利用Langendorff灌流装置建立一种离体快速心房起搏模型

目的:为排除干预因素对其它脏器的影响,制作一种离体的快速心房起搏模型。方法:新西兰大耳白兔12只,随机分为对照组和起搏组(n=6)。开胸取出心脏后,置于Langendorff灌流装置上用台氏液持续灌流,起搏组在灌流的基础上同时给予500次/分的快速心房刺激。分别以400ms、300ms、200ms为起搏周期(S1)测定各组在灌流0h、1h后的心房有效不应期(AERP)。结果:与灌流前(0h)对比,灌流及起搏1h后,起搏组的AERP400、AERP300、AERP200均明显缩短,而单纯灌流组则差别不大;单纯灌流组的AERP400>AERP300>AERP200,而起搏/灌流组的AERP400、AERP300、AERP200三者间无显著差异。结论:起搏离体Langendorff灌流的心脏能够建立有效的快速心房起搏模型。     

Vagal stimulation promotes atrial electrical remodeling induced by rapid atrial pacing in dogs: evidence of a noncholinergic effect

Background: Atrial electrical remodeling (AER) is one of the mechanisms by which atrial fibrillation (AF) begets AF. It is known that vagal activity increases the propensity for AF. However, vagal effects on AER have not been fully investigated. Methods: Adult mongrel dogs were divided in four groups: group I, rapid atria pacing (RAP); group II, RAP plus vagal nerve stimulation (VNS); group III, RAP and VNS with atropine (0.2 mg/kg/h, intravenous), and group IV, group III plus vasoactive intestinal polypeptide (VIP) antagonist ([D‐p‐Cl‐Phe⁶, Leu¹⁷]‐VIP, 0.125 μg/kg/h). VNS was performed bilaterally through vagosympathetic trunks to achieve second‐degree AV block or sinus rate slowing of >30 beats per minute. Atrial effective refractory periods (AERPs) were determined in the coronary sinus and right atrial appendage every hour at drive cycle lengths (DCLs) 350 ms, 300 ms, and 250 ms. Results: During 5 hours RAP with or without VNS, AERP shortened progressively from baseline at both pacing sites and at all DCLs (P < 0.01). Furthermore, RAP‐induced AERP shortening was more pronounced with VNS (P < 0.01). With atropine, the AERP shortening during VNS was blunted (P < 0.01), but was still significantly more pronounced than that in group I (P < 0.05). However, VNS effect on AERP shortening was eliminated completely with the combination of atropine and VIP antagonist (P = 0.15 vs group I). Conclusion: Increased vagal activity promotes RAP‐induced AER, which could not be totally accounted for by cholinergic effect but could be blocked by the combination of atropine and VIP antagonist. Vagally released VIP may have important role in the vagal promotion of AER. (PACE 2011; 34:1092–1099)     

Slow pathway ablation decreases vulnerability to pacing-induced atrial fibrillation: Possible role of vagal denervation

BACKGROUND: Studies indicate that success of radiofrequency (RF) ablation of atrial fibrillation (AF) may be in part due to vagal denervation. RFAof supraventricular tachycardia (SVT) has been associated with vagal denervation. The effects of slow pathway (SP) ablation on AF inducibility have not been studied. OBJECTIVE: To test the hypothesis that SP ablation renders AF less inducible. Methods: Consecutive patients referred for SVT were studied. After atrioventricular nodal reentrant tachycardia (AVNRT) was confirmed they underwent induction of AF. After SP ablation AF induction was reattempted. Vulnerability to AF was reassessed. RESULTS: Twenty-four patients were enrolled; eight were not inducible for AF in the preablative state. Mean CLof the AVNRT was 340 +/- 16 ms. The average RF ablation time was 131 +/- 42 seconds. Presence of junctional rhythm was required. Of the 16 with inducible AF two patients had AF induced during routine invasive electrophysiology study. None of these had inducible AF after SP ablation. Fourteen of 16 patients required specific AF induction. Ten of these were noninducible after SP ablation; two were inducible after SP ablation but with a more aggressive pacing protocol (P < 0.03 compared to preablation) and two had no change in AF vulnerability. Seven of the eight noninducible patients remained noninducible for AF post SP ablation. In the 12 patients who were inducible prior but noninducible after ablation the mean atrial effective refractory period (AERP) increased for both BCL at 400 and 600 ms (400/216 +/- 8 ms preablation vs 400/248 +/- 12 ms postablation, P < 0.03; 600/228 +/- 8 ms preablation vs 600/259 +/- 6 ms postablation, P < 0.04). There were no significant changes in AERP of patients who remained inducible or who were noninducible before ablation. The average ablation time for patients who became noninducible after ablation was significantly higher than those who had no change in inducibility or remained inducible but at a more aggressive pacing threshold (157 +/- 24 seconds vs 35 +/- 5 seconds; P < 0.005). CONCLUSION: SP ablation acutely decreases vulnerability to pacing-induced AF in patients with AVNRT. This may reflect the effect of ablation on atrial vagal tone.     

