatrial conduction, atrial refractoriness, and arrhythmia inducibility in patients with lone paroxysmal AF. An electrophysiological study was performed in 24 patients with a documented history of lone paroxysmal AF but in sinus rhythm at the time of the electrophysiological study. Twelve patients without any history of atrial arrhythmias served as controls. The patients with lone paroxysmal AF showed a significant prolonged local conduction time S1A1 (70 +/- 21 ms vs 36 +/- 12 ms, P < 0.0001), a lack of rate adaptation of the functional refractory period (FRP changes/cycle length changes < 10% in 15 of 24 patients with lone paroxysmal AF vs 1/12 controls, P = 0.002) and a higher incidence of inducible AF with only one extrastimulus (13/24 vs 0/12, P = 0.0014). The total P wave duration in the surface ECG (89 +/- 14 ms vs 83 +/- 8 ms, P = 0.15), the intraatrial conduction time (36 +/- 14 ms vs 28 +/- 8 ms, P = 0.07), the presence of a fragmented atrial electrogram (16/24 vs 7/12, P = 0.62), the absolute value of the effective refractory period (204 +/- 28 ms vs 212 +/- 23 ms, P = 0.42), and the vulnerability index (3.0 +/- 1.5 vs 3.6 +/- 1.5, P = 0.26) were not statistically different between the two groups. The presence of a prolonged (> 50 ms) S1A1 and/or the presence of a lack of rate adaptation of the FRP and/or the presence of inducible AF identified patients with spontaneous lone paroxysmal AF with a sensitivity of 96%, a specificity of 67%, a positive predictive value of 85%, and a negative predictive value of 89%. In patients with lone paroxysmal AF, the electrophysiological study using conventional techniques allows not only to detect AF inducibility using a nonaggressive protocol, but also to reveal several electrophysiological abnormalities related to the atrial substrate itself. This atrial vulnerability may explain the high incidence of recurrences in patients with lone paroxysmal AF.

Simple electrocardiographic markers for the prediction of paroxysmal idiopathic atrial fibrillation

Background The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiologic characteristics in patients with paroxysmal atrial fibrillation (PAF). Methods To search for possible electrocardiographic markers that could serve as predictors of idiopathic PAF, we measured the maximum P-wave duration (P maximum) and the difference between the maximum and the minimum P-wave duration (P dispersion) from the 12-lead surface electrocardiogram of 60 patients with a history of idiopathic PAF and 40 age-matched healthy control subjects. Results P maximum and P dispersion were found to be significantly higher in patients with idiopathic PAF than in control subjects. A P maximum value of 110 msec and a P dispersion value of 40 msec separated patients from control subjects, with a sensitivity of 88% and 83% and a specificity of 75% and 85%, respectively. Conclusions P maximum and P dispersion are simple electrocardiographic markers that could be used for the prediction of idiopathic PAF. (Am Heart J 1998;135:733-8.)

Atrial conduction curves in patients with and without atrial fibrillation.

In order to quantify underlying atrial conduction properties in patients with atrial fibrillation (AF) using clinical electrophysiology techniques, atrial conduction curves relating intra-atrial conduction times to extrastimulus prematurities during programmed atrial stimulation were drawn. Based on the presence or absence of AF episodes, 95 subjects were divided into 2 groups: control (n=42); and AF (n=53). During programmed stimulation introduced from the right atrial appendage, an atrial conduction curve was drawn for each patient. For most of the control subjects, when the extrastimulus prematurity was increased by 10-ms steps, the intra-atrial conduction times also increased gradually; the maximum stepwise prolongation in intra-atrial conduction time was 11.0+/-3.4 msec. For patients with AF, a 10-msec increase in extrastimulus prematurity often produced a sudden marked prolongation in the intra-atrial conduction time; the maximum stepwise prolongation of intra-atrial conduction time was 21.4+/-5.9 msec. In contrast to the gradual atrial conduction curves recorded in control subjects, the sudden prolongation of intra-atrial conduction time was remarkable on the curves obtained in patients with AF. Statistical significance was clearly established (p<0.0001). This difference could be related to differences in the underlying conduction properties in patients with and without AF.

