The influence of atrial activity on ventricular capture by failing artificial pacemakers. I. Report of two new cases and review of the literature.

Atrial activity can influence the ability of a failing artificial pacemaker to excite the heart. An appropriately timed atrial beat may cause failure in excitation by pacemaker stimuli which are usually successful in ventricular capture. Conversely, stimuli which usually fail in excitation may be made to succeed by an appropriately timed atrial beat. Two case reports and a review of the literature are presented. Alternative mechanisms for this influence of atrial activity are electrotonic effects (Wedensky facilitation or inhibition) and mechanical effects (motion of the pacing catheter or ventricular myocardium). The authors consider the latter mechanism preferable.     

Characterization of sustained atrial tachycardia in dogs with rapid ventricular pacing-induced heart failure

INTRODUCTION: Atrial arrhythmias often complicate congestive heart failure (CHF). We characterized inducible atrial tachyarrhythmias and electrophysiologic alterations in dogs with CHF and atrial enlargement produced by rapid ventricular pacing. METHODS AND RESULTS: Endocardial pacing leads were implanted in the right ventricle, right atrium, and coronary sinus in 18 dogs. The right ventricular lead was connected to an implanted pacemaker capable of rapid ventricular pacing. The atrial leads were used to perform electrophysiologic studies in conscious animals at baseline in all dogs, during CHF induced by rapid ventricular pacing at 235 beats/min in 15 dogs, and during recovery from CHF in 6 dogs. After 20 +/- 7 days of rapid ventricular pacing, inducibility of sustained atrial tachycardia (cycle length 120 +/- 12 msec) was enhanced in dogs with CHF. Atrial tachycardia required a critical decrease in atrial burst pacing cycle length (< or = 130 msec) for induction and often could be terminated by overdrive pacing. Calcium antagonists (verapamil, flunarizine, ryanodine) terminated atrial tachycardia and suppressed inducibility. Effective refractory periods at 400- and 300-msec cycle lengths in the right atrium and coronary sinus were prolonged in dogs with CHF. Atrial cells from dogs with CHF had prolonged action potential durations and reduced resting potentials and delayed afterdepolarizations (DADs). Mitochondria from atrial tissue from dogs with CHF were enlarged and had internal cristae disorganization. CONCLUSIONS: CHF promotes inducibility of sustained atrial tachycardia. Based on the mode of tachycardia induction, responses to pacing and calcium antagonists, and presence of DADs, atrial tachycardia in this CHF model has a mechanism most consistent with DAD-induced triggered activity resulting from intracellular calcium overload.     

Atrioventricular Nodal Conduction Rather than Automaticity Determines the Ventricular Rate During Atrial Fibrillation and Atrial Flutter

AV Nodal Conduction During Atrial Fibrillation and Flutter . Introduction: Recent clinical studies have advanced the hypothesis that the atrioventricular (AV) node does not conduct cardiac impulses, but functions as a pacemaker whose discharge rate and rhythm are modulated electrotonically by atrial impulses. Major support for the hypothesis comes from the observation that the short ventricular cycles during atrial fibrillation can be totally eliminated by ventricular pacing at relatively long ventricular cycle lengths. Methods and Results: The hypothesis was tested in ten anesthetized open chest mongrel dogs with sustained atrial fibrillation or atrial flutter (AF). Large differences (> 120 msec) between the ventricular pacing cycle length that achieved > 95% ventricular capture and the shortest spontaneous RR cycle during AF were considered to be consistent with the modulated AV nodal pacemaker hypothesis, while values ≤ 120 msec were not. The results showed that the ventricular pacing cycle length capturing > 95% of ventricular complexes during AF depended on the spontaneous ventricular rate during AF. Short spontaneous RR cycles during AF required short ventricular pacing cycle lengths to achieve > 95% capture, and the difference between the ventricular pacing cycle length and the shortest spontaneous RR cycle length was narrow, i.e., ≤ 120 msec. Slower ventricular rates could be captured at longer ventricular pacing cycle lengths, and the difference between the ventricular pacing cycle length capturing > 95% of the ventricular complexes and the shortest spontaneous RR interval during AF was large, i.e., > 120 msec. A continuum existed, and values ≤ 120 msec could be transformed to values > 120 msec by increasing vagal intensity to slow the ventricular response. We also found in five dogs that we could not achieve overdrive suppression of automaticity of the putative AV nodal pacemaker focus by ventricular pacing at various cycle lengths and durations during atrial fibrillation. Conclusion: In conclusion, data from this study fail to support the modulated AV nodal pacemaker hypothesis and are more consistent with conventional concepts of AV nodal conduction.     