Verapamil suppresses the inhomogeneity of electrical remodeling in a canine long-term rapid atrial stimulation model

Verapamil is known to suppress shortening of the atrial effective refractory period (AERP) during relatively short-term atrial pacing, although the effect of a long-term stimulation model is unclear. The effect of verapamil on electrical remodeling was evaluated in a canine rapid atrial stimulation model. The right atrial appendage (RAA) was continuously paced (400 beats/min) for 2 weeks. Four pairs of electrodes were sutured at four atrial sites; the RAA, right atrium close to the inferior vena cava, Bachmann's bundle, and LA. AERP, AERP dispersion (AERPd), conduction time, and inducibility of AF were evaluated during the pacing phase and the recovery phase. The same protocol was performed under the administration of verapamil. In five control dogs, the AERP shortening was inhomogeneous and the shortening of the AERP was most prominent in the LA. AERPd increased during the rapid pacing phase by 5 +/- 2 ms, but recovered quickly in the recovery phase. The max AERPd was 46 +/- 4 ms in the control group and was larger than that in the verapamil group (31 +/- 3 ms, P = 0.001). At the LA site, the shortening of the AERP was decreased by verapamil administration (-19 +/- 3 vs -5 +/- 2 ms, P = 0.04). However, the AF inducibility was not significantly different between the two groups. The effect of verapamil on electrical remodeling was inhomogeneous, depending on the anatomic portion. As a result, AERPd widening during the rapid pacing phase was suppressed by verapamil, while the AF inducibility was unchanged.     

Tachycardia induced electrical remodeling of the atria and the autonomic nervous system in goats

Atrial fibrillation (AF) shortens the atrial effective refractory period (AERP). To investigate the role of the autonomic nervous system during this so-called electrical remodeling of the atria (ERA) and during recovery from ERA we analyzed heart rate variability (HRV). In 12 goats atrioventricular (300:150 beats/min) pacing was performed for 24 hours, interrupted at 4, 8, 16, and 24 hours for recording of 500 atrial (AA) intervals during sinus rhythm and measurement of the AERP(430ms) at 7.4 +/- 0.6 sites. After 24 hours, pacing was stopped and the electrophysiological study and recording of the AA intervals was repeated at 4, 8, 16, and 24 hours after cessation of pacing. Time- and frequency-domain parameters were computed from each 500 AA interval recording. After 24 hours of rapid pacing the AERP had shortened significantly (147 +/- 5.6 to 102+/- 6.4 ms, P < 0.0001). No significant changes in HRV and dispersion of refractoriness (AAERP) (47 +/- 7.1 to 44 +/- 4.2 ms) were observed. After cessation of pacing, the AERP prolonged again (102 +/-6.4 to 135+/-8.8 ms, P < 0.0001) and was paralleled by a significant increase in AAERP (44 +/- 4.2 to 63+/- 7.1 ms, P = 0.01). Furthermore, HRV increased significantly. At each time point an inverse relation between the logarithmically transformed vagal parameter HF (InHF) and AERP was observed. We calculated the mean InHF for each goat using all time points and used the median value to divide the 12 goats into high and low vagal tone groups. We compared the degree of ERA and recovery from ERA for both groups. The AERP shortened 47.4 +/- 6.5 versus 43.0+/-5.0 ms (NS) for goats with high and low vagal tone, respectively. During recovery from ERA the AERP lengthened 23.6 +/- 4.0 versus 42.5 +/- 1.7 ms (P = 0.001) for goats with high and low vagal tone, respectively. Multivariate regression analysis indicated a short AERP as the single independent determinant of the inducibility of AF during ERA and recovery from ERA (P < 0.0001). During recovery from ERA, the AERP prolonged and vagal tone and AAERP increased. A high vagal tone during recovery from ERA was associated with a short AERP and an attenuated recovery of ERA.     

