The Effect of Ventricular Activation Sequence on Cardiac Performance During Pacing

The aim of this study was to evaluate the importance of a normal ventricular activation pattern for cardiac performance. In nine mongrel clogs, atrial pacing was compared to AV synchronous pacing at three different A V delays (150, 100, and 60 nis). In six dogs, proximal septal AV synchronous pacing was compared to apical A V synchronous pacing at three different A V delays. AV synchronous pacing was performed after RF induced complete heart block. Hemodynarnics were evaluated by assessment of positive and negative dP/dt, cardiac output, and left ventricular and pulmonary pressures. Atrial pacing was superior to AV synchronous pacing with respect to positive and negative dP/dt and cardiac output. This difference was present at all AV delays. Proximal septal pacing was associated with a higher positive and negative dP/dl compared to apical pacing at all AV delays. Left ventricular activation time was significantly shorter during proximal septal pacing than during apical pacing (88 ± 4 vs 115 ± 4 ms, P < 0.001). We conclude that atrial and proximal septal pacing improves cardiac function and shortens the ventricular activation time compared to apical AV synchronous pacing independent of the AV interval.     

Hemodynamic effect of the ventricular pacing site in fetal lambs with complete atrioventricular block

Complete atrioventricular (AV) block in hydrops fetalis is associated with high mortality. Fetal ventricular pacing to restore ventricular rate can be an effective procedure, however, no fetal data has shown an appropriate epicardial ventricular pacing site. To evaluate the hemodynamic effect of right and left ventricular pacing in fetal lambs with complete AV block, a fetal complete AV block model was created. Aortic pressure, central venous pressure, and QRS duration were measured, and right and left ventricular output was estimated in seven fetal lambs. The uterus was opened under maternal anesthesia, and under local anesthesia, catheters were inserted into the fetal superior vena cava and ascending aorta through a neck incision. Pacing leads were then sutured onto the fetal right and left ventricular epicardium via a midline thoracotomy. Complete AV block was created by cryoablation of the AV node. Ventricular output was estimated using echocardiography by a transuterine approach. Fetal hemodynamics were observed before AV block creation (control), and after complete AV block creation with the right and left ventricular pacing set at 150/min. The right ventricular output was 320 +/- 66 mL/kg per minute at control, decreased to 243 +/- 65 mL/kg per minute during right ventricular pacing (P < 0.05), and was 254 +/- 61 mL/kg per minute during left ventricular pacing. The left ventricular output was 224 +/- 98 mL/kg per minute at control, 176 +/- 77 mL/kg minute during right ventricular pacing, and 178 +/- 67 mL/kg per minute during left ventricular pacing. Biventricular (combined ventricular) output was 544 +/- 134 mL/kg per minute at control, 419 +/- 114 mL/kg per minute during right ventricular pacing, and 432 +/- 100 mL/kg minute during left ventricular pacing. Systolic aortic pressure was 62.2 +/- 8.7 mmHg at control, 55.2 +/- 9.5 mmHg during right ventricular pacing, and 53.4 +/- 9.1 mmHg during left ventricular pacing. Central venous pressure (CVP) was 2.6 +/- 0.5 mmHg at control, 4.0 +/- 2.7 mmHg during right ventricular pacing, and 4.4 +/- 2.5 mmHg during left ventricular pacing. The QRS duration was 51 +/- 54 ms at control, but lengthened to 87 +/- 19 ms during right ventricular pacing and to 78 +/- 21 ms during left ventricular pacing (P < 0.05). In conclusion, the right ventricular output decreased during right ventricular pacing in fetal lambs with complete AV block, while it was preserved during the left ventricular pacing. Left ventricular pacing might be superior for treating hydropic fetuses with complete AV block.     