Hypertrophic subaortic stenosis complicated by high degree heart block: successful treatment with an atrial synchronous ventricular pacemaker.

The development of high degree atrioventricular block in a patient with hypertrophic subaortic stenosis underscores the importance of a properly timed atrial contraction in this disorder. Atrial synchronous ventricular pacing therapy, by providing, reliably timed atrial systole and increased left ventricular end-diastolic volume, has an important role in this patient and in similar cases.     

Device-based therapies for atrial fibrillation

Optional statement Ablation of the atrioventricular conduction system and pacemaker implantation is the preferred procedure for patients with atrial fibrillation (AF) in whom a rate control strategy has been selected but in whom rate-controlling medications are intolerable or ineffective. Selection of standard right ventricular (RV) pacing versus biventricular pacing is individualized, based on the degree and etiology of left ventricular dysfunction. Atrial-based pacing is clearly preferable to ventricular-based pacing in patients with sick sinus syndrome, because it leads to a reduction in the development of AF. Emerging evidence indicates that excess RV pacing is deleterious, increasing AF, heart failure, and possibly mortality. Therefore, physiologic pacing with minimization of RV pacing is desirable. Atrial pacing algorithms that increase the frequency of atrial pacing have shown modest efficacy in the prevention of AF. Use of atrial pacing algorithms is reasonable for patients with a history of AF and standard bradycardia indications for permanent pacing in whom maintenance of sinus rhythm is desirable. Studies assessing novel and multiple site atrial pacing therapies have mixed results, without compelling evidence of clinically important benefit. The exceptions are biatrial and right atrial overdrive pacing immediately after cardiac surgery. Several studies have shown effective suppression of postoperative AF with their use. Device therapy (eg, atrial antitachycardia pacing and defibrillation) for the termination of AF is effective in reducing arrhythmia burden. However, improvement in clinically relevant end points is not established and indications are not clearly defined. If a patient lacks an indication for an implantable cardioverter-defibrillator, we do not offer atrial defibrillation as a treatment option. Atrial arrhythmias may be better prevented by programming to avoid ventricular pacing than by specific atrial interventions.     

起搏器植入晚期可逆性阈值升高原因分析及对策

目的 分析起搏器植入患者中,出现晚期可逆性阈值升高的原因,探求解决方法。方法 回顾性分析在2003 -2012年本院植入起搏器的1 143例患者,对出现晚期可逆性阈值升高的7例患者的疾病特点进行总结 。结果 7例患者中,4例出现黑矇或短暂意识丧失,心电图存在失夺获表现;1例心房起搏失夺获,但心室起搏功能良好,无临床症状;2例因安装有具有阈值自动管理功能起搏器,无临床症状。7例的心房基线阈值为0.5 - 0.75 V,心室基线阈值为0. 5 -0.75 V,并发急性病情时,6例心室阈值均超过2.5 V,1例心房阈值超过2.5V。7例患者都有不同的急症,包括大面积烧伤、慢性肾功能不全急性加重、心功能衰竭并呼吸衰竭,导致了酸中毒、高钾血症、心肌缺血缺氧。在急症缓解后,7例心房、心室阈值出现下降,心房阈值降为0. 5 -1. 0 V,心室阈值降为0. 5 - 1. 5 V,起搏器在原有参数设置下工作恢复了正常。 结论 心功能不全、呼吸衰竭、肾功能不全等疾病可引起心肌外环境异常,导致晚期起搏阈值突然升高,具有阈值自动管理功能的起搏器可适时调节起搏阈值。     

The contribution of artificial pacemaking to understanding the pathogenesis of arrhythmias

Right atrial or ventricular pacing was performed on 36 occasions in 26 patients in an attempt to terminate a variety of tachyarrhythmias. Of 16 episodes of atrial flutter, 13 were terminated successfully; in 9 of the 13, sinus rhythm or the patient's pre-flutter rhythm was restored immediately, whereas in 4 patients, intervening atrial fibrillation or unstable atrial flutter occurred. Pacing terminated paroxysmal atrioventricular junctional or paroxysmal atrial tachycardia on 3 occasions; in a fourth patient, this tachyarrhythmia terminated during catheter manipulation. Six episodes of pacemaker-induced ventricular tachycardia were abolished by ventricular pacing. In 2 patients, atrial tachycardia was only transiently suppressed, and in 1 of these patients, d-c cardioversion produced a similar effect. Atrial fibrillation, spontaneously converting to atrial flutter, resulted during pacing for atrial tachycardia with block; the latter arrhythmia returned when the atrial flutter was terminated. Atrial fibrillation in 7 patients remained unaffected by atrial pacing. Based on the different electrophysiologic mechanisms responsible for reentrant excitation and automatic pacemaker discharge, an attempt has been made to determine the pathogenesis of the tachyarrhythmia by its response to pacing.     

Pacemaker pseudodysfunction with a coronary sinus pacemaker

A permanent transvenous coronary sinus pacemaker functioned effectively for 22 months both as an atrial and ventricular pacemaker. Slow atrial flutter resulted in failure of the pacemaker to capture the myocardium and thus incorrectly suggested pacemaker dysfunction. Transtelephonic evaluation of this phenomenon was particularly difficult and could have resulted in unnecessary replacement of the pacing unit     

Echocardiographic documentation of atrial mechanical systole after dual-chamber pacemaker implantation in a patient without electrically evident atrial activity

Documentation of synchronized atrial transport mechanical systole, after dual-chamber pacemaker implantation is generally not sought clinically. In this patient, no electrical atrial activity was seen after elective revision to dual-chamber from single-chamber pacing. M-mode echocardiography provided definitive proof of proper pacemaker function with intact mechanical atrial systole. Echocardiography should be considered in the postoperative evaluation of patients in whom proper atrial or ventricular mechanical function is in doubt.     

Double-counting of intracardiac electrogram during biatrial pacing.

BACKGROUND: Biatrial pacing has a significant problem with memory function that misinterprets normal sinus rhythm as atrial tachyarrhythmias and in addition estimation of the atrial pacing thresholds (biatrial and uniatrial pacing thresholds) is sometimes difficult because of small P waves. METHODS AND RESULTS: The intracardiac electrograms recorded by a pacemaker in 10 patients (age, 66.7+/-10.7 (SD) years) with implanted biatrial pacemakers were analyzed. Atrial sensing within the atrial refractory period after atrial pacing was counted in 6 of the 10 patients (timing of the double counting was 143+/-64 ms) when pacing failed in the left or right atrium. Atrial sensing within the atrial refractory period after atrial pacing disappeared when biatrial pacing was successfully performed. Atrial double-counts depend on interatrial conduction delay. The memory function of implanted pacemaker devices misinterpreted normal sinus rhythm as atrial tachyarrhythmias because of atrial double-counts. On the other hand, the biatrial pacing threshold was easily recognized using this phenomenon. CONCLUSIONS: The memory function of pacemaker devices is unreliable because of atrial double-counting during sinus rhythm in patients with biatrial pacing. However, the biatrial pacing threshold is easily checked using this phenomenon.     

起搏器置入术后并发房颤的危险因素研究进展

房颤(AF)是临床上最常见的心律失常之一。起搏器置入术后房颤的发生率高于普通人群,其中年龄、高血压、左心房扩大、窦房结综合征(SSS)、起搏模式、心房及心室起搏比例、起搏器置入方式等均是影响起搏器置入术后新发房颤的危险因素。本文针对上述因素影响房颤发生的机制作一综述,以期为临床提早预防房颤提供理论参考。     

Echocardiographic assessment of tricuspid regurgitation during ventricular demand pacing

Twenty patients from our pacemaker clinic population were assessed clinically and by saline contrast echocardiography (subxiphoid view) to determine the prevalence of tricuspid regurgitation (TR) and, if TR was present, its mechanism. The patients had no known TR before lead placement, a single transvenous right ventricular pacing lead present more than 6 months (mean 52, range 7 to 138), ventricular demand pacing alternating with sinus rhythm and rate programmability. Each patient was studied in sinus rhythm and during ventricular pacing. Using the criterion of inferior vena cava (IVC) contrast reflux during ventricular systole to diagnose TR, no patient had evidence of TR in sinus rhythm, consistent with clinical examination. During ventricular demand pacing, jugular venous pulse cannon A waves developed in 10 patients, and 18 patients (including these 10) had IVC contrast reflux during ventricular systole. Analysis of the timing of IVC reflux revealed its close temporal relation to the timing of atrial systole rather than a fixed timing during ventricular systole. This reflux occurred with loss of normal atrioventricular (AV) synchrony and the underlying mechanism in all cases was shown to be right atrial contraction against a closed tricuspid valve. Two patients who did not have such a pattern with pacing maintained normal AV synchrony. These observations indicate that: TR is an uncommon accompaniment of ventricular demand pacing; the jugular venous pulse and IVC echocardiographic contrast patterns during ventricular demand pacing simulate TR when AV asynchrony [corrected] occurs; and the IVC contrast pattern of pacing induced AV asynchrony [corrected] is best termed the cannon A wave synchronous pattern.     

Interaction Between Atrial Pacing Lead and Epicardial Ventricular Wire Resulting in Unintended Ventricular Capture by Pacemaker Atrial Output

A 65-year-old man with a history of coronary artery disease underwent coronary artery bypass grafting in 1997 and 1998. He also received a permanent dual chamber pacemaker implantation during the second bypass surgery for complete heart block. He presented a year later to our pacemaker clinic for follow-up. Initial ECG showed ventricular capture by pacemaker atrial output (bottom tracings, left side). When the atrial output was decreased by 0.5V, normal atrial and ventricular pacemaker function was restored (bottom tracings, right side). A chest X-ray revealed an active fixation atrial lead implanted to the right atrium and a passive fixation lead to the ventricle. There was no apparent insulation failure of either lead by X-ray or by impedance measurements. An epicardial pacing lead implanted during bypass surgery for temporary postoperative pacing was not completely removed. The proximity between the retained epicardial wire and the screw of the active fixation atrial lead (arrow) support the hypothesis that the atrial output was conducted by the retained epicardial wire into the ventricles, resulting in unintended ventricular capture by the atrial output. However, we could not exclude the possibility that the atrial lead directly resulted in ventricular capture due to its proximity to the AV grove.     

Effect of atrial fibrillation on atrial blood flow in conscious dogs

This study was undertaken to examine the independent effects of atrial tachycardia, ventricular tachycardia, and atrial fibrillation (AF) on atrial and ventricular blood flow in conscious, heart-blocked dogs using radioactive microspheres. Atrial blood flow averaged 0.54 ± 0.08 ml/min/g during the control period at an atrial rate of 124 beats/min and a ventricular rate of 90 beats/min. Atrial flow increased to 0.72 ± 0.12 ml/min/g during atrial pacing at 236 beats/min, but was not significantly altered by ventricular pacing at 200 beats/min. AF at a ventricular rate of 90 beats/min resulted in atrial flow values of 0.91 ± 0.08 ml/min/g. The ratio of atrial flow to left ventricular flow during AF averaged 1.18 ± 0.08. Administration of a maximal vasodilating dose of adenosine during AF further increased atrial flow to 2.18 ± 0.16 ml/min/g. Atrial tachycardia or AF did not significantly affect ventricular blood flow. These data indicate (1) that atrial blood flow increases significantly during AF, reaching flow values per gram of tissue comparable to those of the left ventricle, and (2) that this flow is regulated by the metabolic needs of the atrial tissue and does not represent maximal vasodilation.     

Efficacy of atrial antitachycardia pacing using the Medtronic AT500 pacemaker in patients with congenital heart disease

Patients with congenital heart disease are vulnerable to atrial tachyarrhythmias, especially after atrial surgeries. We evaluated the efficacy of atrial arrhythmia detection and antitachycardia pacing (ATP) using the Medtronic AT500 pacemaker in 28 patients with congenital heart disease (age 30 +/- 18 years). Of 15 patients with atrial arrhythmias, 14 had atrial tachycardia events that were appropriately detected. ATP was enabled for 167 treatable episodes, successfully converting 90 (54%). Rhythms classified as ventricular tachycardia were detected 127 times, yet most were actually atrial or sinus tachycardia with 1:1 atrioventricular conduction. Atrial tachycardias in congenital heart disease are amenable to ATP algorithms in the AT500 pacemaker.     

Reduction of cardiac ejection fraction as a problem of pacemaker treatment

Ventricular pacing often is associated with a decrease of left ventricular output leading to symptoms of diminished cerebral perfusion. This is caused by a loss of properly timed atrial systole. The contribution of the atrial contribution of the atrial contraction to left ventricular output can reach 40% especially in patients with myocardial failure. A particular diminution of cardiac performance can be observed when ventriculoatrial conduction follows ventricular pacing. AV-sequential pacing, however, with a coordinated atrial systole leads to an obvious increase of cardiac output.     

Atrial pacing for the prevention and termination of atrial fibrillation

Atrial fibrillation (AF) affects about 2% of the general population and 8%–11% of those older than 65 years. The demand for effective therapeutic strategies for AF is anticipated to increase substantially as the proportion of the elderly population increases. Atrioventricular nodal ablation accompanied by permanent pacemaker implantation is an established option in elderly patients with intractable arrhythmia and poor ventricular rate control. However, it renders most patients pacemaker dependent and does not eliminate symptoms associated with loss of atrial transport or reduce the risk of stroke. The considerable limitations of rhythm or rate control strategies prompted interest in preventative atrial pacing, which may reduce the incidence of AF by either eliminating the triggers and/or by modifying the substrate of AF. Atrial or dual-chamber pacing has been proven to prevent or delay progression to permanent AF in elderly patients with sinus node dysfunction as compared with ventricular pacing. Patients with advanced atrial conduction delay may benefit from 'atrial resynchronization' pacing. There may be additional benefits associated with the use of particular sites of pacing, specific pacing algorithms designed to target potential triggers of AF, and pace-termination of atrial tachycardia. Preventive and antitachycardia pacing algorithms incorporated in implantable cardioverter-defibrillators and pacemakers are currently under investigation and may offer a valuable alternative to antiarrhythmic drug therapy in elderly patients with left ventricular dysfunction at high risk of proarrhythmia or worsening heart failure. The evolution of 'hybrid' therapy, in which two or more different strategies are employed in the same patient, may be the most effective approach to management of AF.     

Problems of artificial pacemaker therapy

Four hundred and sixty-seven cases with implantation of an artificial pacemaker were studied. The postoperative survival rate was 63% for 15 years. Seventy-two percent of type III patients of the sick sinus syndrome were free from postoperative thromboembolism and the lowest of the three types of the sick sinus syndrome. Comparing postoperative physical activity, cardiothoracic ratio and exercise tolerance time, physiological pacing was superior to ventricular pacing in hemodynamic effects and clinical symptoms. In a hundred cases of physiological pacing, complications and problems of physiological pacing were discussed. Atrial sensing failure and over-sensing were observed in seven and two cases respectively. A low amplitude of atrial potential and use of unipolar atrial leads were considered to be the main causes of these complications. Bipolar lead should be used as the atrial lead to avoid such complications, because the atrial potential by bipolar leads is not less than that by unipolar leads. Atrial sensing may be more sensitive without electromagnetic interference. The fixed A-V delay time whenever the atrium is sensed or paced, often results in a ventricular fusion beat and hemodynamic change on every beat, according to the interval of atrial and ventricular contractions. The A-V delay time should be changed in accordance with atrial sensing or pacing.     

具有心房自动阈值管理功能起搏器在病窦综合征患者中的临床应用

目的观察具有心房自动阈值管理功能起搏器在病窦综合征患者中的临床应用情况。方法18例病窦综合征患者置人具有心房自动阈值管理功能起搏器（Enpulse系列7例,Sensial系列5例,Adapta系列6例）,于置入时,置入后1周、1个月、6个月采用起搏分析仪及体外起搏器程控仪测定心房起搏阈值和阻抗,利用ACM进行术后阈值和阻抗的动态观察。结果测定的心房阈值与ACM测定值差异无统计学意义;心房起搏阈值均〈1．0V,心房起搏阈值于置入1个月后有下降趋势,阻抗未见明显变化。预期使用寿命6个月时测定为（8．7±2．4）年。结论病窦综合征患者置入具有心房自动阈值管理功能的起搏器心房起搏安全有效,起搏器预期使用寿命延长。     

Beneficial effects of biatrial pacing on cardiac function in patients with bradycardia -- tachycardia syndrome.

BACKGROUND: Biatrial (BiA) pacing prevents atrial fibrillation. By an unknown mechanism. The purpose of this study was to use Doppler echocardiography to evaluate the hemodynamic effects during BiA pacing. METHODS AND RESULTS: The subjects were 7 patients with bradycardia - tachycardia syndrome with an implanted pacemaker. Atrial pacing sites were the right atrial appendage (RAA) and coronary sinus. P wave duration during BiA pacing (123 +/-16 ms) was significantly shorter than during either RAA pacing (167+/-19 ms, p<0.05) or sinus rhythm (148+/-12 ms, p<0.05). Doppler echocardiography revealed a greater cardiac output during BiA pacing than during RAA pacing (4.1+/-1.1 vs 3.5+/-0.7 L/min, p=0.042). The Doppler waveform of transmitral flow indicated that the left ventricular contraction interrupted the atrial filling wave during RAA pacing. The interval between the end of the atrial filling wave of transmitral flow and the mitral valvular closing sound was significantly increased by BiA pacing compared with RAA pacing (56+/-65 vs 40+/-57 ms, p=0.047). CONCLUSION: Cardiac hemodynamics were improved by BiA pacing and reduction of left atrial load may be one of the mechanisms.