Clinical experience with electroanatomic mapping of ectopic atrial tachycardia

The aim of this study was to evaluate the clinical use of a new three-dimensional mapping system as a guide for catheter ablation of ectopic atrial tachycardia. A series of 42 consecutive patients with drug refractory ectopic atrial tachycardia was studied in a prospective observational trial with the electroanatomic mapping system CARTO. The arrhythmogenic focus was found in the right atrium in 30 patients and in the left atrium in 12 patients. The construction of a complete electroanatomic map of the right or left atrium was possible in 37 of 42 consecutive patients with ectopic atrial tachycardia. Mean activation time of the right atrium, including the proximal coronary sinus, was 94 +/- 25 ms for right atrial tachycardias; left atrial activation time during left atrial tachycardias was 86 +/- 17 ms. Average mapping time was 30 minutes for right atrial tachycardias and 22 minutes for left atrial tachycardias, allowing the collection of 86 +/- 50 and 65 +/- 28 catheter positions, respectively. The size of the area of earliest atrial activation calculated from the electroanatomic map amounted to 0.6 +/- 0.4 cm2 in right atrial tachycardias and 1.0 +/- 0.9 cm2 in left atrial tachycardias. In the right atrium the most common locations of the 33 arrhythmogenic foci in 30 patients were the high or mid-lateral right atrium (n = 10) and the inferoparaseptal region near the coronary sinus ostium (n = 7). Ectopic left atrial foci were most commonly located in an inferior position near the mitral annulus (n = 5) and in proximity to the ostium of the pulmonary veins (n = 4). Biatrial electroanatomic mapping allowed visualization of earliest right atrial activation during left atrial tachycardia at the high interatrial septum or near the coronary sinus ostium. Catheter ablation was successful in 85% of right atrial tachycardias and 82% of left atrial tachycardias. In patients with ectopic atrial tachycardia electroanatomic mapping is a safe and feasible technique that allows three-dimensional visualization of the automatic focus in a precise anatomic reconstruction of the atria. This novel mapping technology facilitates catheter ablation of complex ectopic atrial tachycardia.     

快速心室起搏犬心房颤动模型研究

目的建立快速起搏心室致心力衰竭犬房颤模型,研究其电生理及心房结构和功能改变。方法 15只健康杂种犬分两组:对照组6只,实验组9只[240次/min心室起搏(25±3)d]。超声心动图测定起搏前后心房面积、面积缩小分数及左心室功能,利用心内电极测定心房有效不应期、传导速度及房颤诱发情况。结果实验组7只犬完成了实验。快速心室起搏(25±3)d后,犬的收缩末期和舒张末期左、右心房面积显著增大(与起搏前比较,P<0.01),左、右心房面积缩小分数显著减小(左心房:(35.7±1.9)%和(20.7±2.7)%,P<0.01;右心房:(35.0±2.3)%和(18.0±2.3)%,P<0.01),左室射血分数从(65.3±2.1)%降至(31.6±2.8)%(P<0.01)。实验组犬左、右心房有效不应期显著延长,心房内传导速率较对照组减慢。实验组有5只犬诱发出超过30 min的房颤,平均房颤持续时间较对照组显著延长(687±290)s和(13±9)s,P<0.01)。实验组平均房颤持续时间与左、右心房面积及面积缩小分数相关(P<0.05)。结论 快速心室起搏致心衰模型能稳定地诱发出房颤,房颤持续时间与心衰引起的显著心房结构和功能异常相关。     

Evidence for electrical remodelling of the atrial myocardium in patients with atrial fibrillation. A study using the monophasic action potential recording technique

Experimental studies have shown that remodelling of the atrial myocardium is linked to the occurrence and perpetuation of atrial fibrillation (AF). Clinical evidence, however, is insufficient. We recorded monophasic action potentials (MAP) during AF from one to three sites in the right atrium in seven patients with chronic AF (CAF) and in 11 patients with paroxysmal AF (PAF). The fibrillatory (FF) interval between two consecutive upstrokes of the MAP was measured using a computer-assisted manual method. The mean, median, 15th, 10th, 5th percentile and shortest FF intervals were calculated in each patient and used as estimates of the local atrial effective refractory period (AERP) during AF. In three patients burst pacing at 400 and 500 beats min(-1) was delivered during the MAP recording. In nine patients, the AERP was also tested using the extra stimulus technique during sinus rhythm. RESULTS: Thirty-eight recordings were obtained. The shortest FF interval was significantly shorter in patients with CAF as compared with that in patients with PAF (50+/-13 vs. 72+/-31 ms, P<005). Similar differences were seen in the mean, median, 15th, 10th, and 5th percentile FF interval. The AERP during sinusrhythm was significantly longer than the estimated AERPs (P<0 05 to P<0.01) in the nine patients. There was no significant difference in FF interval before and after the burst pacing in the three patients. CONCLUSION: The AERP was significantly shortened during AF, as compared with that during sinus rhythm, and the AERP shortening was more marked in patients with CAF than in patients with PAF. These clinical findings support the connection between the electrical remodelling and the occurrence and/ or perpetuation of the AF.     

