Interatrial Conduction in Patients Undergoing AV Stimulation: Effects of Increasing Right Atrial Stimulation Rate

To evaluate the frequency of spontaneous or rate dependent interatrial blocks, the interatrial conduction time (IACT) was studied on 100 consecutive patients (mean age 78.3 ±7.8 years) during a transvenous dual chamber pacemaker implant. The spontaneous interatrial conduction time (SIACT) was measured from the intrinsic deflection (ID) of the unipolar right atrial signal to the ID of the left atrial signal recorded in a bipoiar way by an esophageal lead. The paced interatrial conduction time (PIACT) was measured from the stimulus artifact to the left atrial ID, when the atrium was paced at a slightly higher rate than the spontaneous rate and during incremental atrial pacing. From these measurements, the maximum increase ofPIACT (MIPIACT) was deduced. In this elderly population, the PIACT was similar (117 ± 26.9 msec) to the data in the literature. However, there were large interindividual variations that were also found in SIACT. We found a close correlation between SIACT and PIACT (P < 0.0001). PIACT was on average 50 msec longer than SIACT. SIACT increased with age (P < 0.03). The MIPIACT was 15.3 ± 15.2 msec. In the majority of patients, the MIPIACT was > 10 msec, and even reached 90 msec in one patient. MIPIACT was longer in patients with a PIACT exceeding 110 msec (P < 0.004). Based on IACT alone, the AV interval must be lengthened on average by 50 msec when changing from atrial tracking-ventricular pacing to atrial pacing-ventricular pacing, but large individual differences must be kept in mind. Elderly people should probably have a longer AV delay.     

Atrial Septal Pacing: A Method for Pacing Both Atria Simuhaneously

By pacing both atria simultaneously, one could reliably predict and optimize left-sided AV timing without concern for IACT. With synchronous depolarization of the atria, reentrant arrhythmias might be suppressed. We studied four male patients (73 ± 3 years) with paroxysmal atrial fibrillation and symptomatic bradyarrhythmias using TEE and fluoroscopy as guides; a standard active fixation screw-in lead (Medtronic model #4058) was attached to the interatrial septum and a standard tined lead was placed in the ventricle. The generators were Medtronic model 7960. The baseline ECG was compared to the paced ECG and the conduction time were measured to the high right atrium, distal coronary sinus and atrial septum in normal sinus rhytbm, atrial septal pacing, and AAT pacing. On the surface ECG, no acceleration or delay in A V conduction was noted during AAI pacing from the interatrial septum as compared with normal sinus rhythm. The mean interatrial conduction time for all 4 patients was 106 ± 2 ms; the interatrial conduction time measured during AAT pacing utilizing the atrial septal pacing lead was 97 ± 4 ms (P = NS). During atrial septal pacing, the mean conduction time to the high right atrium was 53 ± 2 ms. The mean conduction time to the lateral left atrium during atrial septal pacing, was likewise 53 ± 2 ms. We conclude that it is possible to pace both atria simultaneously from a single site using a standard active fixation lead guided by TEE and fluoroscopy. Such a pacing system allows accurate timing of the left-sided AV delay.     

The Importance of the Left Atrioventricular Interval during Atrioventricular Sequential Pacing

