快速右房起搏心房颤动动物模型的建立

目的探讨经快速右房起搏方法制作犬心房颤动动物模型的可行性。方法11只健康杂种犬经右侧颈外静脉途径植入埋藏式高频率心脏起搏器,VOO模式快速(350~430次/m in)起搏右心房8周。观察房颤诱发情况,对起搏前后心电图、超声心动图及电生理检查结果进行比较。结果8只犬完成实验。术后8周停止起搏时出现自发性房颤2只,经程序刺激诱发出房颤4只,爆发刺激诱发出房颤2只,房颤总诱发率100%。结论经快速右房起搏方法制作心房颤动动物模型成功率高、重复性好;可用于房颤发病机理、电生理重构、心肌重构、分子生物学改变等临床研究,也可用于心动过速性心肌病及部分心力衰竭的研究。     

InSync 8040起搏器在充血性心力衰竭治疗中的初步应用

观察InSync 80 40起搏器治疗扩张型心肌病 (DCM)伴充血性心力衰竭 (CHF)的疗效。 8例DCM伴CHF患者 ,男 7例、女 1例。其中伴完全性左束支阻滞 6例 ,左前分支阻滞、右室起搏后宽QRS波 (>0 .2 0s)各 1例。通过冠状静脉窦置入 2 187电极起搏左室 ,右房电极和左、右室电极分别与InSync 80 40起搏器A、V1、V2 孔相连接。术后起搏阈值 3.75± 0 .6 (3.0～ 5 .0 )V。患者CHF的症状明显改善 ,术后左室舒张末径、左室射血分数、左室短轴缩短率、心胸比例较术前均有改善 (分别为 6 6 .1± 6 .93mmvs 72 .5± 8.1mm、0 .374± 0 .0 31vs 0 .2 81± 0 .0 5 3、19.8%± 2 .2 %vs12 .2 %± 2 .7%、0 .5 9± 0 .4vs 0 .6 4± 0 .2 0 ;P均 <0 .0 5 )。结论 :初步临床应用表明 ,以InSync 80 40起搏器行双心室同步起搏治疗CHF疗效肯定     

Chest wall stimulation by pin electrodes in patients with implanted demand pacemakers

In order that we might inhibit their implanted units, 30 patients with permanent R-wave inhibited demand pacemakers underwent chest wall stimulation by impulses delivered from an external pacemaker, first through skin electrodes and then, in the identical positions, through fine platinum subcutaneous pin electrodes of the type used in electroencephalography. A comparison of the suppression characteristics of these electrodes is reported.Both techniques were uniformly successful at low impulse amplitude for the five unipolar pacemakers. In bipolar pacemakers, suppression was achieved in 24 of 25 by pin electrodes, in nine of 25 by skin electrodes, and in one by neither. Of the nine bipolar pacemakers suppressed by both methods, six needed more current amplitude for skin electrodes, while three needed equal current amplitude. In 27 patients the spontaneous rhythm and QRST configuration were determined. One patient had P-waves only and one had no spontaneous electrical activity.Chest wall stimulation through pin electrodes provides a quick, safe, and predictable means of suppressing the R-wave inhibited demand pacemaker.     

Electrocardiographic predictive factors of long-term clinical improvement with multisite biventricular pacing in advanced heart failure

Biventricular pacing has recently been proposed for treating patients with drug refractory heart failure and intraventricular conduction delay. The purpose is to restore ventricular relaxation and contraction sequences as homogeneously as possible. The aim of this study was to determine if some factors could predict the long-term clinical effectiveness of that new treatment. This study included 26 patients, aged 66 ± 7 years, with drug refractory heart failure and wide QRS. Patients were implanted with a biventricular pacemaker. The left ventricle was paced through a coronary sinus tributary. New York Heart Association functional class, exercise tolerance, and left ventricular (LV) ejection fraction were collected at baseline and after pacemaker implantation. Patients were divided into 2 groups: group I = responders; group II = nonresponders. QRS duration and axis at baseline and during biventricular pacing, interventricular conduction time, and LV and right ventricular lead positions were compared between the 2 groups. Group I patients (n = 19) had a mean reduction of 1.3 in functional class and an increase in peak oxygen consumption rate by a mean of 50%. The only parameter that differed between the 2 groups was the QRS duration during biventricular pacing, with a significantly shorter value in group I than in group II (154 ± 17 vs 177 ± 26 ms; p = 0.016). Thus, a positive response to biventricular pacing is correlated with the quality of electrical resynchronization. The optimal positions of the right and LV leads would be those that could induce the greatest shortening of QRS duration.     

Chest wall stimulation for temporary suppression of competitive rhythms due to permanent pacemaker malfunction.

Chest wall stimulation by electrical stimuli was employed to suppress permanent demand (ventricular-inhibited) pacemakers in two patients with competitive ventricular rhythms. The stimuli were nor perceived by either patient, and were continued until surgical intervention was effected. In selected patients with permanent pacemaker malfunction, chest wall stimulation may be appropriate and necessary initial therapy until definitive correction is performed.     

Electrocardiographic Follow‐Up of Biventricular Pacemakers

Multisite pacing for the treatment of heart failure has added a new dimension to the electrocardiographic evaluation of device function. During left ventricular (LV) pacing from the appropriate site in the coronary venous system, a correctly positioned lead V1 registers a right bundle branch block pattern with few exceptions. During biventricular stimulation associated with right ventricular (RV) apical pacing, the QRS is often positive in lead V1. The frontal plane QRS axis is usually in the right superior quadrant and occasionally in the left superior quadrant. Barring incorrect placement of lead V1 (too high on the chest), lack of LV capture, LV lead displacement or marked latency (exit block or delay from the stimulation site), ventricular fusion with the spontaneous QRS complex, a negative QRS complex in lead V1 during biventricular pacing involving the RV apex probably reflects different activation of an heterogeneous biventricular substrate (ischemia, scar, His‐Purkinje participation in view of the varying patterns of LV activation in spontaneous left bundle branch block) and does not necessarily indicate a poor (electrical or mechanical) contribution from LV stimulation. In this situation, it is imperative to rule out the presence of coronary venous pacing via the middle cardiac vein or even unintended placement of two leads in the RV. During biventricular pacing with the RV lead in the outflow tract, the paced QRS in lead V1 is often negative and the frontal plane paced QRS axis is often directed to the right inferior quadrant (right axis deviation). In patients with sinus rhythm and a relatively short PR interval, ventricular fusion with competing native conduction during biventricular pacing may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate biventricular capture. This represents a common pitfall in device follow‐up. Elimination of ventricular fusion by shortening the AV delay, is often associated with clinical improvement. Anodal stimulation may complicate threshold testing and should not be misinterpreted as pacemaker malfunction. One must be cognizant of the various disturbances that can disrupt 1:1 atrial tracking and cause loss of ventricular resynchronization. (1) Upper rate response. The upper rate response of biventricular pacemakers differs from the traditional Wenckebach upper rate response of conventional antibradycardia pacemakers because heart failure patients generally do not have sinus bradycardia or AV junctional conduction delay. The programmed upper rate should be sufficiently fast to avoid loss of resynchronization in situations associated with sinus tachycardia. (2) Below the programmed upper rate. This may be caused by a variety of events (especially ventricular premature complexes and favored by the presence of first‐degree AV block) that alter the timing of sensed and paced events. In such cases, atrial events become trapped into the postventricular atrial refractory period at atrial rates below the programmed upper rate in the presence of spontaneous AV conduction. Algorithms are available to restore resynchronization by automatic temporary abbreviation of the postventricular atrial refractory period.     

Pseudo failure of sensing in patients with universal pacemakers and junctional rhythms

Ventricular fibrillation has been only rarely observed as a complication of cardiac pacing after the advent of demand pacemakers. Automatic AV sequential pacing (DDD) may provide the setting for ventricular fibrillation in patients with junctional rhythms. In this report we present two patients with implanted DDD pacemakers in whom ventricular pacemaker spikes were seen occurring on top of the T wave during episodes of junctional rhythm. This apparent lack of sensing of QRS complexes does not represent pacemaker malfunction, but rather, is the result of physiologic lack of sensing (blanking) which occurs 56 to 100 msec. following the output of the atrial and ventricular channels. During junctional rhythm when the atrial spike occurs at the beginning of a QRS complex the ventricular channel is blanked and does not sense the intrinsic ventricular activity and thus, ventricular output occurs during repolarization. Increasing the maximum pacemaker rate and decreasing the AV delay will reduce the chance occurrence of this phenomenon.     

Assessment of regional wall motion using strain Doppler imaging during right ventricular bifocal pacing in a patient with severe congestive heart failure: a case report

A 79-year-old man presented with dilated cardiomyopathy and chronic atrial fibrillation. A DDD pacemaker was implanted due to sick sinus syndrome. His left ventricular ejection fraction was 23%. He was repeatedly admitted with congestive heart failure. Although cardiac resynchronization therapy was attempted, insertion of a pacing lead into the coronary sinus failed. Right ventricular bifocal pacing was done. The QRS width was shortened to 155 msec during bifocal pacing and 157 msec during right ventricular outflow pacing from 221 msec during right ventricular apical pacing. Heart failure was improved from New York Heart Association class III to II. Regional wall motion was assessed by strain of the myocardium. Bifocal pacing increased stroke volume due to improvement of longitudinal dyssynchrony of the septal and lateral walls. Bifocal pacing is effective for patients with severe congestive heart failure in whom biventricular pacing therapy has failed. Strain Doppler imaging is useful for the assessment of regional wall motion during cardiac pacing.     

The feasibility of utilizing the systolic pre-ejection interval as a determinant of pacing rate

Rate-modulated pacing modes adjust the stimulus rate by responding to sensed alterations in physiologic indexes of metabolic demand. This study was designed to determine whether right ventricular pre-ejection interval, measured in patients by a prototype pacemaker system capable of tracking intraventricular volume, changes predictably with exercise and, if so, whether it can be used in an algorithm to vary heart rate appropriately. This system utilizes intraventricular electrical impedance measurements of injected microampere currents to determine intracavitary volume changes. Five pacemaker-dependent patients underwent temporary insertion of a tripolar electrode connected to an external device that sensed cardiac signals, generated an impedance wave form and produced stimuli at rates dependent on pre-ejection interval. Pre-ejection interval did not change as a result of variations in pacing rate itself (347 +/- 41 ms at 70 beats/min versus 321 +/- 19 ms at 130 beats/min), but consistently decreased during graded exercise (by 23% from baseline). During rate-modulated pacing based on pre-ejection interval, heart rate significantly increased during exercise compared with ventricular demand pacing (by 46 +/- 6 versus 7 +/- 6 beats/min, respectively), and increased appropriately during burst exercise. Thus, the pre-ejection interval appears to be a specific, reliable physiologic determinant of pacing rate during exertion, which may be applicable in implantable rate-modulated pacemakers.     

Right ventricle bipolar pacing may prevent appropriate biventricular pacing from two pacemakers: Case Report

This article reports on practical problems and possible solutions that may occur in case of upgrading a dual-chamber pacemaker by implanting a second left ventricular ventricular pacing, ventricular sensing, ventricular triggering (VVT) pacemaker. This therapeutic strategy was considered appropriate in the case of a 73-year-old patient with severe heart failure, who was scheduled to undergo coronary artery bypass surgery. A right-sided, dual-chamber pacemaker had been already implanted to the patient. The duration of the paced QRS complex was 220 ms and inter- and intraventricular dyssynchrony was documented in the echocardiographic study. We describe the methodological problems and possible solutions related to biventricular pacing following the abovementioned strategy.     

Right ventricle bipolar pacing may prevent appropriate biventricular pacing from two pacemakers. Case report

This article reports on practical problems and possible solutions that may occur in case of upgrading a dual-chamber pacemaker by implanting a second left ventricular ventricular pacing, ventricular sensing, ventricular triggering (VVT) pacemaker. This therapeutic strategy was considered appropriate in the case of a 73-year-old patient with severe heart failure, who was scheduled to undergo coronary artery bypass surgery. A right-sided, dual-chamber pacemaker had been already implanted to the patient. The duration of the paced QRS complex was 220 ms and inter- and intraventricular dyssynchrony was documented in the echocardiographic study. We describe the methodological problems and possible solutions related to biventricular pacing following the abovementioned strategy.     

Termination of recurrent supraventricular tachycardia by right ventricular endocardial pacing but not by left ventricular epicardial pacing

Externally controlled ventricular pacing was employed in a patient with recurrent disabling supraventricular tachycardia and frequent sinus pauses between attacks of tachyarrhythmia. A permanent transthoracic demand pacemaker was inserted after electrophysiologic study demonstrated the effectiveness of ventricular stimulation in terminating induced supraventricular tachycardia. Subsequently, spontaneous recurrences of tachyarrhythmia failed to respond to fixed rate left ventricular stimulation accomplished by placing a magnet externally over the pacemaker pack. During an induced supraventricular tachycardia, repeat electrophysiologic study demonstrated that paced left ventricular beats failed to invade the A-V junctional area before it was depolarized previously by the corresponding tachycardia beat. Right ventricular stimulation from a transvenous pacemaker could depolarize the site of the reentrant circuit and terminate an induced supraventricular tachycardia. The addition of propranolol increased the ease by which spontaneous attacks of tachyarrhythmia could be terminated by right ventricular endocardial pacing.     

Sudden death of a patient with a pacemaker caused by heart rupture in a "cloisonné" pericardium

Myocardial infarction is sometimes accompanied by bradycardia requiring either temporary or permanent cardiac pacing. In addition an MI reduces the amplitude of endocardial action potentials which produces the conditions for defective detection of spontaneous ventricular complexes by the pacemaker. In this particular condition, the competing cardiac rhythm which arises frequently causes malignant arrhythmias which are potentially fatal. This danger is increased even further by endocardial stimulation of the right ventricle with myocardial infarction of the right ventricle. We have reported in this paper the instructive case of a patient with coronary heart disease, hospitalized for third degree AV block with syncope which developed following a massive postero-diaphragmatic MI, but with few symptoms. After secondary extension of the necrotic area, the artificial pacemaker implanted manifested defective firing which resulted in development of ventricular fibrillation. The latter was controlled by cardioversion, but the patient died from disordered conduction after 30 seconds of complete asystole. For one minute, the pacemaker did not stimulate the ventricle because of "electrical stunt to the myocardium", caused by the shock from the defibrillator. Anatomical examination (at autopsy) confirmed the cardiac rupture.     

Unique Interaction Between an Atrial Single-Chamber Pacemaker and a Ventricular Defibrillator

A well described interaction between an antibradycardia pacemaker and a ventricular defibrillator is sensing of pacemaker stimuli by the ventricular defibrillator. This report describes an interaction between an atrial demand pacemaker and a ventricular defibrillator that resulted in ventricular asystole and polymorphic ventricular tachycardia. In this case, the ventricular defibrillator sensed atrial pacing stimuli when complete atrioventricular block with a slow ventricular escape rate developed. Defibrillator-based ventricular demand pacing was inhibited, resulting in prolonged periods of ventricular asystole, polymorphic ventricular tachycardia, and multiple defibrillator shocks. Ventricular defibrillator sensing of atrial pacemaker stimuli in the setting of complete atrioventricular block and ventricular asystole cannot be simulated during defibrillator implantation when atrioventricular conduction is intact. Therefore, a pacemaker programmed to atrial demand pacing in a patient with a ventricular defibrillator can result in inappropriate inhibition of ventricular pacing in the setting of complete heart block. Furthermore, this interaction can be avoided with a dual-chamber pacing ventricular defibrillator.     

Asynchronism and right ventricular pacing

In patients with congenital heart block (CHB), dual-chamber pacing restores physiological heart rate and atrio-ventricular synchronization. However, patients with narrow QRS junctional escape rhythm may be deleteriously affected by long-term, permanent, apical ventricular pacing. We assessed the impact of apical ventricular pacing on echocardiographic ventricular dyssynchrony and hemodynamic parameters. METHODS: Fourteen CHB adults (23 +/- years, 58% male), with a DDD transvenous pacemaker and a junctional escape rhythm (QRS<120 ms) before implantation, were studied. Echocardiography coupled with tissue Doppler imaging (TDI) and Strain rate was performed in spontaneous rhythm (VVI mode 30/mn) and during atrio-synchronized ventricular pacing. RESULTS: The heart rate (43 +/- 09 vs 68 +/- 07: p<0.01), cardiac output (2.9 +/- 0.7 vs 3.7 +/- 0.6 L/min) and left ventricular filling time (325 +/- 38 vs 412 +/- 51 ms; p<0.01) were significantly less in the escape spontaneous rhythm compared with atrio-ventricular synchronized apical pacing. However, interventricular dyssynchrony (28 +/- 12 vs 59 +/- 25 ms, p<0.05), intra-left ventricular dyssynchrony (36 +/- 11 vs 57 +/- 29 ms; p<0.05), extent of left ventricular myocardium displaying delayed longitudinal contraction (26 +/- 10 vs 39 +/- 17%: p<0.05) were significantly less in the escape rhythm compared with paced rhythm. CONCLUSION: Once implanted with a DDD pacemaker, CHB patients present with increased cardiac output secondary to the restoration of physiological heart rate and improved diastolic function. However, the apical site is not optimal, as it creates detrimental ventricular dyssynchrony in patients with previous nearly physiological ventricular activation. Alternative pacing sites should be investigated.     

经CT定位不同部位间隔起搏的心电图特征分析

目的 探讨不同间隔部位起搏的体表心电图特征.方法 观察31例永久性心脏起搏器间隔起搏患者体表心电图特征,使用64排双源CT精确定位起搏导线在间隔部的具体位置,比较不同位置间隔起搏的心电图参数变化.结果 ①仅根据X线植入的起搏导线,起搏导线误置于前壁的占12.9%.②前壁起搏的QRS间期（148±19）ms,宽于高位间隔起搏QRS间期（118±24）ms（P＜0.05）.③中位间隔起搏QRS波群移行6.00±0.76,晚于高位间隔（4.13±1.56）和低位间隔（3.75±2.99）（均P＜0.05）.④高位间隔起搏RIII（1.11±0.70）mV,大于低位间隔起搏RⅢ（0.038±0.075）mV（P＜0.05）.⑤高位间隔起搏（46.7%）及中位间隔起搏（37.3%）I出现q波或QS的比例有多于前壁起搏的趋势.结论经CT定位不同部位间隔起搏的体表心电图存在明显不同,一些参数有助于判断导线位置.     

External cardiac pacing in right ventricular infarction

A patient with acute inferior wall myocardial infarction presented with clinical evidence of right ventricular infarction complicated by bradycardia and cardiogenic shock. Pharmacologic interventions produced no change in heart rate or blood pressure, and a transvenous pacemaker failed to capture the infarcting right ventricle. An external transthoracic pacemaker immediately increased the heart rate with a marked hemodynamic improvement. In the setting of right ventricular infarction, external pacing may be more effective than transvenous pacing, perhaps due to its ability to pace the left ventricle.     

Placement of permanent epicardial pacemaker in a newborn with congenital complete AV block

Isolated congenital atrioventricular block is reported in one out of 20,000 live births. The optimistic view on the prognosis and indications for permanent pacing have been modified in the last 35 years. The purpose of this report is to present a prenatally diagnosed case, outlining the surgical technique for permanent pacing. The infant was a male born by cesarean section, weighted 3030 grs and had a structurally normal heart. His ECG showed complete AV block with narrow QRS, atrial rate was 140 and ventricular rate was 55. We implanted a epicardial pacemaker VVIR by midline laparatomy. The lead was unipolar 35 cms long screw-in type and was placed in the right ventricle through the xiphoid process. The pacemaker was placed in a GoreTex bag and fixed intraperitoneal to the abdominal wall. The infant did well after the procedure and he was discharged in good condition one week later. We conclude that it is appropriate to implant a permanent pacemaker in these patients with low ventricular rate thus reducing the risk of sudden cardiac death. The surgical technique is safe and makes easy the generator replacement.     

Use of temporary pacemaker programming in VVT mode for the treatment of recurrent ventricular tachycardia

This is a report of a 59-year-old man with a Bj?rk aortic prosthetic valve and mitral commissurotomy with left ventricular dysfunction and recurrent ventricular tachycardia (VT) in spite of antiarrhythmic therapy with amiodarone. Serial electrophysiologic studies were performed using standard ventricular extrastimulation technique. During these studies, sustained VT was induced and terminated by programmable extrastimulus pacing. The usual rhythm of the patient was atrial fibrillation with slow ventricular rate. The Medtronic Spectrax model 5985 pulse generator was implanted. A temporary program converts this device from inhibited (VVI) to triggered (VVT) mode, permitting programmed ventricular stimulation through synchronization with chest wall stimulation by a standard external programmable stimulator. During episodes of VT the pacemaker was temporary programmed to the VVT mode with a refractory period of 220 msec. With the chest wall stimulation by a electrophysiology stimulator it was possible to convert the VT with 2 or 3 synchronised extra stimulus. Thanks to the triggered mode the pacemaker will fire when the chest wall is stimulated, working as an external electrophysiology stimulator.     

Loss of Left Bundle Branch Block following Biventricular Pacing Therapy for Heart Failure: Evidence for Electrical Remodeling?

Cardiac resynchronization therapy has been proven to improve symptoms and indices of left ventricular function in patients with heart failure and intraventricular conduction delays. We present a case of a patient with New York Association Class III heart failure and left bundle branch block, who received a biventricular pacemaker in order to achieve cardiac resynchronization. Her symptoms improved markedly, as did left ventricular ejection fraction and dimensions. In addition, her intrinsic QRS duration normalized. This may represent a salutory effect of biventricular pacing on electrical remodeling.