Electrophysiological characteristics of junctional rhythm during ablation of the slow pathway in different types of atrioventricular nodal reentrant tachycardia

BACKGROUND: Junctional rhythm (JR) is commonly observed during radiofrequency (RF) ablation of the slow pathway for atrioventricular (AV) nodal reentrant tachycardia. However, the atrial activation pattern and conduction time from the His-bundle region to the atria recorded during JR in different types of AV nodal reentrant tachycardia have not been fully defined. METHODS: Forty-five patients who underwent RF ablation of the slow pathway for AV nodal reentrant tachycardia were included; 27 patients with slow-fast, 11 patients with slow-intermediate, and 7 patients with fast-slow AV nodal reentrant tachycardia. The atrial activation pattern and HA interval (from the His-bundle potential to the atrial recording of the high right atrial catheter) during AV nodal reentrant tachycardia (HA(SVT)) and JR (HA(JR)) were analyzed. RESULTS: In all patients with slow-fast AV nodal reentrant tachycardia, the atrial activation sequence recorded during JR was similar to that of the retrograde fast pathway, and transient retrograde conduction block during JR was found in 1 (4%) patient. The HA(JR) was significantly shorter than the HA(SVT) (57 +/- 24 vs 68 +/- 21 ms, P < 0.01). In patients with slow-intermediate AV nodal reentrant tachycardia, the atrial activation sequence of the JR was similar to that of the retrograde fast pathway in 5 (45%), and to that of the retrograde intermediate pathway in 6 (55%) patients. Transient retrograde conduction block during JR was noted in 1 (9%) patient. The HA(JR) was also significantly shorter than the HA(SVT) (145 +/- 27 vs 168 +/- 29 ms, P = 0.014). In patients with fast-slow AV nodal reentrant tachycardia, retrograde conduction with block during JR was noted in 7 (100%) patients. The incidence of retrograde conduction block during JR was higher in fast-slow AV nodal reentrant tachycardia than slow-fast (7/7 vs 1/11, P < 0.01) and slow-intermediate AV nodal reentrant tachycardia (7/7 vs 1/27, P < 0.01). CONCLUSIONS: In patients with slow-fast and slow-intermediate AV nodal reentrant tachycardia, the JR during ablation of the slow pathway conducted to the atria through the fast or intermediate pathway. In patients with fast-slow AV nodal reentrant tachycardia, there was no retrograde conduction during JR. These findings suggested there were different characteristics of the JR during slow-pathway ablation of different types of AV nodal reentrant tachycardia.     

Atrial refractoriness and action potential duration after sudden reversal of atrioventricular sequence

To address the potential of atrioventricular (AV) asynchrony to provoke cardiac arrhythmias, atrial electrophysiology was examined during normal and reversed AV interval in anesthetized pigs. A new automatic stimulation technique was adapted to monitor rapid changes in the effective refractory period (ERP), using continuous AV sequential pacing, incremental extrastimulus interval scanning, and automatic detection of capture. Right atrial ERP using 2-8 ms stimulus interval increments and right atrial and ventricular monophasic action potential (MAP) duration were determined simultaneously when the AV interval was changed from normal (+80 ms) to reversed (-40 ms) and back. During reversed AV interval the peak right atrial pressure increased from 8 +/- 3 to 14 +/- 4 mmHg (P < 0.001) and mean arterial pressure decreased from 86 +/- 18 to 65 +/- 21 mmHg (P < 0.001). At new steady state, atrial ERP and MAP duration at 90% level of repolarization were lengthened by 22 +/- 16 and 42 +/- 12 ms respectively (P < 0.001). Ventricular MAP duration did not change. A statistically significant lengthening in atrial ERP could be demonstrated in 5-10 seconds. After reversion of the AV sequence, the ratio of atrial ERP to MAP duration decreased from 1.27 to 0.94 (P < 0.001) on average for 15 seconds, the change being thought to favor reentry. Thus atrial wall stress from contraction during ventricular systole even for a short period of time modifies atrial electrophysiology. Deficient AV synchrony may immediately contribute to the development of atrial arrhythmias.     