During atrioventricular (AV) sequential pacing from the right heart, the interval between the left atrium and ventricle may vary from the programmed AV interval depending on the position of the atrial and ventricular electrodes and interatrial and interventricular conduction. The aim of this study was to determine the hemodynamic effects of altering the left AV interval while keeping the programmed AV interval constant. Four male and 17 female patients, aged 49 ± 15 years were studied. The left AV interval was measured by a catheter in the coronary sinus. Stroke volume and mitral flow were measured by simultaneous echo Doppler during AV sequential pacing from the right atrial appendage and right ventricular apex at programmed AV intervals of 100. 60, and 6 ms. The atrial catheter was then positioned on the atrial septum and the measurements repeated. With the atrial catheter in the right atrial appendage, interatrial activation time (118 ± 20 ms) was similar to interventricular activation time (125 ± 21 ms) and the left AV interval was almost identical to the programmed right AV interval. There was a significant correlation between interatrial and interventricular activation times (r = 0.8; P < 0.001). Positioning the atrial electrode on the septum decreased interatrial activation time by 39 ± 12 ms and increased the left AV interval by a similar amount. At a programmed AV interval of 60 ms, the left AV interval increased from 67 ± 15 ms to 105 ± 17 ms after the atrial catheter was repositioned from the appendage to the septum (P < 0.001). Compared to pacing from the right atrial appendage, atrial septal pacing increased mitral A wave velocity integral (2.8 ± 1.4 vs 4.4 ±1.7 cm at a programmed AV interval of 60 ms, P < 0.01), decreased E wave velocity integral (8.1 ± 2.2 vs 6.1 ± 2.4 cm, P < 0.001) but did not alter stroke volume (44.8 ± 10.6 vs 44.9 ± 10.1 mL). In contrast, a 40 ms decrease in the programmed right AV interval from 100 to 60 ms decreased stroke volume from 48.0 ± 10.0 to 44.9 ± 10.2 mL (P < 0.001). There was a strong relationship between interatrial and interventricular conduction so that patients with prolonged interatrial conduction still had equivalent left and right AV intervals during atrioventricular sequential pacing from the right atrial appendage and right ventricular apex. Positioning the atrial electrode on the septum decreases interatrial activation time and increases the left AV interval by about 40 ms but has minimal hemodynamic effect in patients without heart failure.     

Interatrial conduction correlates with optimal atrioventricular timing in cardiac resynchronization therapy devices

Background: Echocardiographic optimization of the atrioventricular delay (AV) may result in improvement in cardiac resynchronization therapy (CRT) outcome. Optimal AV has been shown to correlate with interatrial conduction time (IACT) during right atrial pacing. This study aimed to prospectively validate the correlation at different paced heart rates and examine it during sinus rhythm (Sinus). Methods: An electrophysiology catheter was placed in the coronary sinus (CS) during CRT implant (n = 33). IACT was measured during Sinus and atrial pacing at 5 beats per minute (bpm) and 20 bpm above the sinus rate as the interval from atrial sensing or pacing to the beginning of the left atrial activation in the CS electrogram. P‐wave duration (PWd) was measured from 12‐lead surface electrocardiogram, and the interval from the right atrial to intrinsic right ventricular activation (RA‐RV) was measured from device electrograms. Within 3 weeks after the implant patients underwent echocardiographic optimization of the sensed and paced AVs by the mitral inflow method. Results: Optimal sensed and paced AVs were 129 ± 19 ms and 175 ± 24 ms, respectively, and correlated with IACT during Sinus (R = 0.76, P < 0.0001) and atrial pacing (R = 0.75, P < 0.0001), respectively. They also moderately correlated with PWd (R = 0.60, P = 0.0003 during Sinus and R = 0.66, P < 0.0001 during atrial pacing) and RA‐RV interval (R = 0.47, P = 0.009 during Sinus and R = 0.66, P < 0.0001 during atrial pacing). The electrical intervals were prolonged by the increased atrial pacing rate. Conclusion: IACT is a critical determinant of the optimal AV for CRT programming. Heart rate‐dependent AV shortening may not be appropriate for CRT patients during atrial pacing. (PACE 2011; 34:443–449)     

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.     