Origin of electrical activation within the right atrial and left ventricular walls: differentiation by electrogram characteristics using the noncontact mapping system

Clinical data using the noncontact mapping system (Ensite 3000) suggest that characteristics of the reconstructed unipolar electrograms may predict the origin of electrical activation within the atrial and ventricular walls (endocardial vs myocardial vs epicardial origin). Experimental data are lacking. In ten open-chest pigs (mean body weight 62 kg) cardiac pacing was performed at a cycle length of 600 ms with a pulse width of 2 ms and twice diastolic threshold from the endo-, the myo-, and the epicardium, respectively. Pacing was undertaken at three right atrial and three left ventricular sites, and cardiac activation was recorded with the Ensite system. Reconstructed unipolar electrograms at the location of earliest endocardial activation assessed by color coded isopotential maps were analyzed systematically for differences in morphology. The positive predictive value of atrial electrograms exhibiting an initial R wave during pacing for a subendocardial origin (i.e., myocardial or epicardial) was 0.96. The negative predictive value was 0.48. Electrograms generated during myocardial pacing exhibited increased maximal negative voltage and maximal dV/dt (-3 +/- 1.8 mV, -798 +/- 860 mV/ms, respectively) than the electrograms obtained during endocardial (-2 +/- 1 mV, -377 +/- 251 mV/ms, respectively) and epicardial pacing (-2.1 +/- 0.7 mV, -440 +/- 401 mV/ms, respectively, P<0.01 for both parameters). During pacing at the left ventricular wall, occurrence of an initial R wave did not differ significantly between electrograms reconstructed during endocardial and subendocardial pacing. All other characteristics of the unipolar ventricular electrograms analyzed, except latency, did not differ significantly when compared to stimulation depth. Morphological characteristics of unipolar electrograms generated by the noncontact mapping system during pacing of the atrium allowed for discrimination of an endocardial versus a subendocardial origin of activation. At the ventricular level, characteristics of unipolar electrograms did not predict the origin of cardiac activation in this experimental setting.     

Distinct Activation Patterns of Idioventricular Rhythms and Sympathetically-Induced Ventricular Tachycardias in Dogs with Atrioventricular Block

To investigate mechanisms of ventricular impulse formation in response to sympathetic stimulation in the healthy canine heart in situ, we compared the patterns of ventricular activation during the idioventricular rhythms arising after complete atrioventricular (AV) block and ventricular tachycardias induced by RSG or LSG stimulation. Isochronal maps were generated by computer from 116-127 unipolar electrograms recorded from the entire ventricular epicardium in 15 open chest, anesthetized dogs. In eight of these, bipolar electrograms were recorded with plunge electrodes from 11 selected endocardial sites located below epicardial breakthrough areas. Intracardiac recordings from the His-Purkinje system were made with electrode catheters. After electrograms were recorded during sinus rhythm, complete AV block was induced by injecting formaldehyde into the AV node and idioventricular rhythms occurred spontaneously at a rate of 37 +/- 12 beats/min (mean +/- SD, n = 25). During idioventricular rhythms, endocardial activation preceded the earliest epicardial breakthrough, which occurred in either the right anterior paraseptal region, antero-apical left ventricle, or postero-apical left ventricle. These sites were consistent with a focal origin in the subendocardial His-Purkinje system. Total epicardial activation times lasted for 47 +/- 13 msec (n = 40). Idioventricular rhythms were suppressed by overdrive pacing (intermittent trains of ten beats with decremental cycle length from 500 to 200 msec) or by intravenous calcium infusion (to plasma levels of 10.1-15.2 mM). Right or left stellate ganglion stimulation increased idioventricular rhythm rates (to 52 +/- 13 beats/min, n = 28) and also induced, in all preparations, ventricular tachycardias that had significantly faster rates (189 +/- 55 beats/min, n = 27, P less than 0.005). Ventricular fibrillation was induced after brief runs of ventricular tachycardia in five of the preparations. During ventricular tachycardias, epicardial activation occurred on the right ventricular outflow tract or the postero-lateral wall of the left ventricle, and preceded endocardial activation in 50% of cases. Total epicardial activation times (103 +/- 29 beats/min) were significantly longer than during idioventricular rhythms (P less than 0.005). Ventricular tachycardias displayed overdrive excitation at critical pacing cycle lengths (360-280 msec) and were not suppressed by calcium infusion. Thus, differential mechanisms of impulse formation with distinct localizations can be elicited from healthy ventricular myocardium.     