Effect of Different Pacing Protocols on the Induction of Atrial Fibrillation in a Transvenously Paced Sheep Model

In different animal models rapid atrial stimulation led to a shortening and maladaptation to rate of the atrial effective refractory period (AERP). This atrial electrical remodeling resulted in an increased vulnerability to atrial fibrillation (AF). These experimental findings formed the rationale for a stringent pursuit of sinus rhythm in patients with AF, since this would prevent or reverse atrial remodeling. This study tested the hypothesis that a reduction of arrhythmia burden would lead to a decreased vulnerability for AF. Different rapid atrial pacing protocols in a sheep model were used. During 15 weeks, 13 animals were continuously rapid paced and 7 animals were intermittently burst-paced, resulting in rapid atrial activation during 100% versus 33 +/- 4% of the time, respectively. In the continuously paced group, 77% of the animals developed sustained AF (i.e., > 1 hour) versus only 29% in the burst-paced group (P < 0.05). However, there was no difference in mean AERP shortening over time, nor maximal AERP shortening per animal, between both protocols. Minimal AERP was 103 +/- 5 ms in the continuously paced group and 107 +/- 5 in the burst-paced group (P = NS). Significant changes could be identified in effect on P wave duration, AVN function, and atrial dilation. Conduction slowing was more pronounced in the continuously paced group with a maximal P wave duration of 136 +/- 4 ms in this group versus 116 +/- 5 in the burst-paced group (P < 0.05). In the continuously paced group, the right atrial area significantly increased from 2.5 +/- 0.1 cm2 at baseline to 4.2 +/- 0.2 cm2. In the burst-paced group there was no significant atrial dilatation (from 2.6 +/- 0.1 to 2.8 +/- 0.1 cm2). In conclusion, limiting atrial arrhythmia burden slowed the development of sustained AF in this sheep model. This was not mediated by a decreased influence on atrial refractoriness but seemed to be dependent on smaller changes in atrial conduction and dimensions.     

Characteristic P wave morphology in patients undergoing the atrial compartment operation for chronic atrial fibrillation with mitral valve disease

The P wave in the surface ECG represents atrial electrical activation and may be altered in certain pathological conditions. Atrial compartment operation has been used to convert chronic AF to sinus rhythm. However, this procedure may result in changes of impulse conduction in various atrial compartments and alters the P wave morphology. This study sought to elucidate the P wave changes after the atrial compartment operation for AF. Fifteen patients undergoing the atrial compartment operation for chronic AF were studied. In the operation, the atrium was divided into three compartments, namely the left atrium, the atrial septum including sinus and AV nodes, and the right atrial compartment. The anatomic connection between adjacent compartments were preserved at the posterior lower margin of incisions. The surface lead P waves were correlated with intracardiac recording and stimulation in various atrial compartments. Fifteen age- and sex-matched control patients without structural heart diseases were compared. The results showed that patients undergoing the atrial compartment operation had a prolonged P wave duration (190 +/- 27 v s95 +/- 14 ms, P < 0.001), a prolonged PR interval (207 +/- 23 vs 155 +/- 20 ms, P < 0.001), and a shortened PR segment (17 +/- 19 vs 60 +/- 17 ms, P < 0.001). The increase in P wave duration was primarily due to a conduction delay from the sinus node to the other atrial compartments as the conduction time from the high right atrium to the right atrial appendage was 132 +/- 57 ms(vs 21 +/- 6 ms for control,P < 0.001), and the conduction time from the high right atrium to the distal coronary sinus was 140 +/- 55 ms(vs 70 +/- 15 ms, P < 0.001). However, the conduction from the high right atrium to the low septal right atrium, which were located in the same compartment, was not impaired. Also, the conduction in the AV node and His-Purkinje system were not impaired. The mean axis of P waves varied greatly, but was not statistically different from that of the control group (60 +/- 48 degrees vs 52 +/- 18 degrees,P > 0.05). Although the patients undergoing atrial compartment operation had a larger left atrial size, their P wave amplitude was smaller (1.0 +/- 0.3 vs 1.3 +/- 0.3 mm, P < 0.01), and an increased negative terminal force in V1 was not seen (0.02 +/- 0.02 vs 0.02 +/- 0.01 mm/s, P > 0.05). Alteration in P wave morphology was seen in 14 patients. All the P waves showed a biphasic configuration with an initial positive and a terminal slurred negative deflection in leads II, III, and aVF. The terminal components represented the activation of right atrial appendage in 5 patients, the left atrium in 1, and the combined activation of right atrial appendage and the left atrium in 8 patients. The P wave morphology suggested that activation of both the right atrial appendage and the left atrial compartments proceeded in a caudocranial direction as a result of the atrial incisions. In conclusion, atrial compartment operation altered the conduction time and direction in the atria and resulted in characteristic P wave changes.     