Different effects of class Ic and III antiarrhythmic drugs on vagotonic atrial fibrillation in the canine heart.

Effects of class Ic drug pilsicainide and class III drug MS-551 were determined in the canine model of atrial fibrillation (AF) induced under vagal stimulation. Pilsicainide injected intravenously at a dose of 1.0 mg/kg over 3 min terminated AF in six of six dogs. After pilsicainide injection, the effective refractory period (ERP) of the right atrium (RA) increased (104 +/- 22 to 122 +/- 31 ms; p < 0.05), and intraatrial conduction time (CT) increased (24%; p < 0.05) in the RA during vagal stimulation. Wavelength index (WLI; ERP/CT), an estimate of the wavelength for reentry, was decreased slightly but significantly (-2%; p < 0.05) in the RA after pilsicainide. MS-551 injected intravenously at a dose of 0.5 mg/kg over a 3-min period terminated AF in three of eight dogs. An additional dose of 0.5 mg/kg of MS-551 terminated AF in three of the remaining five dogs. After MS-551 injection, ERP increased (100 +/- 30 to 143 +/- 28 ms; p < 0.05), but CT remained unchanged in the RA, and therefore WLI was increased significantly (48%; p < 0.01). Immediately before termination of AF with test drugs, mean AF intervals (FF intervals) increased, whereas the standard deviation of FF intervals did not change significantly. In conclusion, both pilsicainide and MS-551 effectively terminated vagotonic AF after an increase in FF intervals. However, changes in WLI were different between the two test drugs. Vagotonic AF could, therefore, be terminated either by prolongation of ERP or suppression of conduction with antiarrhythmic drugs.

Atrial electrophysiological features in patients with Wolff-Parkinson-White and atrial fibrillation: absence of rate adaptation of intraatrial conduction time parameters.

Clinical electrophysiology has not yet clearly defined atrial features that can predict spontaneous occurrence of atrial fibrillation (AF). The aim of this work was to identify atrial electrophysiological features that can distinguish Wolff-Parkinson-White patients with spontaneous AF from those without this arrhythmia. Sixty-nine patients with Wolff-Parkinson-White were divided into three groups: group I (16 patients) with spontaneous AF; group II (35 patients) with reciprocating tachycardia but not AF; and group III (18 patients) asymptomatic without documented arrhythmias. Atrial effective refractory periods (ERPs) and intraatrial conduction times in response to premature extrastimuli were analyzed. The latter were evaluated as the A1A2 interval minus the correspondent S1S2 interval (A1A2-S1S2), S1A2 and the interval A1A2 following the shortest S1S2 producing atrial activation (FRP'). All the parameters have been evaluated in two atrial sites and at two atrial pacing cycle lengths (600 and 400 ms). For all the parameters, the difference ("gradient") was calculated between the values of the same parameter measured at the atrial pacing cycle length of 600 ms and that found at the atrial pacing cycle length of 400 ms in the same recording site in each patient was calculated. Atrial ERP did not differ significantly in the three groups. Intraatrial conduction parameters, evaluated in the high right atrium (HRA), were longer when measured at an atrial pacing of 400 ms and showed a lack of rate adaptation in patients with spontaneous AF. In group I patients in particular, FRP' became longer with the increase of atrial rate, while in groups 2 and 3, it usually shortened. The mean gradient of HRA FRP' was -15.0 +/- 19 ms in group I as compared to 5.7 +/- 13 ms in group II and 6.4 +/- 13 ms in group III (P < 0.001); sensitivity, specificity, and negative predictive value of a negative gradient in the identification of patients with spontaneous AF, were, respectively, 83%, 75%, and 93%. Patients from groups 2 and 3 did not differ in any of the analyzed parameters. Patients with Wolff-Parkinson-White and spontaneous AF showed prolonged intraatrial conduction times and a different behavior in response to modification of heart rate.