Interatrial Conduction During Cardiac Pacing

DDD pacemakers sense and pace right-sided cardiac chambers. The relationship of atrial to ventricular systole on the left side of the heart is of importance for systemic hemodynamics. Effective atrioventricular synchrony is partially determined by interatrial conduction time (IACT). At the time of DDD pacemaker implantation, interatrial conduction was measured using an intraesophageal pill electrode in 25 patients who were on no cardiac medications. Mean interatrial conduction time for all patients prolonged from 95 ± 18 ms during sinus rhythm to 122 ± 30 ms during right atrial pacing (p < 0.001). In 16 patients with P wave duration < 110 ms interatrial conduction prolonged from 85 ± 10 ms during sinus rhythm to 111 ± 9 ms during right atrial pacing (p < 0.01) compared to 114 ± 20 ms prolonging to 111 ± 19 ms (p < 0.01] in 9 patients with P wave duration > 110 ms. In each patient, while atrioventricular conduction prolonged with incremental right atrial pacing, interatrial conduction times did not vary. Interatrial conduction prolongs from baseline during atrial pacing and remains constant at all paced rates from 60–160 heats per minute. In addition to longer interatrial conduction times during sinus rhythm, patients with electrocardiographic P wave prolongation have longer interatrial conduction times during right atrial pacing than do normals (p < 0.0001). Based on interatrial conduction times alone, the AV interval during DDD cardiac pacing should be approximately 25 ms longer during AV pacing as compared to atrial tracking.     

The effect of the atrial pacing site on the total atrial activation time

The effect of dual site pacing for prevention of atrial fibrillation may be due to synchronization of right and left atrial activation. Little is known, however, about the effect of pacing from single right atrial sites on differences in interatrial conduction. Twenty-eight patients without structural heart disease were studied following radiofrequency catheter ablation of supraventricular arrhythmias. Pacing was performed using standard multipolar catheters from the presumed insertion site of Bachmann's bundle, the coronary sinus ostium, the high lateral right atrium, and the right atrial appendage (n = 8 patients). Bipolar recording was performed from the distal coronary sinus, the high and low lateral right atrium, and the posterolateral left atrium (n = 13 patients). The longest conduction time from each pacing to each recording site was considered the total atrial activation time for the respective pacing site. During high right atrial pacing, the total atrial activation time was determined by the conduction to the distal coronary sinus (118 +/- 18 ms), during coronary sinus ostium pacing by the conduction to the high right atrium (94 +/- 18 ms), and during Bachmann's bundle pacing by the conduction to the distal coronary sinus (74 +/- 18 ms). The total atrial activation time was significantly shorter during pacing from Bachmann's bundle, as compared to pacing from other right atrial sites. Thus, in normal atria, pacing from the insertion of Bachmann's bundle causes a shorter total atrial activation time and less interatrial conduction delay, as compared to pacing from other right atrial sites. These findings may have implications for alternative pacing sites for prevention of atrial fibrillation.     

Nonphysiological Left Heart AV Intervals as a Result of DDD and AAI "Physiological" Pacing

DDD and AAI pacemakers are considered physiological, since they preserve atrioventricular (AV) synchrony. Artificial pacing, however, is performed largely from right heart chambers, causing aberrant depolarization pathways. Pacing at the right atrial appendage (RAP) is known to delay left atrial contraction due to interatrial conduction time (IACT), and right ventricular (RV) apical pacing (RVP) delays left ventricular (LV) contraction due to interventricular conduction time (TVCT). These delays may render the left heart AV intervals (LAV) either too short or too Jong, thus affecting LV systolic function. The purpose of this study was to evaluate the actual LAV intervals during conventional, right heart AAI and DDD pacing. Resulting LAV intervals were compared to programmed AV values during all DDD pacing modalities. Ten patients with DDD and six patients with AAI pacemakers were studied. IACT was measured from the atrial spike to the onset of left P wave, as recorded by an esophageal lead. Systolic time intervals were measured using either a carotid pulse tracing or a densitogram (photoplethysmography). LV function was appraised by measuring rate-corrected LV ejection time (LVETc). IVCT was measured indirectly as the lengthening of LV preelection period (PEPJ caused by RV pacing, as compared to normal depolarization pathway. Intrinsic‘ACT and IVCT were considered zero. Right heart AV intervals (RAV) were measured from surface ECG and LAVs were calculated according to the following equations: Sinus Rhythm: LAV = RAV; Atrial Pace 4- Ventricular Sense: LAV= RAV ? IACT; Atrial Sense + Ventricular Pace: LAV = RAV + IVCT; Sequential AV Pace: LAV = RAV ? IACT + IVCT, Results: 1. IACT: mean = 73 msec, range: 35–130; IVCT: mean = 50 msec, range: 44–100. 2. Compared to RAVs, LAVs were either too short or too long (?130 to + 300 msec: P < 0.001 J in RAP 4- RVS and RAS + RVP. Conclusions: 1. LAV differed significantly from RAV during AP + VS and AS + VP. 2. “Physiological” RAV intervals in DDD and AAI may cause nonphysiological LAV, possibly affecting LV function. 3. IACT and IVCT should be accounted for when programming DDD PM to provide physiological LAV.     