Effects of sex and age on electrocardiographic and cardiac electrophysiological properties in adults

Although differences in patient sex in heart rate and QT interval have been well characterized, sexual differences in other cardiac electrophysiological properties have not been well defined. The study population consisted of 354 consecutive patients without structural heart disease or preexcitation who underwent clinically indicated electrophysiological testing in the drug-free state. Atrial, AV nodal, and ventricular effective refractory periods (AERP, AVNERP, VERP) were determined at a pacing cycle length of 500 ms using an 8-beat drive train and 3-second intertrain pause. There were 124 men and 230 women with a mean age of 45 +/- 19 and 47 +/- 18 years, respectively. The sinus cycle length (SCL) was longer in men than in women (864 +/- 186 and 824 +/- 172 ms, respectively, P < 0.05). The QRS duration was significantly longer in men (90 +/- 12 ms) than women (86 +/- 13 ms) (P < 0.005). The HV interval was 48 +/- 9 ms in men and 45 +/- 8 ms in women (P < 0.05). The sinus node recovery time (SNRT) was significantly longer in men than in women (1215 +/- 297 ms and 1135 +/- 214 ms, respectively, P < 0.05). AERP and VERP were similar in both sexes. Aging did not influence sexual differences in cardiac electrophysiological properties, although, it independently prolonged the SCL, PR, and QT intervals, AH and HV intervals, SNRT, AVNERP, and the AV Wenckebach cycle length. The SCL, QRS duration, HV interval, and SNRT were significantly longer in men than in women. Aging prolonged cardiac conduction and increased the SCL but the effects were similar in both sexes. AERP and VERP were unaffected by aging or sex.     

Alcohol intake is significantly associated with atrial flutter in patients under 60 years of age and a shorter right atrial effective refractory period

Background: Although evidence suggests that alcohol is associated with atrial fibrillation (AF), the association between alcohol and atrial flutter (AFL) has not been examined. The mechanism connecting alcohol and atrial arrhythmias is unknown.
Methods: Alcohol intake was determined in 195 consecutive patients with AF and AFL. Control subjects included patients with other supraventricular arrhythmias (n = 132) and healthy subjects (n = 54). Because of important competing risk factors for atrial arrhythmias in the elderly, stratification by age was performed. In a subset, atrial effective refractory periods (AERPs) were obtained from the high right atrium and proximal and distal coronary sinus.
Results: AF and AFL patients were significantly more likely to be daily alcohol drinkers (27% vs 14% of controls, P = 0.001). In multivariable analysis, AFL patients ≤ 60 years of age were significantly more likely to be daily drinkers than to drink no alcohol compared to controls (odds ratio 17, 95% confidence interval 1.6–192.0, P = 0.019). Progressively more frequent alcohol intake was significantly associated with a progressively greater odds of AFL in patients ≤ 60 years of age (P = 0.045). Neither AF subjects of any age nor AFL subjects > 60 years of age exhibited significant associations with alcohol after multivariable adjustment. Right AERPs shortened significantly with increasing amounts of alcohol intake (P = 0.025), whereas left AERPs were not associated with alcohol intake.
Conclusions: Alcohol intake is positively associated with AFL in younger patients. The mechanism may be related to a shortening of the right AERP.     

