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.     

Evaluation of atrial conduction time at various sites of right atrial pacing and influence on atrioventricular delay optimization by surface electrocardiography

Cardiac function and electrical stability may be improved by programming of optimal AV delay in DDD pacing. This study tested the hypothesis if the global atrial conduction time at various pacing sites can be derived from the surface ECG to achieve an optimal electromechanical timing of the left heart. Data were obtained from 60 patients following dual chamber pacemaker implantation. Right atrial septal pacing was associated with significantly shorter atrial conduction time (P < 0.0005) and P wave duration (P < 0.005), compared to standard right atrial pacing sites at the right atrial appendage or at the right free wall. The last two pacing sites showed no significant difference. In a group of 31 patients with AV block, optimal AV delay was achieved by programming a delay of 100 ms from the end of the paced P wave to peak/nadir of the paced ventricular complex. Optimization of AV delay resulted in a relative increase of echocardiographic stroke volume (SV) (10.9 +/- 13.7%; 95% CI: 5.9-15.9%) when compared to nominal AV delay (170 ms). Optimized AV delay was highly variable (range 130-250 ms; mean 180 +/- 35 ms). The hemodynamic response was characterized by a weak significant relationship between SV increase and optimized AV delay (R2 = 0.196, R = 0.443, P = 0.047). The study validated that septal pacing is advantageous for atrial synchronization compared to conventional right atrial pacing. Tailoring the AV delay with respect to the surface ECG improved systolic function significantly and was superior to nominal AV delay settings in the majority of patients.     

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.     

Continuously adjusting CRT therapy: clinical impact of adaptive cardiac resynchronization therapy

Cardiac resynchronization therapy (CRT) is a well-established therapy to reduce morbidity and mortality in patients with moderate and severe symptomatic congestive heart failure. Left ventricular (LV) pacing that fuses with intrinsic right ventricular (RV) conduction results in similar or even better cardiac performance compared to biventricular (Biv) pacing. Optimal programming of the atrio-ventricular (AV) and inter-ventricular (VV) delays is crucial to improve LV performance since suboptimal programming of AV and VV delays affect LV filling as well as cardiac output. CRT optimization using echocardiogram is resource-dependent and time consuming. Adaptive CRT (aCRT) algorithm provides a dynamic, automatic, ambulatory adjustment of CRT pacing configuration (Biv or LV pacing) and optimization of AV and VV delays. aCRT algorithm is safe and efficacious for CRT-indicated patients without permanent atrial fibrillation. It has been shown to improve CRT response and reduce morbidity and mortality for patients with normal AV conduction.     

Atrial Flutter Ablation using a Technique for Detection of Conduction Block within the Posterior Isthmus

Catheter ablation orientated on the induction of a functional intraatrial block within the posterior isthmus of the tricuspid annulus has been shown to effectively abolish atrial flutter. In order to improve and simplify the current technique, a strategy based on an electrode catheter for combined right atrial and coronary sinus mapping and stimulation was explored prospectively. Twenty-four consecutive patients referred for catheter ablation of recurrent type I atrial flutter were included. A steerable 7 Fr catheter (Medtronic/Cardiorhythm) composed of two segments with 20 electrodes was used for right atrial and coronary sinus activation mapping and stimulation. Multiple steering mechanisms allowing intubation and positioning of the distal part within the coronary sinus were incorporated into the device. Adequate positioning of the mapping catheter was achieved solely via a transfemoral approach in all patients after 7.7 +/- 4.6 minutes, providing stable electrogram recordings during the entire ablation procedure. Radiofrequency current ablation (16.3 +/- 9.6 pulses) caused a significant bidirectional increase of the mean intraatrial conduction times via the posterior isthmus irrespective to the stimulation interval. Significant changes of intraatrial conduction properties were induced during ablation in 22 of 24 patients (bidirectional block: n = 18, unidirectional block: n = 3, conduction delay: n = 1, unchanged conduction: n = 2). Following ablation atrial flutter was noninducible in all patients. Twenty-two of 24 patients (92%) remained free of atrial flutter episodes during a follow-up of 12.5 +/- 5.7 months. Two of six patients without a bidirectional conduction block had a recurrence of atrial flutter. Atrial flutter ablation guided by the induction of an intraatrial conduction block can be effectively performed with this novel strategy for combined mapping of the posterior tricuspid isthmus, including coronary sinus and right atrial free wall. This transfemoral approach has a high accuracy with respect to the detection of radiofrequency current-induced changes of intraatrial conduction patterns.     