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。     

Left Origin of the Atrial Esophageai Signal as Recorded in the Pacing Site

Clear atrial depolarizations from inside the esophagus have always been recorded in electrocardiology, but their precise origin is still under discussion. Though atriol signals are recorded along most of the esophagus, pacing of the atria is possible only in a short tract, probably where the esophagus is in contact with the posterior left atrium wall. In order to ascertain which portion of atria gives rise to the esophageai atrial signal recorded in the atrial pacing segment, we examined 37 patients with normal P waves on the standard ECG by inserting esophageai and endocavitary catheters. The interval between the earliest start of the P wave and the bipolar atrial deflection, was measured both through the esophagus (PA-Eso) and the Hisian region (PA-His) (the latest depolarization of interatrial septum). The former was longer than the latter (P < 0.001) in 36 of 37 patients, showing that the esophagus recorded atrial signal, at the site of effective pacing, originates outside the interatrial septum. As the atrial depolarization recorded through the esophagus is significantly delayed compared with the Hisian region recording, a pure left origin of the esophageai signal can be hypothesized. This is supported by the well-known delayed depolarization, during sinus rhythm, of the left atrium posterior wall compared with the right atrium and interatrial septum. Measuring the interval between the standard ECC P wave and atrial depolarization recorded through esophagus in the site of effective pacing, provides a reliable noninvasive estimate of interatrial time conduction.     

Time interval determination from left atrial appendage ejection flow in patients with mitral stenosis

The feasibility of determining the time interval from left atrial appendage (LAA) flow was examined using transesophageal Doppler echocardiography. Time intervals were compared between LAA flow and mitral flow patterns during late diastole in 8 patients with mitral stenosis and in 12 controls. The start of ejection flow from the LAA was later than the initiation of mitral flow, but the termination was same in both flows, indicating the contribution of LAA ejection to the latter half of the left atrial booster pump function. The pre-ejection time and the time interval from P-wave to end-ejection correlated significantly with left atrial dimensions (r = 0.55, and r = 0.70, respectively). The pre-ejection time, duration of the ejection flow from the LAA, and duration of mitral flow in the atrial contraction phase were significantly longer in patients with mitral stenosis (126 ± 14 msec, 131 ± 36 msec, and 167 ± 28 msec, respectively) than in the controls (109 ± 13 msec, 108 ± 15 msec, and 141 ± 17 msec, respectively). These results indicate that electrical conduction time from the right atrium to LAA can be estimated from the LAA ejection flow, and the time is related to the left atrial size. In patients with mitral stenosis, LAA contraction may contribute to left ventricular filling in the latter half of the atrial contraction phase. © 1997 John Wiley & Sons, Inc. J Clin Ultrasound 25 : 97–102, 1997.     

Adenosine Induced Intraatrial Block

Adenosine, an endogenous nucleoside with potent negative chronotropic and dromotropic effects on the sinus and AV nodes, is thought to have little if any antiarrhythmic effect on normal atrial tissue. However, there may be an electrophysiological basis for an adenosine effect on atrial tissue with atypical conduction properties. We examined the electrophysiological effects of adenosine in a patient with decremental atrial conduction properties. During incremental pacing from the high right atrium there was gradual prolongation of the intraatrial interval between the high right atrium and the low septal atrium, from 180 to 280 msec, until 2:1 intraatrial block occurred at a pacing cycie length of 280 msec. Adenosine (6 mg IV) resulted in transient intraatrial block followed by prolonged intraatrial conduction during high right atrial pacing at a cycle length of 400 msec. Thus, similar to its effects on the AV node and decremental AV accessory pathways, adenosine may also slow and abolish conduction in decremental atrial issue, an effect that is likeiy attributed to adenosine induced hyperpolarizing K⁺ current in partially depolarized atrial tissue.     