Atrial pacing lead location alters the effects of atrioventricular delay on atrial and ventricular hemodynamics

The combined role of atrial pacing lead location and AV timing on cardiovascular performance has not been defined. This study tested the hypothesis that atrial pacing lead location can change the dependence of LA and LV hemodynamics on AV timing in vivo. Dogs anesthetized with isoflurane (n = 8) were instrumented for measurement of hemodynamics including LA pressure, LA volume, and pulmonary venous bloodflow. Data were recorded during normal sinus rhythm, and atrial overdrive pacing from the right atrial appendage (RAA), proximal coronary sinus (CS), and LA lateral wall (LAW). The AV node was then ablated and measurements repeated during synchronous ventricular pacing and during dual chamber pacing from each atrial lead location at various AV delays (20, 60, 120, 180, 240, and 350 ms). Hemodynamics during intrinsic sinus rhythm and overdrive atrial pacing from different sites were similar. In contrast, ventricular or dual chamber pacing caused significant (P < 0.05) changes in cardiac output with different AV timing during RAA (3.5 +/- 0.2 vs 2.9 +/- 0.2 L/min at 120 and 350 ms, respectively) and LAW pacing but not CS pacing. A significant interaction between atrial lead location and AV delay was observed for changes in stroke volume, pulmonary venous blood transport, LA volume, and LV preload. The results indicate that the atrial contribution to cardiac output depends on AV timing and atrial lead location in isoflurane-anesthetized dogs with AV nodal conduction block.     

Importance of the Site of Ventricular Tachycardia Origin on Left Ventricular Hemodynamics in Humans

Experimental animal data have indicated that the site of ventricular tachycardia origin and, hence, the degree of asynchronous contraction, may influence the hemodynamic tolerance during sustained ventricular tachycardia. However, data in man are scarce. We studied patients with preserved left ventricular function and absence of significant coronary artery disease. Ventricular tachycardia was simulated with rapid pacing (at 120 and 150 beats/min), performed randomly, from the right ventricular apex or the right ventricular outflow tract. Following pacing from one site, it was repeated from the alternate site. Compared to outflow tract pacing, QRS duration was significantly longer during rapid pacing from the apex. Left ventricular pressure was recorded using a micromanometer-tipped catheter. During sinus rhythm, peak systolic pressure was 142 ± 14 mmHg: at 120 beats/min, it decreased to 109 ± 12 mmHg during pacing from the apex and to 127 ± 21 mmHg during pacing from the outflow tract (P = 0.008). This difference diminished at 150 beats/min (101 ± 16 mmHg vs 112 ± 16 mmHg, respectively, P = 0.21). During sinus rhythm end-diastolic pressure was 13 ± 1 mmHg, which did not change significantly during pacing at 120 beats/min. During pacing at 150 beats/min, end-diastolic pressure increased to 21 ± 3 mmHg during pacing from the apex and to 16 ± 2 mmHg during pacing from the outflow tract (P = 0.005). Changes in first derivative of pressure and in isovolumic relaxation time constant were comparable during pacing from the two sites. Thus, it seems that tachycardias originating from the right ventricular outflow tract result in more favorable left ventricular hemodynamics, compared to those from the right ventricular apex     

A Comparison of Ventricular Function During High Right Ventricular Septal and Apical Pacing after His-Bundle Ablation for Refractory Atrial Fibrillation