Reduction of right ventricular pacing in patients with sinus node dysfunction through programming a long atrioventricular delay along with the DDIR mode

Background  

Right ventricular (RV) pacing increases the incidence of atrial fibrillation (AF) and hospitalization rate for heart failure. Many patients with sinus node dysfunction (SND) are implanted with a DDDR pacemaker to ensure the treatment of slowly conducted atrial fibrillation and atrioventricular (AV) block. Many pacemakers are never reprogrammed after implantation. This study aims to evaluate the effectiveness of programming DDIR with a long AV delay in patients with SND and preserved AV conduction as a possible strategy to reduce RV pacing in comparison with a nominal DDDR setting including an AV search hysteresis.     

Mechanism of Double Ventricular Response to a Single Atrial Extrastimulus in Patients with Wolff-Parkinson-White Syndrome

The purpose of this study is to elucidate electrophysiological determinants of double ventricular response (DVR) to a single atrial extrastimulus in Wolff-Parkinson-White (WPW) syndrome. DVR was observed in 5 (3.4%) out of 146 consecutive patients with WPW syndrome. The site of accessory pathway was located in left lateral free wall in four patients and posterior septum in one. DVR was induced by extrastimulus from coronary sinus in four patients with left-sided accessory pathway, and from both coronary sinus and high right atrium in a patient with septal accessory pathway. However, it was not possible to induce DVR from high right atrium in patients with left-sided accessory pathway, because 50 to 80 ms are needed for intra-atrial conduction from high right atrium to coronary sinus. Critical prolongation of normal AV conduction allowing DVR was seen in the slow pathway of AV node in four patients. In the remaining patients requisite conduction delay occurred in both AV node and His-Purkinje system. Single right ventricular extrastimulus could easily elicit orthodromic AV reciprocating tachycardia or echo beat in four out of five patients and incremental ventricular stimulation induced it in the remaining patient, indicating the presence of retrograde block in the normal AV pathway. As requisites of DVR to a single atrial extrastimulus in WPW syndrome: (1) slow antegrade conduction and retrograde block in the normal AV pathway; and (2) stimulation site in the vicinity of accessory pathway, are needed.     

Right atrial tachycardia in a patient with severe atrial conduction disturbances and an anatomically normal heart

We describe a case of abnormal right atrial (RA) conduction in a patient with atrial tachycardia (AT) but no history of structural heart disease or cardiac surgery. Following ablation of AT, the patient experienced typical atrial flutter (AFL) and a postcardioversion ECG suggestive of low atrial rhythm. Repeat EPS and three-dimensional electroanatomic activation mapping showed unusual RA activation during SR. This case illustrates the possibility that abnormal intraatrial conduction may lead to unusual patterns of activation in the RA which can serve as a necessary substrate for the initiation and maintenance of macro-reentry circuits.     

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.     

双腔起搏器房室间期自动搜索功能对右心室起搏比例影响的临床研究

目的比较植入双腔起搏器患者房室（AV）间期自动搜索功能（Search AV）打开与固定长AV间期起搏,对右心室起搏比例的影响。方法入选60例病态窦房结综合征或间歇性Ⅱ度或Ⅲ度AV传导阻滞患者,均安装双腔起搏器。程控首先关闭Search AV功能,固定长AV间期（起搏房室间期220ms,感知房室间期200ms）起搏3个月,后程控打开Search AV 3个月,自身对照,比较其心房起搏比例、心室起搏比例及高频心房事件次数。再根据患者是否1：1房室传导分为2个亚组,自身对照分别比较其心房起搏比例、心室起搏比例及高频心房时间次数。结果58倒患者完成随访,固定长AV间期起搏时比Search AV（＋）自动搜索功能打开时的心室起搏比例、高频心房事件次数都高,分别为（70．5±12．4）％vs（22．4±8．3）％,（86±16）次VS（31±11）次（P=0．007,P=0．006）;而心房起搏比例二者差异无统计学意义。在1：1房室传导组（33例）及非1：1房室传导组（25例）两亚组比较中,均得出相同结果。结论Search AV功能可以减少不必要的右心室起搏,减少高频心房事件。     

Electroanatomical mapping in partial atrial standstill for visualization of atrial viability and a suitable pacing site

Partial atrial standstill is characterized by the failure of atrial activity either spontaneously or in response to electrical stimulation in restricted site of atria. In this case with bradycardia, atrial standstill was restricted to the lateral and posterior right atrium. The markedly prolonged intraatrial conduction delay was observed in the superior to septal region of the right atrium. The electroanatomical mapping was successfully utilized to estimate atrial activity and to find a suitable site for atrial lead placement. The electroanatomical mapping may become an innovated strategy to estimate atrial electrical status in partial atrial standstill.     