Proposal of a Method for Automatic Optimization of Left Heart Atrioventricular Interval Applicable to DDD Pacemakers

Electrical pacing of the right heart is known to cause delays in the depolarization of left heart chambers, leading to abnormal left heart AV sequence. Interatrial conduction time, defined as the time from the right atrial pacing pulse or intrinsic P to the onset of left atrial P wave, and P wave sensing delay cause a shorter left heart AV interval during atrial pacing-ventricular sensing and atrial sense-ventricular pace. Interventricular conduction time (the time from the right ventricular pacing pulse to the onset of left ventricular depolarization), lengthens left heart AV interval during atrial sensing-ventricular pacing. These delays may add up or partly cancel out, depending on pacing mode. Thus, an algorithm for DDD pacemakers to optimize left heart AV interval by compensating for the above delays is proposed. This algorithm takes into account pacing and sensing delays to deliver a certain AV sequence to the right heart, aimed at producing a physiological left heart AV interval. The optimization of left heart AV interval is achieved by automatically changing right heart AV interval and pacing mode in accordance with known interatrial and interventricular conduction delays, and P wave sense offset.     

Modulation of the Arterial Coronary Blood Flow by Asynchronous Activation with Ventricular Pacing

This study aims to test the assumptions that: (1) coronary arterial flow is attenuated in an early activated region by ventricular pacing; (2) asynchronous mechanical activation caused by ventricular pacing under controlled perfusion pressure and intact coronary tone is associated with reduced coronary flow compared to atrial pacing; and (3) abolishment of vascular tone under controlled perfasion pressure diminishes the expected difference in blood flow between atrial and ventricular pacing. Blood flow velocity (BFV) in the left anterior descending (LAD) and the left circumflex arteries (CFX) and a wall thickening index were measured in 14 open-chest dogs under normal conditions, and constant perfasion pressure. Four pacing sites were used: right atrium (RAJ, mid-right ventricle (RVyJ, mid-left ventricle (LVp), and left ventricular apex (Apex. Pacing modes were either sequential ventriculoatrial (VA) (protocol A, n = 7), or sequential atrioventricalar (AV) (protocol B, n = 7), with a shorter AV difference (30 msec) than normal. Residis: BFV was decreased in the LAD during HV and Apex, pacingby 9.7%-12.9% versas LV^p and by 1.6%-14.6% versus LV^p (P < 0.05). No BFV variations were observed in the CFX. Flow velocity conductance (FVC = mean blood flow velocity divided by the mean aortic pressure) was higher by 16%-28% in the CFX for the three ventricular pacing sites versus the airial pacing, and higher by 14.1%± 6.1% only in LV_p versus RA_p pacing in the LAD (P < 0.05). Wall thickening index reduced during ventricular pacing in all three ventricular sites by 50%-64% (P < 0.05) compared to atrial pacing. Under constant perfusion pressure, LAD blood flow decreased with ventricular pacing as compared to right atrial pacing; this was particularly pronounced during the diastolic phase (16.6%?45.5%, P < 0.02). Normalized oscillatory flow amplitude (OFA.J was reduced in RVy, pacing compared to RA_p and LV_p pacing (16.2 ± 3.5 and 21.7%± 4.1%, respectively, P < 0.03). The variations in blood flow and OFAn disappeared with adenosine-mediated maximum vasodilatation. Summary; (1) Mean and phasic flows are reduced in the early activated LAD region by ventricular pacing (RV_p, Apex. (2) Under controlled perfusion pressure and intact vascular tone, ventricular pacing compromises blood flow compared with atrial pacing. (3) This effect disappears when vascular tone is eliminated by intracoronary injection of adenosine, suggesting that the coronary autoregulation is responsible for some of the effects.     