This study compares LV performance during high right ventricular septal (RVS) and apical (RVA) pacing in patients with LV dysfunction who underwent His-bundle ablation for chronic AF. We inserted a passive fixation pacing electrode into the RVA and an active fixation electrode in the RVS. A dual chamber, rate responsive pulse generator stimulated the RVA through the ventricular port and the RVS via the atrial port. Patients were randomized to initial RVA (VVIR) or RVS (AAIR) pacing for 2 months. The pacing site was reversed during the next 2 months. At the 2 and 4 month follow-up visit, each patient underwent a transthoracic echocardiographical study and a rest/exercise first pass radionuclide ventriculogram. We studied nine men and three women (mean age of 68 +/- 7 years) with congestive heart failure functional Class (NYHA Classification): I (3 patients), II (7 patients), and III (2 patients). The QRS duration was shorter during RVS stimulation (158 +/- 10 vs 170 +/- 11 ms, P < 0.001). Chronic capture threshold and lead impedance did not significantly differ. LV fractional shortening improved during RVS pacing (0.31 +/- 0.05 vs 0.26 +/- 0.07, P < 0.01). RVS activation increased the resting first pass LV ejection fraction (0.51 +/- 0.14 vs 0.43 +/- 0.10, P < 0.01). No significant difference was observed during RVS and RVA pacing in the exercise time (5.6 +/- 3.2 vs 5.4 +/- 3.1, P = 0.6) or the exercise first pass LV ejection fraction (0.58 +/- 0.15 vs 0.55 +/- 0.16, P = 0.2). The relative changes in QRS duration and LV ejection fraction at both pacing sites showed a significant correlation (P < 0.01). We conclude that RVS pacing produces shorter QRS duration and better chronic LV function than RVA pacing in patients with mild to moderate LV dysfunction and chronic AF after His-bundle ablation.     

Effect of right ventricular apex pacing on the Tei index and brain natriuretic peptide in patients with a dual-chamber pacemaker

BACKGROUND: Asynchronous electrical activation induced by right ventricular apex (RVA) pacing can cause various abnormalities in left ventricular (LV) function, particularly in the context of severe LV dysfunction or structural heart disease. However, the effect of RVA pacing in patients with normal LV and right ventricular (RV) function has not been fully elucidated. The aim of this study was to characterize the effects of RVA pacing on LV and RV function by assessing isovolumic contraction time and isovolumic relaxation time divided by ejection time (Tei index) and by assessing changes in plasma brain natriuretic peptide (BNP). METHODS: Doppler echocardiographic study and BNP measurements were performed at follow-up (mean intervals from pacemaker implantation, 44+/-75 months) in 76 patients with dual chamber pacemakers (sick sinus syndrome, n=30; atrioventricular block, n=46) without structural heart disease. Patients were classified based on frequency of RVA pacing, as determined by 24-hour ambulatory electrocardiogram (ECG) that was recorded just before echocardiographic study: pacing group, n=46 patients with RVA pacing>or=50% of the time, percentage of ventricular paced 100+/-2%; sensing group, n=30, patients with RVA pacing<50% of the time, percentage of ventricular paced 3+/-6%. RESULTS: There was no significant difference in mean heart rate derived from 24-hour ambulatory ECG recordings when comparing the two groups (66+/-11 bpm vs 69+/-8 bpm). LV Tei index was significantly higher in pacing group than in sensing group (0.67+/-0.17 vs 0.45+/-0.09, P<0.0001), and the RV Tei index was significantly higher in pacing group than in sensing group (0.34+/-0.19 vs 0.25+/-0.09, P=0.011). Furthermore, BNP levels were significantly higher in pacing group than in sensing group (40+/-47 pg/mL vs 18+/-11 pg/mL, P=0.017). With the exception of LV diastolic dimension (49+/-5 mm vs 45+/-5 mm, P=0.012), there were no significant differences in other echocardiographic parameters, including left atrium (LA) diameter (35+/-8 mm vs 34+/-5 mm), LA volume (51+/-27 cm3 vs 40+/-21 cm3), LV systolic dimension (30+/-6 mm vs 29+/-7 mm), or ejection fraction (66+/-9% vs 63+/-11%), when comparing the two groups. CONCLUSIONS: These findings suggest that the increase of LV and RV Tei index, LVDd, and BNP are highly correlated with the frequency of the RVA pacing in patients with dual chamber pacemakers.     