Pacemaker Syndrome in a Patient with DDD Pacemaker for Long QT Syndrome

A patient with long QT syndrome was treated with beta blockers and had a permanent DDD pacemaker implanted. The lower rate was set to 85 beats/min because this provided the best shortening of QT interval at the lowest paced heart rate. The atrioventricular (AV) delay was programmed to 250 msec to allow native AV conduction. Patient returned complaining of symptoms suggestive of pacemaker syndrome. ECG during one of these episodes showed AV sequential pacing. Doppler echocardiography of hepatic vein flow suggested atrial contraction against a closed tricuspid valve. Endocardial electrogram telemetry demonstrated ventriculoatrial (VA) conduction with the retrograde atrial electrogram falling within the atrial refractory period and thus was not sensed. The following atrial stimulus did not capture because of the atrial refractoriness. Ventricular pacing proceeded after the programmed AV delay. Reprogramming the AV delay to 200 msec restored AV synchrony by allowing the atrial stimulus to capture by placing it outside of the refractory period of the atrium. No further symptoms reported during six months of follow-up.     

Failure of coronary sinus pacing in reducing local atrial conduction delay in patients with atrial fibrillation after successful internal cardioversion

Recent studies suggested that distal coronary sinus (CS) pacing may prevent atrial fibrillation (AF) by reducing site dependent intraatrial conduction delay. The aim of this study was to investigate the effect of high right atrial (HRA) and distal CS pacing on local conduction delay in patients with AF. The study population consisted of 10 patients with persistent AF after transvenous atrial defibrillation and 10 control subjects. The local conduction delays along the anterolateral right atrium (RA), in the CS, and at the right atrial septum (RAS), and the incidence of AF in response to an atrial extrastimulus during HRA and distal CS pacing at a drive cycle length of 400, 500, and 600 ms were evaluated. In patients with AF, distal CS and HRA pacing are associated with more prominent and similar extent of conduction delay within the atria, without any significant difference in the dispersion of conduction delay and susceptibility to AF induction (70% vs 60%, P = 0.9). In normal controls, distal CS pacing reduces the conduction delay at the RAS and CS ostium and decreases the dispersion of conduction delay and the propensity for AF induction (0% vs 50%, P = 0.03) compared to HRA pacing. The pacing drive cycle length has no significant effect on conduction delay in patients with AF and normal controls (P > 0.05). Compared to normal controls, patients with AF have significantly longer conduction delay at the RAS and along the anterolateral RA during HRA and distal CS pacing. The result of this study demonstrates that the effect of HRA and distal CS pacing on the local atrial conduction delay in patients with and without AF differ significantly. These patients with AF may have more diffuse atrial anisotropy causing the changes in conduction, and pacing from distal CS in these patients dose not reduce the propensity for AF.     

Reduction of right ventricular pacing with advanced atrioventricular search hysteresis: results of the PREVENT study

Background: Right ventricular pacing predisposes to the development of heart failure and atrial fibrillation. Automatic atrioventricular search hysteresis (AVSH) is a commonly used strategy to decrease the percentage of right ventricular pacing (%VP) in patients without permanent AV block, but the results have not been optimal. Methods: The randomized, crossover PREVENT study evaluated whether an enhanced AVSH with two new features can reduce %VP compared with standard AVSH. The new features are the repetitive hysteresis [switch from extended to basic AV delay after a consistent loss of intrinsic AV conduction (IAVC) lasting for six consecutive atrial cycles] and the scan hysteresis (periodic IAVC search extension over six consecutive atrial cycles). Both standard AVSH and enhanced AVSH performed a periodic IAVC search every 180 cardiac cycles and operated with a basic AV‐delay of 225 ms and a rate‐independent maximum AV‐delay of 300 ms for paced and sensed atrial events. Results: Among 178 patients, 53.4% had no evidence of AV block at enrollment and 46.6% had history of intermittent AV block. The median %VP was decreased by enhanced AVSH compared to standard AVSH (4.0% vs 5.5%, P < 0.001), particularly in patients with a history of AV block (21.4% vs 25.5%, P < 0.001). The primary study hypothesis that 25% of all patients would experience > 20% relative %VP reduction was not met as 46 (25.8%) patients (95% confidence interval, 20.5–31.8%) presented such relative reduction. Conclusion: The enhanced AVSH algorithm reduces %VP compared with standard AVSH in patients with intermittent AV block. (PACE 2011; 34:975–983)     