Can Simple Doppler Measurements Estimate Interatrial Conduction Time?

COZMA, D., et al.: Can Simple Doppler Measurements Estimate Interatrial Conduction Time? Prolongation of the interatrial conduction time (ia-CT) is considered an important factor in the pathophysiology of atrial fibrillation (AF) and as a criterion to perform multisite atrial pacing. Measurement of ia-CT requires an electrophysiologic study. The aim of this study was to compare echocardiographic with electrophysiologic measurements to determine if they are correlated. Methods and Results: The study included 32 consecutive patients who underwent electrophysiologic studies. We measured ia-CT between the high right atrium and the distal coronary sinus. In all patients we measured P wave duration, left atrial diameter and area, and ia-CT by Doppler echocardiography was measured as the difference in time intervals between the QRS onset and the tricuspid A wave, and the QRS onset and the mitral A wave (DT). Ia-CT was statistically correlated with DT  (r = 0.79, P < 0.0001)  , but not with P wave duration or left atrial dimensions. Conclusions: Measurement DT may be reliable to estimate ia-CT without invasive procedure. Accordingly, DT could be used as a simple selection criterion when considering patients for atrial resynchronization therapy. (PACE 2003; 26[Pt. II]:436–439)     

VDD Pacing at Short Atrioventricular Intervals Does Not Improve Cardiac Output in Patients with Dilated Heart Failure

Atrial synchronous pacing with short, nonphysiologicai atrioventricular (AV) intervals has been reported to increase cardiac output in selected patients with severe dilated heart failure. The aim of this study was to determine the acute effect of atrial synchronous pacing with short AV intervals in a consecutive series of patients with dilated heart failure. Twelve patients with a mean ejection fraction of 21 %± standard error 2.5% were studied. Pacing catheters were placed in the high right atrium and right ventricular apex and a balloon flotation catheter in the pulmonary artery for measurement of cardiac output. Simultaneous transthoracic echocardiography was performed for measurement of left ventricular filling time and mitral regurgitation. In a randomized crossover design, measurements were made during VDD pacing at programmed AV intervals of 100 and 60 msec and during a control period in sinus rhythm. Left ventricular filling time increased at AV intervals of 100 and 60 msec (mean difference 37 ± 9 and 34 ± 11 msec, respectively, both P < 0.01 compared to control). Despite increases in ventricular filling time, stroke, and cardiac index declined with short atrioventricular intervals (at an AV interval of 60 msec, stroke index fell by 2.1 ± 0.5 mL/m², P < 0.05 and cardiac index by 125 ± 45 mL/m²; P = NS). Heart rate was unchanged at both AV intervals (78 ± 4.9 at control, 78 ± 5.2 at 100 msec and 79 ± 4.9 beats/min at 60 msec; P = NS). The decrease in stroke index at an AV Interval of 60 msec was inversely related to control left ventricular filling time (r = 0.74; P = 0.01) and ejection fraction (r = 0.69; P = 0.02) and directly related to heart rate (r = 0.77; P < 0.01). The change in stroke index at an AV delay of 60 msec was also inversely related to the change in mitral regurgitation induced by pacing (r = 0.84; P = 0.01). Thus, in a group of patients with stable dilated heart failure, atrial synchronous pacing with short AV intervals did not improve cardiac output. The change in cardiac output with pacing was inversely related to baseline left ventricular function and to the change in mitral regurgitation induced by pacing.     

Acute Hemodynamic Improvement by Pacing in Patients with Severe Congestive Heart Failure

Since the first report on dual chamber pacing for congestive heart failure (CHF) in 1991, a number of investigators have explored the topic with conflicting results. These conflicts may arise from an incomplete understanding of the mechanisms by which pacing improves cardiac function. Potential mechanisms include: (1) increase in filling time: (2) decrease in mitral regurgitation: (3) optimization of left heart mechanical atrioventricular delay (left heart MAVD); and (4) normalization of ventricular activation. One or more of these mechanisms may be operative in an individual patient, implying that patients may require individuol optimization. Acute pacing studies were conducted on nine CHF patients, NYHA Class II-III to Class IV. Measurements of conduction times in sinus rhythm revealed: (1) normal interatrial conduction times (59 ± 5 ms) in all patients, with wide variations in interventricular conduction times (range, ?15–105 ms); and (2) a wide range of left heart MAVD (range, 97–388 ms). While pacing the right, left, or both ventricles, measurement of high fidelity aortic pressure and mitral and aortic velocities revealed the following: (1) 6 of 9 patients increased mean pulse pressure over sinus value during RV orLV pacing at an optimal A V delay: (2) the maximum aortic pulse pressure was achieved when the atrium was not paced: an 8% increase over sinus pulse pressure with paced RV versus a 5% decrease for paced atrium and RV at optimum AV delay (paired Student's t-test, P = 0.01), and a 0% increase over sinus with paced LV versus 7% decrease for paced atrium and LV at optimum AV delay, P < 0.05: (3) significant dependence on pacing site was noted, with 4 patients doing best with RV pacing. 3 patients achieving a maximum with LV pacing, and 2 patients showing no preference; and (4) 2 of 4 patients with restrictive filling patterns were converted to nonrestrictive patterns with optimum pacing. Patient hemodynamics appear to benefit acutely from individually optimized pacing. Increases in filling time, optimization of left heart MAVD, and normalization of intraventricular activation are the most significant mechanisms. Atrial pacing is inferior to atrial sensed modes if the patient has a functional sinus node.     

Assessment of atrial conduction time in patients with coronary artery ectasia

Background: Coronary artery ectasia (CAE) is associated with increased sympathetic activity, plasma levels of inflammatory markers, and oxidative stress. These factors can also cause arrhythmias such as atrial fibrillation. Atrial conduction abnormalities in patients with CAE have not been investigated in terms of atrial electromechanical delay obtained by tissue Doppler echocardiography. Methods: Ninety patients with pure CAE (n = 30), nonobstructive coronary artery disease (NO‐CAD) (n = 30), and angiographically normal coronary arteries “controls” (n = 30) were compared in terms of electrocardiographic P‐wave measurements, echocardiographic atrial electromechanical coupling (AEC) parameters, and interatrial conduction delay. Results: The mean left atrium diameter in the CAE group was similar to the NO‐CAD group but significantly greater than the control group (3.62 ± 0.28 vs 3.46 ± 0.32 vs 3.41 ± 0.31 cm, P = 0.021). P maximum and P‐wave dispersion were significantly increased in the CAE group compared to the NO‐CAD group and the control group (108.6 ± 6.6 vs 97.9 ± 6.6 vs 93.5 ± 6.2, P = 0.0001; 34.4 ± 7.6 vs 23.2 ± 7.8 vs 19.4 ± 7.7 ms, P < 0.0001). Mitral AEC, septal AEC, and tricuspid AEC were significantly higher in the CAE group than the NO‐CAD group and the control group (68 ± 4.5 vs 57 ± 4.5 vs 53 ± 4.6 ms, P < 0.0001; 50.7 ± 7 vs 42.7 ± 7 vs 41.7 ± 7.2 ms, P = 0.0001; 47 ± 6.7 vs 39.1 ± 6.7 vs 38.1 ± 6.6 ms, P < 0.0001). Interatrial conduction delay was significantly increased in the CAE group compared to the NO‐CAD group and the control group (21 ± 5.5 vs 17.8 ± 5.6 vs 15 ± 5.6 ms, P < 0.0001).The correlation analysis demonstrated that the interatrial conduction delay and P‐wave dispersion (Pd) were positively correlated with number of ectatic segments (ESN) (r = 0.41, P = 0.024 vs r = 0.49, P = 0.006). Stepwise multiple linear regression analysis revealed that the ESN was the only independent determinants of interatrial conduction delay (P = 0.024). Conclusion: Pd and interatrial conduction delay are prolonged in patients with CAE compared to NO‐CAD patients and the healthy controls. (PACE 2011; 34:1468–1474)     