Atrial Septal Pacing to Synchronize Atrial Depolarization in Patients with Delayed Interatrial Conduction

The current method of pacing the right atrium from the appendage or free wall is often the source of delayed intraatrial conduction and discoordinate left and right atrial mechanical function. Simultaneous activation of both atria with pacing techniques involving multisite and multilead systems is associated with suppression of supraventricular tachyarrhythmias and improved hemodynamics. In the present study we tested the hypothesis that pacing from a single site of the atrial septum can synchronize atrial depolarization. Five males and two females (mean age 58 ± 6 years) with drug refractory paroxysmal atrial fibrillation (AF) were studied who were candidates for AV junctional ablation. All patients had broad P waves (118 ± 10 ms) on the surface ECG. Multipolar catheters were inserted and the electrograms from the high right atrium (HRA) and proximal, middle, and distal coronary sinus (CS) were recorded. The atrial septum was paced from multiple sites. The site of atrial septum where the timing between HRA and distal CS (d-CS) was ≤ 10 ms was considered the most suitable for simultaneous atrial activation. An active fixation atrial lead was positioned at this site and a standard lead was placed in the ventricle. The interatrial conduction time during sinus rhythm and AAT pacing and the conduction time from the pacing site to the HRA and d-CS during septal pacing were measured. Atrial septal pacing was successful in all patients at sites superior to the CS os near the fossa ovalis. During septal pacing the P waves were inverted in the inferior leads with shortened duration from 118 ± 10 ms to 93 ± 7 ms (P < 0.001), and the conduction time from the pacing site to the HRA and d-CS was 54.3 ± 6.8 ms and 52.8 ± 2.5 ms, respectively. The interatrial conduction time during AAT pacing was shortened in comparison to sinus rhythm (115 ± 18.9 ms vs 97.8 ± 10.3 ms, P < 0.05). In conclusion, simultaneous activation of both atria in patients with prolonged interatrial conduction time can be accomplished by pacing a single site in the atrial septum using a standard active fixation lead placed under electrophysiological study guidance. Such a pacing system allows proper left AV timing and may prove efficacious in preventing various supraventricular tachyarrhythmias.     

Atrioventricular Nodal Conduction and Refractoriness Following Abrupt Changes in Cycle Length

The properties of the atrioventricular (AV) nodal conduction and effective refractory period in man are generally evaluated at a constant basic cycle length (CL) and, in most cases, they demonstrate an inverse relationship to the drive cycle. The response of AV node to abrupt change in CL is less defined. We therefore studied the effects of abrupt changes in CL on AV nodal conduction time and refractoriness in 18 patients. AV nodal conduction time, and effective and functional refractory periods were measured during: (1) a constant long CL, (2) a constant short CL, and (3) after an abrupt increase in CL just prior to the introduction of extrastimuli. In 10 of the 18 patients a constant long CL of 600 ms, a constant short CL of 400 ms and a sudden short-to-long change in CL (400 to 600 ms) were tested. AV nodal conduction times (A2H2) were measured at the shortest and longest comparable A1A2 intervals. The mean value of the shortest A2H2 intervals for constant CL of 600 ms was 144 +/- 18 ms; for a constant CL of 400 ms it was 162 +/- 17 ms; after a sudden short-to-long change in CL (400 to 600 ms) it was 142 +/- 14 ms. The mean value of the longest A2H2 intervals at a constant CL of 600 ms was 185 +/- 18 ms; at a constant CL of 400 ms it was 236 +/- 26 ms (p less than 0.01) and after a short-to-long change in CL (400 to 600 ms) 199 +/- 21 ms. AV nodal effective refractory periods measured at the same three CLs had mean values of 279 +/- 13 ms; 300 +/- 15 ms and 294 +/- 13 ms, respectively. Similar results were obtained when other CLs such as 700 to 900, 500 to 900, and 400 to 700 ms were tested. The data suggest that after abrupt short-to-long changes in CL, AV nodal function curves shift from long constant CL toward short constant CL as the coupling intervals decrease, indicating a cumulative pattern. Although the return to baseline conduction time after the fast basic rate is known to be slow, the limitation of this effect to the very early premature beat in the human has not been reported previously.     

Hemodynamically optimized temporary cardiac pacing after surgery for congenital heart defects

Disturbance of normal AV synchrony and dyssynchronous ventricular contraction may be deleterious in patients with otherwise compromised hemodynamics. This study evaluated the effect of hemodynamically optimized temporary dual chamber pacing in patients after surgery for congenital heart disease. Pacing was performed in 23 children aged 5 days to 7.7 years (median 7.3 months) with various postoperative dysrhythmias, low cardiac output, and/or high inotropic support and optimized to achieve the highest systolic and mean arterial pressures. The following four pacing modes were used: (1) AV synchronous or AV sequential pacing with individually optimized AV delay in 11 patients with first- to third-degree AV block; (2) AV sequential pacing using transesophageal atrial pacing in combination with a temporary DDD pacemaker for atrial tracking and ventricular pacing in three patients with third-degree AV block and junctional ectopic tachycardia, respectively, who had poor signal and exit block on atrial epicardial pacing wires; (3) R wave synchronized atrial pacing in eight patients with junctional ectopic tachycardia and impaired antegrade AV conduction precluding the use of atrial overdrive pacing; (4) Atrio-biventricular sequential pacing in two patients. Pressures measured during optimized pacing were compared to baseline values at underlying rhythm (13 patients with first-degree AV block or junctional ectopic tachycardia) or during pacing modes commonly used in the given clinical situation: AAI pacing (1 patient with slow junctional rhythm and first-degree AV block during atrial pacing), VVI pacing (2 patients with third-degree AV block and exit block and poor sensing on epicardial atrial pacing wires) and dual-chamber pacing with AV delays set to 100 ms (atrial tracking) or 150 ms (AV sequential pacing) in 7 patients with second- to third-degree AV block and functional atrial pacing wires. Optimized pacing led to a significant increase in arterial systolic (mean) pressure from 71.5 +/- 12.5 (52.3 +/- 9.0) to 80.5 +/- 12.2 (59.7 +/- 9.1) mmHg (P < 0.001 for both) and a decrease in central venous (left atrial) pressure from 12.3 +/- 3.4 (10.5 +/- 3.2) to 11.0 +/- 3.0 (9.2 +/- 2.7) mmHg (P < 0.001 and < 0.005, respectively). In conclusion, several techniques of individually optimized temporary dual chamber pacing leading to optimal AV synchrony and/or synchronous ventricular contraction were successfully used to improve hemodynamics in patients with heart failure and selected dysrhythmias after congenital heart surgery.     

Effects of An Acute Increase in Atrial Pressure on Atrial Refractoriness in Humans

Contraction-excitation feedback has been studied extensively in mammalian ventricles. In contrast, little is known about contraction-excitation feedback in mammalian atria. The objective of this study was to investigate the effect of acute alterations in atrial pressure, induced by varying the atrioventricular (AV) interval, on atrial refractoriness. Twenty patients without structural heart disease participated in the study. In each patient the atrial effective (ERP) and absolute refractory periods (ARP) were measured during AV pacing at a cycle length of 500 msec and an AV interval of 120 msec. Acute increases in atrial pressure were induced by pacing the atrium and ventricle simultaneously for the final two beats of the drive train. The ERP was defined as the longest extrastimulus coupling interval that failed to capture with an extrastimulus current strength of twice the stimulation threshold. The ARP was defined in a similar manner with an extrastimulus current strength of 10 mA. The ERP and ARP were determined using the incremental extrastimulus technique. A subset of patients had the pacing protocol performed during autonomic blockade. As the AV interval of the final two beats of the drive train was shortened from 120 msec to 0 msec, the peak right atrial pressure increased from 7 ± 3 mmHg to 15 ± 5 mmHg (P < 0.001). The increase in atrial pressure associated with simultaneous pacing of the atrium and ventricle resulted in shortening of the atrial ERP and ARP by 7.3 ± 5.2 and 6.2 ± 3.5 msec, respectively (P < 0.0011). Similar results were obtained during autonomic blockade. These findings confirm the presence of contraction-excitation feedback in normal human atria.     

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

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

Atrial and Ventricular Vulnerability in a Patient with the Wolff-Parkinson-White Syndrome

An electrophysiologic study was carried out in a patient with the Wolff-Parkinson-White syndrome and a history of spontaneous atrial fibrillation but with no evidence of organic cardiac disease. A single induced premature ventricular depolarization resulted in ventricular tachycardia followed by ventricular fibrillation. Similarly, atrial pacing or premature atrial stimulation resulted in frequent episodes of atrial fibrillation or flutter, The atrial and ventricular effective refractory periods were 180 ms and < 160 ms, respectively, at a driven cycle length of 480 ms. Intravenous administration of procainamide resulted in lengthening of the refractory periods and failure to induce either atriaJ or ventricular arrhythmias with pacing. In most patients with enhanced atrioventricular nodal or accessory atrioventricular nodal bypass, the mechanism of ventricular tachycardia is related to an inordinately rapid ventricular response during supraventricular arrhythmias. In our patient, a unique mechanism was apparent: atrial and ventricular vulnerability to fibrillation was associated with extremely short myocardial effective refractory periods. The relationship of this finding to sudden cardiac death bears further study.