Method of atrioventricular programming in atrial flutter in patients with biventricular pacemaker

BACKGROUND: Atrial flutter is a common cause of exacerbation of congestive heart failure (CHF). Typically, during atrial tachycardia, pacemakers, both dual and biventricular, are programmed to ignore atrial tracking. Virtually all current pacemakers and defibrillators use a programmable mode switch algorithm to switch between atrial tracking modes (DDD, DDDR) to nontracking modes (DDIR, DDI, VVI) during episodes of atrial tachycardia. METHODS: In this report, we describe a novel method of atrioventricular (AV) pacemaker programming in four patients with atrial flutter and CHF who remained symptomatic postbiventricular pacemaker implantation. All patients had chronic atrial flutter upon interrogation; adjustment of AV delay and postventricular atrial refractory period (PVARP) was performed to enable sensing of every second to fourth atrial flutter beat by the atrial lead. Mode switch was turned "OFF" in all points, and lower and upper rate limits were set to 50 and 100 bpm. Once sequential early and late diastolic filling was seen on mitral inflow pulsed-wave (PW) Doppler, further adjustment of AV delay and PVARP was performed until the highest and broadest atrial velocity occurred on mitral inflow PW Doppler. RESULTS: All patients developed improvement in aortic ejection duration and peak ejection velocity during AV optimization. Repeat ECG in these patients at 8 months, 7 days, 2 days, and 2 months postoptimization showed no change in P and QRS relationship. All patients developed improvement in CHF symptoms postbiv pacemaker optimization. CONCLUSION: In symptomatic patients with CHF and stable atrial flutter who have a biventricular pacemaker, atrial mechanical contribution to cardiac output can be achieved by adjusting PVARP and AV delay during echo-guided pacemaker programming.     

Atrial and Ventricular Pressures in Atrial Flutter

The hemodynamic effects of atrial flutter (AF) are unknown. The purpose of the present study was to investigate the changes in atrial and ventricular pressures after induction of AF. In 23 patients with paroxysmal AF (age 59 ± 9 years), a hemodynamic study was performed both during sinus rhythm and after induction of the tachyarrhythmia. During AF, 13 patients showed a fixed 2:1 AV conduction and 10 patients showed variable conduction. Mean right and left atrial pressures increased (P < 0.001) and right and left ventricular end-diastolic pressures decreased (P < 0.001) after induction of AF. Roth the increase in mean atrial pressures and the decrease in ventricular end-diastolic pressures were present either in the patients with fixed 2:1 AV (heart rate: 133 ± 15 beats/min) or in those with variable conduction (heart rate 96 ± 15 beats/min), but were more marked in the former. AF produces an impairment of atrial function, as evidenced by the increase in mean atrial pressures and reduction in ventricular end-diastolic pressures in the absence of an elevated heart rate. The mechanisms responsible for the increase in mean atrial pressures are unknown; however, atrial contractions against closed AV valves seem to play an important role.     

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.     

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.     

An Optimized AV Delay Algorithm for Patients with Intermittent Atrioventricular Conduction

Detection and promotion of an intermittent atrioventricular (A V) conduction is the objective of an AV delay hysteresis algorithm in dual chamber pacemaker (DDDj pacing. The AV delay following an atrial event is automatically extended by a programmable interval (AV hysteresis interval) if the previous cycle showed spontaneous AV conduction, i.e., a ventricular event was detected within the previous AV delay. An automatic search mode scans for spontaneous ventricular events during the hysteresis interval: a single AV delay extension (equal to the programmed AV delay hysteresis) will occur after a successive, programmable number of AV cycles with ventricular pacing. If a spontaneous AV conduction is present, the AV delay will remain extended by the hysteresis interval. Our first results in 17 patients with intermittent AV block disclosed a satisfactorily working algorithm with effective reduction of ventricular stimuli. In relation to the underlying conduction disturbance and pacemaker settings, the majority of our patients showed a reduction of ventricular pacing events up to 90% without any adverse hemodynamic or electrophysiological changes. Based on clinical (promotion of a physiological activation and contraction sequence) and technical (reduction of power consumption) advantages, the AV hysteresis principle could be of incremental value for future dual chamber pacing in patients with intermittent complete heart block.