Effects of Procainamide on Refractoriness, Conduction, and Excitable Gap in Canine Atrial Reentrant Tachycardia

The effects of procainamide were studied in a model of atrial flutter around the tricuspid valve in seven open chest, chloralose-anesthetized dogs (31 ± 3 kg). A Y-shaped incision in the intercaval area extending to the right atrial appendage was made and five bipolar electrodes were sutured on the atrial epicardium around the tricuspid valve. Reentry tachycardia was induced in the absence and presence of drug by burst pacing. Procainamide (5 mg/kg bolus followed by 0.075 mg/kg/min infusion) produced stable plasma levels (38 ± 9μ) during the study. At a pacing cycle length of 200 msec, mean (± SD) diastolic threshold at the five sites increased from 1.6 ± 1,5 to 2,0 ± 1.7 mA and mean atrial effective refractory period from 128 ± 9 to 140 ± 16 msec on drug (P < 0.05). Procainamide prolonged the cycle length of atrial flutter from 144 ± 10 to 160 ± 13 msec and slowed conduction velocity during atrial flutter around the tricuspid valve from 73 ± 6 to 66 ± 6 cm/sec (P < 0.05). A reset response curve was determined by introducing premature stimuli during atrial flutter. Procainamide prolonged effective refractory period during atrial flutter from 101 ± 13 to 116 ± 17 msec but did not change the duration of the excitable gap (38 ± 9 vs 40 ± 18 msec). Although the reset response curve was predominantly increasing, in six of seven experiments there was present a flat portion at long coupling intervals approaching the atrial flutter cycle length that comprised 23%± 10% of the excitable gap. Procainamide shifted the reset response curve upward and to the right but did not change its slope or the duration of the flat portion. Thus, in the majority of experiments the reset response curve in atrial flutter about the tricuspid valve in vivo suggests that procainamide prolongs atrial flutter cycle length directly by slowing conduction through fully excitable tissue rather than indirectly by increasing refractoriness at the head of the wave front.     

Relationship between P-wave duration and atrial electromechanical delay assessed by tissue Doppler echocardiography

Background: The aim of the study was to assess the relationship between P‐wave duration on the surface electrocardiogram (ECG) and echocardiographic parameters of atrial electromechanical delay (EMD), as well as contraction synchrony during different atrial pacing modalities. Methods: In 57 patients with sinus node disease and prolonged sinus P‐wave duration treated with multisite atrial pacing (MSAp), the EMD was measured by tissue Doppler in several left and right atrial sites during sinus rhythm, MSAp, and single‐site pacing at right atrial appendage (RAAp), Bachmann's bundle (BBp) region, and coronary sinus (CSp) ostium. Regional atrial synchrony was calculated on the basis of EMD. Results: P‐wave duration was 141 ± 16, 120 ± 17, 138 ± 17, 144 ± 16, and 160 ± 19 ms during sinus rhythm, MSAp, BBp, CSp, and RAAp, respectively (P < 0.001 RAAp and MSAp vs other). P‐wave duration correlated with all atrial EMDs as well as interatrial and intraleft atrial parameters of dyssynchrony. In multivariate analysis, the EMD in lateral left atrial wall was the strongest predictor of P‐wave duration (β 0.41; P < 0.001). The relationship between P‐wave duration and the atrial EMDs was most prominent during RAAp (all left atrial walls r > 0.51; P < 0.01) and BBp (all atrial walls r > 0.42; P < 0.05), while during sinus rhythm and CSp, only weak correlation between echo and ECG was found. Neither of the tissue Doppler parameters correlated with P‐wave duration during MSAp. Interatrial dyssynchrony correlated with P‐wave duration during sinus rhythm and RAAp and intraleft atrial dyssynchrony only during sinus rhythm. Conclusions: P‐wave duration of the surface ECG is highly correlated with the atrial EMD, the relationship is specific for each pacing modality. (PACE 2011; 23–31)