右心室心尖不同部位起搏时左心室收缩时序的超声研究

目的探讨右心室心尖不同部位起搏时左心节段性室壁的收缩特征及时序。方法利用实时三维超声心动图技术确定右心室心尖起搏电极顶端在右心室心尖部的准确空间附着位点。运用应变显像技术，测定左心室壁各节段收缩期应力的达峰时间，即自心电图Q波起点至收缩期峰值应变时限（interval between Q wave of surface ECG and peak strain，QPSI），反映左心室各室壁的收缩时序；并计算QPSI的离散度，即最大QPSI减去最小QPSI的时限差，代表左心室内收缩延迟时间。观察正常对照组、右心室心尖不同部位起搏组左心室壁的节段性运动，评价各组左心室壁的收缩（或应变）时序及收缩协调性。结果右心室心尖起搏组的左心室壁收缩时序较正常对照组发生改变。右心室心尖侧壁起搏与右心室心尖间隔起搏组的左心室壁收缩时序不同，左室间隔心尖段、后壁基底段差异存在统计学意义（P〈0．05）。右心室心尖起搏时左室壁整体的收缩发生延迟，并且右心室心尖侧壁起搏组左室壁的收缩延迟时间明显大于右心室心尖间隔起搏组（P〈0．05）。结论右心室心尖不同部位起搏可以导致左心室不同的收缩模式改变，提示右心室心尖不同部位起搏所引起的电激动顺序及对心脏血流动力学的影响也存在差异。     

Septal Short Atrioventricular Delay Pacing: Additional Hemodynamic Improvements in Heart Failure

Controversy exists as to whether short AV delay pacing is beneficial in left ventricular dysfunction with the studies performed coming to disparate conclusions. The right ventricular apical pacing previously studied results in asynchronous contraction and relaxation sequences and may limit the potential benefits of short AV delay pacing. In this study the hemodynamic effects of septal (resulting in a more physiological activation sequence) and apical right ventricular activation were compared in 15 patients with heart failure. VDD pacing with AV delays of 50,100, and 150 msec was evaluated. Apical VDD pacing did not increase the cardiac output significantly, 4.1 ± 0.75 to 4.45 ± 0.74 L/min, whereas septal VDD pacing increased the cardiac output to 4.86 ± 0.79 L/min (P = 0.037). Apical pacing increased the cardiac output in 10 patients and septal pacing in 11 patients. We conclude that selected patients with ventricular dysfunction benefit from short AV delay pacing. Septal ventricular activation confers significant hemodynamic improvements over apical activation.     

Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks.

To test the hypothesis that a defibrillation shock is unsuccessful because it fails to annihilate activation fronts within a critical mass of myocardium, we recorded epicardial and transmural activation in 11 open-chest dogs during electrically induced ventricular fibrillation (VF). Shocks of 1-30 J were delivered through defibrillation electrodes on the left ventricular apex and right atrium. Simultaneous recordings were made from septal, intramural, and epicardial electrodes in various combinations. Immediately after all 104 unsuccessful and 116 successful defibrillation shocks, an isoelectric interval much longer than that observed during preshock VF occurred. During this time no epicardial, septal, or intramural activations were observed. This isoelectric window averaged 64 +/- 22 ms after unsuccessful defibrillation and 339 +/- 292 ms after successful defibrillation (P less than 0.02). After the isoelectric window of unsuccessful shocks, earliest activation was recorded from the base of the ventricles, which was the area farthest from the apical defibrillation electrode. Activation was synchronized for one or two cycles following unsuccessful shocks, after which VF regenerated. Thus, after both successful and unsuccessful defibrillation with epicardial shocks of greater than or equal to 1 J, an isoelectric window occurs during which no activation fronts are present; the postshock isoelectric window is shorter for unsuccessful than for successful defibrillation; unsuccessful shocks transiently synchronize activation before fibrillation regenerates; activation leading to the regeneration of VF after the isoelectric window for unsuccessful shocks originates in areas away from the defibrillation electrodes. The isoelectric window does not support the hypothesis that defibrillation fails solely because activation fronts are not halted within a critical mass of myocardium. Rather, unsuccessful epicardial shocks of greater than or equal to 1 J halt all activation fronts after which VF regenerates.     

Electroanatomic mapping of endocardial right ventricular activation as a guide for catheter ablation in patients with arrhythmogenic right ventricular dysplasia

Arrhythmogenic right ventricular dysplasia is a structural heart disease characterized by fibrofatty degeneration of right ventricular myocardium and arrhythmias of right ventricular origin. The aim of this study was to characterize endocardial right ventricular activation by electroanatomic mapping as a guide for catheter ablation in patients with arrhythmogenic right ventricular dysplasia. Electroanatomic mapping and entrainment procedures were performed in 5 patients with arrhythmogenic right ventricular dysplasia. Endocardial mapping during ventricular tachycardia demonstrated a focal activation pattern with radial spreading of activation from a site of earliest ventricular activation in all directions. Right ventricular activation time (127 +/- 34 ms) was markedly shorter than tachycardia cycle length (415 +/- 92 ms). The site of earliest ventricular activation was found in an aneurysmal outflow tract (n = 2), at the border of aneurysms near the tricuspid annulus (n = 2), and at the apex of the right ventricle (n = 1). Entrainment mapping criteria of these areas of earliest endocardial activity were consistent with exit sites of a reentrant circuit in an area of abnormal myocardium. Fractionated potentials were found 61 +/- 29 ms before the onset of the QRS complex at these sites. Catheter ablation rendered the "clinical" ventricular tachycardia noninducible in four patients but "nonclinical" faster ventricular tachycardias were inducible in three patients. During the follow-up of 7 +/- 3 months after ablation, the frequency of therapies in 4 patients with an implantable cardioverter defibrillator decreased from 49 +/- 61 episodes per month before ablation, to 0.3 +/- 0.5 episodes per month after ablation (P < 0.05). Electroanatomic mapping during ventricular tachycardia facilitates localization of exit sites in relation to aneurysms in diseased right ventricle and may guide catheter ablation in patients with arrhythmogenic right ventricular dysplasia.     

Permanent and atrial-synchronized ventricular stimulation for clinically stable patients with normal or impaired left ventricular systolic function

BACKGROUND: Ventricular desynchronization imposed by permanent dual-chamber ventricular pacing (VDD) may compromise ventricular function. METHODS: We investigated the impact of background VDD pacing on the right and left ventricular (LV) function on 129 clinically stable outpatients (mean age 69 +/- 10) implanted chronically with a dual-chamber pacemaker or an automatic defibrillator by using echocardiographic techniques including tissue doppler imaging (TDI) and color M-mode (CMM) examinations, and B-type natriuretic peptide (BNP) measurements. Patients were divided into two groups of normal (n = 65) or impaired (n = 64) LV systolic function (ejection fraction 63 +/- 6% and 38 +/- 10%, respectively) according to clinical and echocardiographic criteria. Each patient group included two subgroups on the basis of the underlying permanent and atrial-synchronized heart rhythm: either intrinsic ventricular activation (IVA) or VDD pacing. RESULTS: The BNP levels (mean, 95% CI) of patients with impaired LV systolic function were approximately threefold higher than those of patients with normal LV systolic function [189 (145-245) pg/mL vs 65 (50-85) pg/mL, P < 0.0001], but did not differ between subgroups of patients with IVA vs VDD pacing. By two-way analysis of variance and analysis of covariance, and after adjustment for age and gender, significant VDD pacing effects were found in terms of lower E/A ratio (P < 0.05) and increased LV end-systolic volume (P < 0.05). VDD pacing did not significantly affect the BNP levels and the LV filling pressures, as determined by the E/Ea and E/Vp ratios. CONCLUSIONS: Long-term VDD pacing may not be harmful in clinically stable patients with normal or moderately reduced LV systolic function.     

频发性室性期前收缩的射频导管消融治疗

目的探讨射频导管消融治疗室性期前收缩（PVC）的疗效及安全性。方法对129例PVC[右心室流出道（RVOT）107例,右心室流人道游离壁近瓣环处4例、前壁间隔部近瓣环处1例,左心室前上间隔3例、左心室流出道（LVOT）左冠窦内5例、左冠窦下1例,左心室下后间隔5例,左心室前侧壁、左心室前侧壁近瓣环处、右心室心尖部各1例]分别采用起搏标测或起搏与激动顺序标测结合的方法进行消融。结果消融即刻成功122例、失败7例。手术操作时间12—171min,X线曝光时间2—48min。术后随访3个月～4年,4例复发。结论射频导管消融治疗PVC是一种安全、有效的方法,其适应证可适当放宽。     

Pacing-induced electrophysiological remodeling in hypertrophic obstructive cardiomyopathy--observations on cardiac memory

BACKGROUND: Hypertrophic cardiomyopathy carries an increased risk for sudden cardiac death. While pacing therapy reduces the left ventricular outflow tract gradient and improves symptoms in a subgroup of hypertrophic obstructive cardiomyopathy (HOCM) patients, its electrophysiological consequences are unknown and were therefore assessed in this prospective study. METHODS AND RESULTS: Fifteen consecutive HOCM patients were studied and compared with 14 patients without HOCM paced because of sinus bradycardia. ECG intervals were measured before pacemaker implantation and after > or =3 months of DDD pacing in HOCM patients and > or =5 weeks in controls. Both groups showed similar ECG signs of cardiac memory development. In HOCM patients, with baseline QTc 447 +/- 33 ms, cardiac memory development was not associated with any significant changes in ECG intervals. In contrast, baseline repolarization in control patients was significantly prolonged by 6% (QTc 429 +/- 33 vs 454 +/- 46 ms; P < 0.05). Furthermore, in HOCM patients repolarization was 7% shorter during DDD pacing compared to sinus rhythm (JTc 329 +/- 25 vs 353 +/- 21 ms; P < 0.05), despite a significantly prolonged ventricular activation time (QRS duration 155 +/- 16 vs 91 +/- 9 ms; P < 0.01). CONCLUSIONS: Importantly, the development of cardiac memory-induced different repolarization responses depending on baseline structure and electrophysiology. In HOCM patients repolarization was shorter during right ventricular apical pacing than during normal activation despite prolonged activation time.     

Influence of Ventricular Fibrillation Duration on Defibrillation Energy in Dogs Using Bidirectional Pulse Discharges

The automatic implantable defibrillator device typically discharges 5-30 seconds after detection of ventricular fibrillation. To investigate the importance of the duration of ventricular fibrillation on defibrillation, the effects of ventricular fibrillation durations of 5, 15, and 30 seconds on the energy requirements for successful internal defibrillation were compared in 15 closed chest dogs with internal electrodes. The electrode configuration utilized a transvenous right heart catheter with two electrodes and a precordial subcutaneous patch electrode, with a single bidirectional pulse discharged between the distal catheter electrode and the proximal catheter and patch electrodes. Curves of energy vs. percentage of successful defibrillation were constructed and logistic regression was used to derive 90% and 50% successful energy doses (ED90 and ED50). The mean ventricular fibrillation activation interval just prior to defibrillation was determined from discrete RV endocardial electrograms. Four dogs died during testing, all because of inability to defibrillate after 30 s of ventricular fibrillation. In the remaining 11 dogs, the ED90 increased from (mean +/- SD) 27 +/- 13J at 5 s to 41 +/- 14J at 30 s (p less than .01). The mean ventricular fibrillation activation interval decreased from 107 +/- 21 ms at 5 s to 95 +/- 18 ms at 30 s (p less than .01). In conclusion, the energy required for internal defibrillation in dogs using this electrode configuration increases with longer durations of ventricular fibrillation, and is associated with more rapid ventricular fibrillation activation intervals.     

Importance of using standard rather than torso surface electrocardiographic leads for pacemapping at the right ventricular outflow tract

Although pacemapping has been used to localize the origin of ventricular tachycardia, the effect of changes in the position of ECG electrodes during ventricular pacing remains unknown. To clarify the relationship between the position of ECG limb electrodes and QRS configuration during pacemapping at the right ventricular outflow tract (RVOT), RVOT pacing was performed on 12 patients at eight pacing sites located in the anterior, septal, lateral, and posterior portions each in the high and low RVOT. Standard and torso ECGs were recorded simultaneously during each pacing protocol, and the QRS axis and amplitude were compared between the two ECGs. Differences between sites in the horizontal plane and in the longitudinal direction were also compared. The QRS axis on the torso ECG was significantly more rightward than that on the standard ECG at all eight pacing sites (72.1+/-17.4 vs 64.0+/-21.9 degrees). The magnitude of differences in the QRS axis and amplitude between the anterior and other sites at the same height was significantly greater in the standard ECG in all locations and in 7 of 18 comparable leads, respectively. The magnitude of differences between high and low sites was significantly greater in the standard ECG in three of four locations and in 5 of 12 comparable leads, respectively. In conclusion, the torso ECG is less sensitive to changes in pacing site at the RVOT than the standard ECG. The torso ECG is, therefore, not proper for pacemapping in attempts to ablate ventricular tachycardia arising from the RVOT.     

右室间隔部与心尖部起搏影响心功能的对比分析

目的对比分析右室间隔部起搏和心尖部起搏对患者心功能的长期影响。方法连续选取高度以上房室传导阻滞患者分别行右室间隔部起搏和心尖部起搏,随访观察两组手术情况、电极参数变化、心电图、并发症、超声心动图改变。结果两组在手术时间、感知阈值、起搏阈值、QRS波宽度改变上差异有统计学意义,在电极阻抗方面差异无统计学意义;长期随访右室心尖部起搏组LVEDD、LVESD均较间隔部起搏者增加,LVEF减低。结论长期右室间隔部起搏较心尖部起搏对心功能影响更小。     

Hemodynamic Responses to Rapid Pacing: A Model for Tachycardia Differentiation

The hemodynamic responses to rapid atrial and ventricular pacing were examined in 10 closed-chest anesthetized dogs in an attempt to distinguish hemodynamically stable from unstable tachycardias. Pressure monitoring catheters were placed in the femoral artery, right atrium, and right ventricle to measure mean arterial pressure, mean right atrial pressure, and mean right ventricular pressure at baseline heart rate and after rapid high right atrial and right ventricular apex pacing. Pressures recorded during rapid pacing (average of the pressures at 30 and 60 seconds of pacing) at pacing rates of 180, 250, and 280/minute were compared to those recorded initially at baseline heart rates. Rapid right ventricular apex pacing resulted in significant increases in mean right atrial pressure (from 6 ± 1 mmHg (mean ± standard error) to 12 ± 1 mmHg, a 100% increase, P < 0.001) and mean right ventricular pressure (from 11 ±1 mmHg to 16 ± 1 mmHg, a 45% increase, p < 0.02) with marked hemodynamic compromise (mean arterial pressure decreased from 85 ± 6 mmHg to 50 ± 6 mmHg, a 41% decrease, P < 0.01). These parameters remained stable (no statistically significant difference from baseline) during high right atrial pacing. In half of the dogs high right atrial pacing at rates 250 resulted in atrioventricular Wenckebach. