Detection of atrial late potentials with P wave signal averaged electrocardiogram among patients with paroxysmal atrial fibrillation

The analysis of the QRS-complex with signal averaged ECG (SAECG) has been evaluated for patients affected by ventricular tachycardia for a long time. A longer filtered QRS-complex was a marker of a slower ventricular conduction velocity and reentry tachycardia. This method was modified for an analysis of the P wave (P-SAECG). Different filter methods were evaluated for the analysis of atrial late potentials. METHOD: We measured the bidirectional P wave signal averaged ECG of 45 consecutive patients with (group A) and without (group B) paroxysmal atrial fibrillation (PAF) and 15 young volunteers without a cardiac disease (group C). RESULTS: As a result patients with PAF had a significantly lower root mean square voltage of the last 20 ms (RMS 20) (2.59 +/- 0.89) vs 4.08 +/- 1.45 microV, p < 0.0003) and a significantly longer filtered P wave duration (FPD) than patients of the control collective (139.2 +/- 17.5 vs 115.1 +/- 17.7 ms, p < 0.0001) and the young volunteers (3.44 +/- 0.95 microV, p < 0.0001/101.9 +/- 14.2 ms, p < 0.009). Furthermore we found an age-dependent relationship of FPD between group B and C (115.1 +/- 17.7 vs 101.9 +/- 14.2 ms, p < 0.05) but not an age-dependent relationship of the RMS 20 (4.08 +/- 1.45 vs 3.44 +/- 0.95 microV, p = n.s.). A specificity of 80% and a sensitivity of 78% was achieved for identifying patients with atrial fibrillation by using a definition of atrial late potentials as FPD > 120 ms and a RMS 20 < 3.5 microV. CONCLUSIONS: The analysis of the P-SAECG can be used as a non-invasive method for identifying atrial late potentials. Atrial late potentials might be a reason for PAF. The predictive power of atrial late potentials has to be examined by prospective investigations of a larger patient population.     

Electrophysiologic characteristics in initiation of paroxysmal atrial fibrillation from a focal area

OBJECTIVES: We investigated the electrophysiologic characteristics in the initiation of paroxysmal atrial fibrillation (PAF) from a focal area. BACKGROUND: The electrophysiologic characteristics in the initiation of PAF are still not clear. METHODS: The study group consisted of 77 patients (M/F = 65/12, age 66 +/- 12 years) with frequent episodes of PAF; we analyzed: 1) 15 cycle lengths of electrical activity before the onset of atrial fibrillation (AF); 2) coupling interval (CI) of the first ectopic beat just before the initiation of AF; and 3) the prematurity of an ectopic beat (prematurity index [PI] = CI/mean of preceding 15 cycle lengths). RESULTS: A total of 111 episodes of sustained AF were identified. Two patterns of AF initiation were observed: group I (59/111, 53%) included the episodes preceded by cycle length oscillation, and group II (52/111, 47%) included the episodes initiated by a single ectopic beat with preceding cycle length relatively constant. The PI of group I episodes was significantly greater than that of group II (0.41 +/- 0.12 vs. 0.34 +/- 0.10, p < 0.01). The CI (267 +/- 54 ms vs. 217 +/- 55 ms, p < 0.05), AF1 (194 +/- 36 ms vs. 153 +/- 37 ms, p < 0.05) and PI (0.49 +/- 0.13 vs. 0.37 +/- 0.11, p < 0.01) of the AF episodes from the superior vena cava (SVC) were significantly longer and greater than those of AF episodes from pulmonary veins (PVs). CONCLUSIONS: In patients with PAF originating from PVs or the SVC, two major initiating patterns were found. Moreover, the electrophysiologic characteristics in the initiation of AF originating from the SVC were also different from those of AF initiating from the PVs.     

Inducibility of atrial fibrillation during electrophysiologic evaluation is associated with increased dispersion of atrial refractoriness

The impact of atrial dispersion of refractoriness (Disp_A) in the inducibility and maintenance of atrial fibrillation (AF) has not been fully resolved. AIM: To study the Disp_A and the vulnerability (A_Vuln) for the induction of self-limited (<60 s) and sustained episodes of AF. METHODS AND RESULTS: Forty-seven patients with paroxysmal AF (PAF): 29 patients without structural heart disease and 18 with hypertensive heart disease. Atrial effective refractory period (ERP) was assessed at five sites--right atrial appendage and low lateral right atrium, high interatrial septum, proximal and distal coronary sinus. We compared three groups: group A - AF not inducible (n=13); group B - AF inducible, self-limited (n=18); group C - AF inducible, sustained (n=16). Age, lone AF, hypertension, left atrial and left ventricular (LV) dimensions, LV systolic function, duration of AF history, atrial flutter/tachycardia, previous antiarrhythmics, and Disp_A were analysed with logistic regression to determine association with A_Vuln for AF inducibility. The ERP at different sites showed no differences among the groups. Group A had a lower Disp_A compared to group B (47+/-20 ms vs 82+/-65 ms; p=0.002), and when compared to group C (47+/-20 ms vs 80+/-55 ms; p=0.008). There was no significant difference in Disp_A between groups B and C. By means of multivariate regression analysis, the only predictor of A_Vuln was Disp_A (p=0.04). Conclusion: In patients with PAF, increased Disp_A represents an electrophysiological marker of A_Vuln. Inducibility of both self-limited and sustained episodes of AF is associated with similar values of Disp_A. These findings suggest that the maintenance of AF is influenced by additional factors.     

Electrocardiographic signal-averaging during atrial pacing and effect of cycle length on the terminal QRS in patients with and without inducible ventricular tachycardia

Electrocardiographic signal-averaging during sinus rhythm (61 to 99 beats/min) and atrial pacing (100 to 171 beats/min) were performed to determine the effect of heart rate on late potentials in 15 patients without (group 1) and 7 patients with (group 2) inducible sustained ventricular tachycardia (VT). In sinus rhythm (79 +/- 12 vs 77 +/- 12 beats/min, difference not significant), the duration of the low-amplitude signal less than 40 microV was longer in group 2 than group 1 (43 +/- 21 vs 26 +/- 8 ms, p = 0.034) and more patients had late potentials (57 vs 7%, p = 0.021), but QRS duration (121 +/- 32 vs 98 +/- 19 ms) and terminal voltage (33 +/- 33 vs 50 +/- 26 ms) were not significantly different. With atrial pacing in group 1 (128 +/- 16 beats/min), 3 patients developed a simultaneous decrease in terminal voltage and an increase in terminal QRS duration consistent with a late potential, but mean total and terminal durations were unchanged. Terminal voltage increased (50 +/- 26 to 59 +/- 40) but not significantly. With atrial pacing in group 2 (119 +/- 12 beats/min) all patients either had a late potential or developed a simultaneous decrease in terminal voltage and an increase in terminal QRS duration (p = 0.001 vs group 1). Root mean square (p = 0.001 vs group 1). Root mean square voltage decreased (33 +/- 23 to 22 +/- 23) and became significantly different from group 1 (p = 0.017). Mean QRS duration, root mean square terminal voltage and low-amplitude terminal QRS duration, however, were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

P wave signal averaged ECG and chemoreflexsensitivity in paroxysmal atrial fibrillation

Detailed analysis of the QRS-complex and autonomic dysfunction can identify patients at risk to suffer from ventricular arrhythmias. To determine whether patients at risk for paroxysmal atrial fibrillation (PAF) could be identified while in sinus rhythm, a P wave triggered signal averaged ECG and an analysis of the autonomic function by chemoreflexsensitivity (CHRS) were examined. The ratio between the difference of RR intervals in the ECG and the venous partial pressure of oxygen before and after 5-min oxygen inhalation was measured for the determination of CHRS. We examined 224 patients (group A) who suffered from PAF, 250 patients (group B) without arrhythmic history and 30 young volunteers (group C). The filtered P wave duration (FPD) was significantly longer in group A than in group B (140.9+/-21.0 vs. 118.2+/-9.4 ms, p<0.0001) or C (105.2+/-14.1 ms, p<0.0001) while the root mean square voltage of the last 20 ms of the P wave (RMS 20) was significantly lower in group A than in group B (2.68+/-1.12 vs. 4.06+/-1.57 microV, p<0.0001) or C (3.97+/-1.36 microV, p<0.0001). Atrial late potentials (ALP) were defined as a FPD>120 ms and a RMS 20< or =3.5 microV. ALP could identify patients of group A with a specificity of 78% and a sensitivity of 83%. Patients with PAF (2.32+/-1.15 ms/mm Hg) showed a significantly lower CHRS than group B (4.14+/-1.58 ms/mm Hg, p<0.0001) or group C (4.98+/-1.51 ms/mm Hg, p<0.0001). The sensitivity for the presence of atrial fibrillation was 71% for a CHRS below 3.0 ms/mm Hg with a specificity of 70%. A combination of both methods showed a specificity of 85% and a sensitivity of 65% when ALP and pathological CHRS were present. The results of our study suggest that risk of atrial fibrillation could be detected by P wave signal averaged ECG and CHRS. An analysis of CHRS seems to be an appropriate method to demonstrate a neurovegetative imbalance, which might be one possible trigger mechanism.     

New observations on atrial fibrillation before and after surgical treatment in patients with the Wolff-Parkinson-White syndrome.

The records of 342 patients who received surgical treatment for the Wolff-Parkinson-White syndrome between 1968 and 1986 were reviewed to evaluate the characteristics of atrial fibrillation. The patients were classified into two groups according to the presence (n = 166) or absence (n = 176) of documented episodes of atrial fibrillation preoperatively. The mean follow-up duration was 6 years (range 2 to 20). As compared with reports based on smaller patient groups and shorter follow-up, the study revealed several new findings. 1) During follow-up, nine patients in the atrial fibrillation group developed recurrent atrial fibrillation after a successful operation; five of these nine patients did not have associated heart disease. 2) All three patients with a history of atrial fibrillation and an accessory pathway conducting in the anterograde direction only had a successful surgical procedure and no postoperative atrial fibrillation. 3) The cycle length of atrioventricular (AV) reciprocating tachycardia was significantly shorter in the atrial fibrillation group (304 +/- 42 ms, mean +/- SD) than in the no-atrial fibrillation group (321 +/- 54 ms, p less than 0.005), and the cycle length of AV reciprocating tachycardia that degenerated into atrial fibrillation (289 +/- 26 ms) was shorter than that for the AV reciprocating tachycardia without subsequent atrial fibrillation (316 +/- 51 ms, p less than 0.005). 4) Sustained atrial fibrillation was induced in 30% of patients without a history of atrial fibrillation. 5) Atrial fibrillation occurred in four patients with an accessory pathway that conducted only in the retrograde direction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Activation patterns in experimental canine atrial flutter produced by right atrial crush injury.

OBJECTIVES. This study was designed to localize and characterize the atrial flutter reentrant circuit and the electrophysiologic effects of right atrial crush injury in a new canine model. BACKGROUND. In previous studies sustained atrial flutter was induced in the canine heart by rapid atrial pacing after a linear crush injury was placed in the right atrial free wall. METHODS. Eight dogs (group 1) with three electrode plaques on the right and left atria and Bachmann's bundle and seven dogs (group 2) with a single high density electrode plaque on the right atrium were studied with use of a 64-channel computerized mapping system. RESULTS. At baseline, during sinus rhythm and right and left atrial pacing, activation spread uniformly without areas of slow conduction. Crush injury produced marked conduction delay or complete block during sinus rhythm, increasing the mean difference in activation times across the injury compared with control values (group 1, 31 +/- 4 vs. 14 +/- 5 ms, p less than 0.01; group 2, 28 +/- 10 vs. 7 +/- 2 ms, p less than 0.01). Rapid atrial pacing (S1S1 200 ms) above and below the crush injury revealed a line of complete block across which adjacent electrodes recorded markedly different activation times (33 +/- 5 and 38 +/- 12 ms difference, respectively) and around which activation wave fronts proceeded, colliding opposite the stimulating electrodes. The mean atrial flutter cycle length of 11 episodes induced in group 1 and 14 episodes in group 2 was 157 +/- 16 and 140 +/- 16 ms, respectively (p = NS). Activation mapping revealed a reentrant circuit in the right atrium around the crush injury in all episodes. Although the reentrant circuit did not contain a discrete area of slow conduction, activation time below was longer than that above the crush injury (92 +/- 14 vs. 66 +/- 8 ms and 82 +/- 12 vs. 59 +/- 9 ms in groups 1 and 2, respectively, p less than 0.01 for both). Rapid atrial pacing or premature stimuli produced progressive conduction delay and unidirectional block between the crush injury and the tricuspid anulus, inducing atrial flutter directly in 9 of 25 episodes. In 16 episodes, atrial flutter developed after transient induction of atrial fibrillation. CONCLUSIONS. 1) Atrial flutter in this model is due to reentry in the right atrium; 2) the crush injury functions as an anatomic obstacle around which reentry may occur; and 3) the reentrant circuit does not contain a discrete area of slow conduction but, rather, generally slower conduction below the crush injury.     

Mode of onset of atrial fibrillation in the Wolff-Parkinson-White syndrome: how important is the accessory pathway?

The mode of onset of 103 episodes of atrial fibrillation lasting greater than or equal to 30 s was studied in 79 patients with the Wolff-Parkinson-White syndrome during electrophysiologic study. No patient had organic heart disease, and 31 had clinical atrial fibrillation before study. These 79 patients were then compared with a control group of 53 patients with Wolff-Parkinson-White syndrome in whom atrial fibrillation could not be induced. Ninety-five of the 103 episodes were technically suitable for analysis. Atrial fibrillation invariably began with rapid atrial tachycardia that became progressively disorganized within 10 to 20 cycles. It was initiated during right atrial stimulation (n = 52), right ventricular stimulation (n = 8), reciprocating tachycardia (n = 33) and spontaneously (n = 2). Most episodes started at a high right atrial site regardless of accessory pathway location, with only 19% of episodes starting at the electrode closest to the accessory pathway. During reciprocating tachycardia (n = 33), either atrial (n = 8) or ventricular (n = 5) extrastimuli initiated atrial fibrillation. Atrial fibrillation started at the accessory pathway site in 6 of 20 episodes occurring spontaneously during reciprocating tachycardia. Patients with atrial fibrillation had a longer PA interval (54 +/- 14 versus 42 +/- 12 ms, p less than 0.0001), shorter atrial functional refractory period (226 +/- 38 versus 240 +/- 30 ms, p = 0.049) and shorter anterograde effective refractory period of the accessory pathway (279 +/- 26 versus 304 +/- 75 ms, p = 0.03). Clinical reciprocating tachycardia was documented with equal frequency in both the atrial fibrillation and control groups (59.5% versus 52.9%, p = 0.58).(ABSTRACT TRUNCATED AT 250 WORDS)     

Pre-excited RR intervals during atrial fibrillation in the Wolff-Parkinson-White syndrome: influence of the atrioventricular node refractory period

The ventricular rate and percent of pre-excited QRS complexes during atrial fibrillation were compared in two groups of patients with the Wolff-Parkinson-White syndrome. Group A consisted of 22 patients whose anterograde effective refractory period of the accessory pathway was longer than that of the atrioventricular (AV) node. Group B consisted of 23 patients in whom this relation was reversed. No patient had organic heart disease. Both groups had a similar effective refractory period of the accessory pathway (288 +/- 37 vs. 280 +/- 26 ms), whereas that of the AV node was shorter in group A than group B (242 +/- 25 vs. 285 +/- 27 ms, p = 0.0001). Patients in group A had a lower percent of pre-excited QRS complexes during atrial fibrillation (39 +/- 43% vs. 93 +/- 20%, p = 0.0001). In the 21 patients whose refractory period was measured, the difference was plotted against the percent of pre-excited QRS complexes; there was a significant correlation between the two (r = -0.83, p less than 0.001). In patients in whom pre-excited RR intervals were present, the pre-excited RR intervals were compared between the two groups. Both groups had similar effective refractory periods of the accessory pathway (265 +/- 22 vs. 280 +/- 27 ms) and ventricle (200 +/- 17 vs. 211 +/- 26 ms). The effective refractory period of the AV node was shorter in group A (248 +/- 22 vs. 285 +/- 28 ms, p = 0.0005). The shortest pre-excited RR interval did not show any difference (244 +/- 37 vs. 265 +/- 41 ms). However, both the average (328 +/- 39 vs. 397 +/- 56 ms, p = 0.001) and longest (495 +/- 109 vs. 666 +/- 205 ms, p = 0.02) pre-excited RR intervals were shorter in group A.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transesophageal atrial pacing: a first-choice technique in atrial flutter therapy

Here we report on a study of 181 episodes of spontaneous atrial flutter (AF) (mean atrial cycle length 250 +/- 32 msec) treated by transesophageal atrial pacing (TAP) in 138 patients (92 men and 46 women; mean age 59.5 +/- 12.6 years). TAP was effective in 163 episodes (90%); sinus rhythm resumption was immediate in 36 (19.9%) and followed a short period of atrial fibrillation in 64 (35.3%); in 63 episodes (34.8%) a stable atrial fibrillation was obtained. TAP was unsuccessful in 18 cases (10%). All the patients tolerated the procedure well. A statistical elaboration with the Fisher exact test did not evidence a correlation between efficacy and age, sex, atrial cycle length, or underlying heart disease but showed a significant correlation between efficacy and AF duration of less than 1 day (p less than 0.05) and absence of antiarrhythmic pharmacologic pretreatment (p less than 0.01). These data strongly support the immediate first-choice use of TAP in AF therapy.     

Efficacy of a dual chamber defibrillator with atrial antitachycardia functions in treating spontaneous atrial tachyarrhythmias in patients with life-threatening ventricular tachyarrhythmias.

BACKGROUND: Atrial fibrillation has a high incidence in patients wearing an implantable cardioverter defibrillator for ventricular tachyarrhythmias and may lead to palpitations, heart failure, angina, stroke and inappropriate defibrillator discharge. The aim of the study was to evaluate the efficacy of a dual chamber defibrillator with atrial antitachycardia functions in treating spontaneous atrial tachyarrhythmias. METHODS: One hundred and twelve patients, 88 male, mean age 64+/-11 years, were enrolled. Seventy-six had ischaemic heart disease, 21 idiopathic dilated cardiomyopathy, nine other heart diseases, six no structural heart disease. The mean left ventricular ejection fraction was 40+/-11%. Sixty-two had prior atrial tachyarrhythmias. RESULTS: Follow-up lasted 11+/-9 months (range 1-42). Among 933 ventricular tachyarrhythmia episodes, 100% of ventricular fibrillation and 92% of ventricular tachycardia were successfully cardioverted. Among 414 detected sustained atrial tachyarrhythmias, 195 were classified as atrial tachycardia (47.1%), 192 as atrial fibrillation (46.4%) and 27 (6.5%) as sinus rhythm. The detection-positive predictive value was 93.5%. Therapy success rates: antitachy pacing on atrial tachycardia = 71.3% (crude estimate); 66.1% (adjusted estimate); 50 Hertz on atrial fibrillation=36.2% (crude estimate); 13.5% (adjusted estimate); atrial shock on atrial fibrillation = 62.5% (mean energy 7.8+/-14.1J). Shock efficacy was 32% when delivered energy was < or = 2 atrial defibrillation threshold at implant and 92% when >2. Duration of successfully treated atrial episodes was significantly lower than that of unsuccessfully treated (6+/-26 min vs 42+/-60). CONCLUSIONS: Atrial antitachy pacing and shock therapies demonstrated very high efficacy in treating atrial tachyarrhythmias in defibrillator patients.     

Electrophysiological determinants of atrial fibrillation in sinus node dysfunction despite atrial pacing.

AIMS: The effectiveness of atrial pacing in reducing the incidence of atrial fibrillation in patients with sinus node dysfunction is incomplete, and the correlation between electrophysiological atrial properties and the effect of permanent atrial pacing has been poorly investigated. Accordingly, the aim of the present study was to correlate electrophysiological data, in terms of atrial refractoriness, conduction parameters, and propensity to atrial fibrillation induction, and the likelihood of atrial fibrillation after DDD device implantation. METHODS AND RESULTS: The authors reviewed electrophysiological data of 41 patients with sinus node dysfunction (mean age 70 +/- 8 years, who were investigated free of anti-arrhythmic treatments before pacemaker implantation. At a drive cycle length of 600 ms, effective and functional refractory periods, S1-A1 and S2-A2 latency, A1 and A2 width, and latent vulnerability index (effective refractory period [ERP] A2), were measured. Atrial fibrillation induction was tested with up to three extrastimuli in 34 patients. Induction of sustained atrial fibrillation (> 1 min) was considered as the end-point. P-wave duration on the surface ECG in lead II/V1 was also measured. Minimal atrial rate was programmed between 60 and 75 bpm (mean: 64 +/- 4 bpm). After implantation, the patients were followed-up for 28 +/- 17 months, and ECG-documented occurrence of atrial fibrillation was determined. Electrophysiological characteristics of patients with (n = 12) or without (n = 29) paroxysmal atrial fibrillation before implantation were similar. When comparing patients with (n = 11) or without (n = 30) post-pacing atrial fibrillation occurrence, no differences were found in age, underlying heart disease, left atrial size, minimal pacing rate, and follow-up duration. Additionally, between the two former groups, there was no significant difference in terms of effective refractory periods (233 +/- 47 ms vs 239 +/- 25 ms), functional refractory periods (280 +/- 48 ms vs 272 +/- 21 ms), S1-A1 (44 +/- 20 ms vs 37 +/- 13 ms) and S2-A2 latency (77 +/- 28 ms vs 66 +/- 22 ms), and A1 duration (60 +/- 23 ms vs 53 +/- 16 ms). In contrast, in patients with post-pacing atrial fibrillation occurrence, the P wave was more prolonged (116 +/- 22 ms vs 98 +/- 13 ms; P < 0.01), A2 was longer (116 +/- 41 ms vs 87 +/- 27 ms; P < 0.01), effective refractory periods/A2 was lower (2.1 +/- 0.4 cm vs 3.1 +/- 1.4 cm; P < 0.05), and rate of atrial fibrillation induction was higher (8/11 patients vs 8/23 patients; P < 0.05). Electrophysiological characteristics of patients free of post-pacing atrial fibrillation with associated (n = 6) or unassociated (n = 24) paroxysmal atrial fibrillation history before implantation were quite similar. In patients with post-pacing atrial fibrillation with associated (n = 6) or unassociated atrial fibrillation history (n = 5) before implantation, effective refractory periods was statistically different (207 +/- 23 ms vs 264 +/- 46 ms; P < 0.05). Values of effective refractory periods < 220 ms were significantly more frequent in patients with post-pacing atrial fibrillation than in patients without (4/11 patients vs 2/30 patients; P < 0.05). When comparing patients with post-pacing atrial fibrillation with effective refractory periods > or = 220 ms (n = 7) and < 220 ms (n = 4), A2 duration was remarkably prolonged (145 +/- 42 ms vs 90 +/- 11 ms; P < 0.05) in those with effective refractory periods > or = 220 ms. By contrast, between the two groups, effective refractory periods/A2 were identical (2.08 +/- 0.6 cm vs 2.15 +/- 0.3 cm; P = n.s.). CONCLUSION: Prolonged atrial refractoriness, lesser degrees of conduction disturbance and a lower rate of atrial fibrillation induction seem to be predictive of stable sinus rhythm. In contrast, patients with persistence of atrial fibrillation despite pacing have a more abnormal and inhomogeneous atrial substrate, as well as a higher rate of atrial fibrillation induction. Prolonged P wave, shortened refractoriness, or remarkably abnormal conduction disturbances in the presence of prolonged refractoriness limit the effectiveness of standard atrial pacing in atrial fibrillation prevention. Identification of predictive criteria of failure of single-site atrial pacing may be used to consider dual-site atrial pacing in such patients with sinus node dysfunction.     

Electrophysiologic studies in atrial fibrillation. Slow conduction of premature impulses: a possible manifestation of the background for reentry

Extrastimulus-induced intraatrial conduction delays were measured in 12 patients with documented episodes of atrial fibrillation (AF) by recording atrial electrograms at the high right atrium, His bundle region, and coronary sinus. Seventeen patients with and without heart disease, but without atrial arrhythmias served as the control group. During baseline-paced atrial rhythms, a conduction delay zone could be delineated, near the atrial effective refractory period, during which all extrastimuli produced conduction delays. When compared at the same paced cycle lengths (500 to 650 ms), the patients with AF had shorter atrial effective refractory periods (mean +/- standard deviation 206 +/- 24.1 versus 233 +/- 28.2 in control patients, p less than 0.02), wider conduction delay zones (79 +/- 21.7 ms versus 52 +/- 21 in control patients, p less than 0.01), and longer conduction delays both to the His bundle region (64 +/- 18.3 ms versus 35 +/- 21.7 in control patients, p less than 0.005) and the coronary sinus (76 +/- 18.9 ms versus 35 +/- 16.1 in control patients, p less than 0.001). Repetitive atrial responses were recorded in 6 patients with AF and in 9 control subjects. Sinus nodal function abnormalities were detected in 6 of the patients with fibrillation. Patients with AF had a higher tendency than control subjects to develop slow intraatrial conduction, as well as shorter effective refractory periods. Since both features would favor reentry, they may be the electrophysiologic manifestations of the abnormalities making these patients prone to atrial reentrant arrhythmias. Repetitive atrial responses were of no predictive value. Sinus nodal dysfunction was frequently found, but was not essential for the occurrence of AF.     

Usefulness of handgrip to improve ibutilide efficacy in organizing atrial electrical activity during atrial fibrillation

We analyzed the effect of handgrip on atrial electrical activity during atrial fibrillation (AF) by recording right and left atrial activity in 15 patients with persistent AF under baseline conditions and after saline and ibutilide infusions. The handgrip test for 15 seconds, which was always associated with a significant increase in mean atrial cycle length, was recorded in both atria (right atrium: saline vs saline + handgrip 141 +/- 29 vs 171 +/- 24 ms, p <0.001; ibutilide vs ibutilide + handgrip: 197 +/- 43 vs 221 +/- 39 ms, p <0.005). Handgrip favorably modifies atrial electrophysiologic properties during AF.     

The signal-averaged P-wave duration is longer in hypertensive patients with history of paroxysmal atrial fibrillation as compared to those without

BACKGROUND: Onset of atrial fibrillation in hypertensive patients is usually associated with a high occurrence of cardiovascular complications. Therefore, it is important to assess non-invasively the risk of developing paroxysmal atrial fibrillation (PAF) in hypertensive patients during sinus rhythm. This study was undertaken to determine if hypertensive patients with history of PAF could be identified while in sinus rhythm by measurement of signal-averaged ECG P-wave duration. METHODS: Signal-averaged electrocardiography (SAECG) P-wave recording was performed in 44 hypertensive patients (30 men and 14 women; mean age 60+/-11 years, group A) who had a history of paroxysmal AF and in 50 hypertensive patients without history of AF (33 men and 17 women; mean age 57+/-12, group B). All patients were also evaluated by using echocardiography to measure left ventricular ejection fraction (LVEF) and left atrial diameter (LAD). RESULTS: SAECG P-wave duration was found to be significantly higher in group A than in group B (146+/-14 ms vs. 128+/-11 ms, p<0.001). Left atrial diameter was not significantly different (40.1+/-3.4 mm vs. 39.3+/-3.0 mm, p>0.05), whereas LVEF was significantly lower in group A than group B (63+/-5% vs. 67+/-4%, p=0.03). There was a correlation between SAECG P-wave duration and age (r=0.32, p<0.05). In univariate analysis, SAECG P-wave duration and LVEF were significant predictors of PAF, but only SAECG P-wave duration remained a significant independent predictor of PAF in multivariate analysis. CONCLUSION: The results of this study indicate that hypertensive patients with history of PAF can be detected while in sinus rhythm by signal-averaged ECG P-wave duration.     

Chemoreflexsensitivity among patients with paroxysmal atrial fibrillation

Atrial fibrillation is the most common cardiac arrhythmia with typical complications of thromboembolisms. The autonomic nervous system is an important factor for the initiation of arrhythmias. A vagally or adrenergically hyperfunction could cause the initiation of paroxysmal atrial fibrillation (PAF). METHOD: We measured the chemoreflexsensitivity (CHRS) among 110 patients to determine a disturbed autonomic function as risk factor for PAF. We examined 45 patients with PAF (group A), 45 patients with sinus rhythm (group B) and 20 young volunteers (group C). The ratio between the difference of RR intervals in ECG and venous pO(2) was measured for the determination of CHRS. The margin of the CHRS was 3 ms/mmHg. RESULTS: Patients of group A had a significantly lower CHRS compared to group B (1.56+/-1.46 vs 6.29+/-3.71 ms/mmHg, p<0.0008) or group C (1.56+/-1.46 vs 6.35+/-4.29 ms/ mmHg, p<0.0003). A significant difference between group B and C could not be observed (6.29+/-3.71 vs. 6.35+/-4.29 ms/mmHg, p = n.s.). A specificity of 74% and a sensitivity of 71% was achieved for identifying patients with PAF by using a margin of 3 ms/mmHg for the CHRS. CONCLUSIONS: An analysis of CHRS seems to be an appropriate method to demonstrate a neurovegetative imbalance which might be one possible trigger mechanism of PAF. The predictive power has to be examined by prospective investigations of a larger patient population.     

Effect of experimentally induced atrial fibrillation on coronary circulation in dogs

The influence of atrial fibrillation on coronary circulation was studied in 21 anesthetized open-chest dogs. Atrial fibrillation was induced either by local application of acetylcholine (10% in normal saline) on the left atrial appendage or by electric stimulation (2-7 volts, 2 ms, 50 Hz). When atrial fibrillation was induced (n = 10), mean aortic pressure fell and heart rate rose significantly; coronary blood flow (CBF) remained unchanged (78 +/- 6 vs. 75 +/- 5 ml/min X 100 g) while coronary vascular resistance (CVR) (1.16 +/- 0.05 vs. 0.87 +/- 0.07 [m Hg X min X 100 gl/ml [RU], p less than 0.0001) and sinus oxygen saturation (26 +/- 2 vs. 22 +/- 1%, p less than 0.05) decreased. Following the application of carbochromen (5 mg/kg in 3 min i.v.) resulting in maximal coronary dilatation, atrial fibrillation resulted in a reduction in CBF (311 +/- 48 vs. 205 +/- 30 ml/min X 100 g, p less than 0.01) and coronary sinus oxygen saturation (65 +/- 6 vs. 42 +/- 6%, p less than 0.01), while CVR (0.27 +/- 0.03 vs. 0.37 +/- 0.04 RU, p less than 0.0001) was 38 +/- 8% (p less than 0.0005) higher during atrial fibrillation than at sinus rhythm. When hearts were paced to a rate which was identical to the average heart rate at atrial fibrillation (n = 11), CBF (92 vs. 125 +/- 14 ml/min X 100 g, p less than 0.001) and sinus oxygen saturation (24 +/- 2 vs. 30 +/- 2%, p less than 0.0025) were higher and CVR (1.16 +/- 0.11 vs. 0.97 +/- 0.10 RU, p less than 0.0005) lower than during atrial fibrillation; during maximal coronary dilatation by carbochromen, pacing also resulted in a higher CBF (233 +/- 24 vs. 168 +/- 16 ml/min X 100 g, p less than 0.0005) and sinus oxygen saturation (70 +/- 3 vs. 57 +/- 2%, p less than 0.0005), while CVR (0.25 +/- 0.02 vs. 0.46 +/- 0.02 RU, p less than 0.0005) was lower than during atrial fibrillation. Thus atrial fibrillation results in a decrease in coronary vascular resistance but an increase in coronary oxygen extraction. When heart rate is controlled, the vasoconstrictor effect of atrial fibrillation becomes unmasked. Coronary vasoconstriction during atrial fibrillation appears to be greater during maximal coronary dilatation than during control.     

Characteristics of frequency content of atrial signal-averaged electrocardiograms during sinus rhythm in patients with paroxysmal atrial fibrillation.

To clarify the characteristics of the frequency content of atrial signal-averaged electrocardiograms (ECGs) during sinus rhythm in patients with paroxysmal atrial fibrillation, P wave-triggered signal-averaged ECGs were recorded in 28 patients with and 34 control patients without paroxysmal atrial fibrillation. Fast Fourier transform analysis was performed on the 100-ms segment starting 75 ms before the end of the P wave. An area ratio (AR50) was calculated by dividing the area under the spectrum curve between 20 and 50 Hz, multiplied by 100, by the area between 0 and 20 Hz. Magnitude ratios (MR20, MR30, MR40 and MR50) were calculated by dividing the magnitude at 20, 30, 40 and 50 Hz, respectively, multiplied by 100, by the maximal magnitude of the entire signal. AR50 was significantly greater in patients with than without paroxysmal atrial fibrillation (62.3 +/- 34.2 vs. 42.4 +/- 18.4). MR20 and MR30 were also significantly greater in patients with than without paroxysmal atrial fibrillation (MR20 76.1 +/- 15.2 vs. 60 +/- 20.2; MR30 41 +/- 18.8 vs. 26.6 +/- 14.4), although no significant differences in MR40 or MR50 were observed between the two patient groups. The difference in MR30 between groups remained significant even after taking into account the presence of organic heart disease. It is concluded that, irrespective of the presence of organic heart disease, the terminal portion of the P wave contained significantly more components in the 20- to 50-Hz range, especially around 30 Hz, in patients with than in patients without paroxysmal atrial fibrillation. These results suggest that frequency analysis could characterize atrial signal-averaged ECGs of patients at risk for paroxysmal atrial fibrillation.     

Termination of acute atrial fibrillation in the Wolff-Parkinson-White syndrome by procainamide and propafenone: importance of atrial fibrillatory cycle length

The effects of intravenous procainamide (n = 30) or propafenone (n = 25) were evaluated in 55 patients with acute atrial fibrillation and the Wolff-Parkinson-White syndrome. All patients received either procainamide (12 to 15 mg/kg body weight) or propafenone (1 to 2 mg/kg) during sustained (greater than 10 min) atrial fibrillation or after termination of nonsustained atrial fibrillation. Termination of atrial fibrillation was attributed to a drug if it occurred less than or equal to 15 min after infusion. Measurements included mean cycle length of fibrillatory electrograms (mean AA interval) as measured at the high right atrium and shortest RR interval between pre-excited cycles during atrial fibrillation. Atrial fibrillation terminated more frequently after procainamide administration (65%) than after propafenone (46%), although this difference was not significant. Procainamide prolonged the shortest pre-excited RR interval (228 +/- 41 to 339 +/- 23 ms, p = 0.0001) as did propafenone (215 +/- 40 to 415 +/- 198 ms, p = 0.0001) and the magnitude of increase was greater for propafenone (p = 0.048). Patients with sustained atrial fibrillation had shorter mean AA intervals than did their counterparts with nonsustained atrial fibrillation (123 +/- 25 versus 186 +/- 35 ms, p = 0.0001). Termination of sustained atrial fibrillation by either drug was accompanied by prolongation of the mean AA interval but not necessarily by the shortest pre-excited RR interval. Termination of atrial fibrillation was heralded by a 68% increase in the mean AA interval after procainamide administration compared with a 30% increase when the arrhythmia persisted. For propafenone the increases were 90% and 68%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intravenous sotalol decreases transthoracic cardioversion energy requirement for chronic atrial fibrillation in humans: assessment of the electrophysiological effects by biatrial basket electrodes

OBJECTIVES: This study was undertaken to assess the effects of sotalol on the transthoracic cardioversion energy requirement for chronic atrial fibrillation (AF) and on the atrial electrograms during AF recorded by two basket electrodes. BACKGROUND: The effects of sotalol infusion on transthoracic electrical cardioversion for chronic atrial fibrillation in humans have not been well investigated. METHODS: We included 18 patients with persistent AF for more than three months. Atrial electrograms were recorded by two basket electrodes positioned in each atrium respectively. Transthoracic cardioversion was performed before and after sotalol 1.5 mg/kg i.v. infusion. RESULTS: In the 14 patients whose AF could be terminated by cardioversion before sotalol infusion, the atrial defibrillation energy was significantly reduced after sotalol infusion (236 +/- 74 jules [J] vs. 186 +/- 77 J; p < 0.01). Atrial fibrillation was refractory to cardioversion in four patients at baseline and was converted to sinus rhythm by cardioversion after sotalol infusion in two of them. We further divided the patients into two groups. Group A consisted of 10 patients in whom the energy requirement was decreased by sotalol while group B consisted of eight patients in whom the energy requirement was not decreased. The mean A-A (atrial local electrogram) intervals during AF were significantly increased after sotalol infusion in both groups, but the increment of A-A interval was significantly larger in group A than it was in group B patients (36 +/- 13 ms vs. 22 +/- 8 ms for the right atrium; 19 +/- 7 ms vs. 9 +/- 7 ms for the left atrium; both p < 0.05). The spatial and temporal dispersions of A-A intervals were not significantly changed after sotalol infusion in both atria in both groups. CONCLUSIONS: Sotalol decreases the atrial defibrillation energy requirement by increasing atrial refractoriness but not by decreasing the dispersion of refractoriness.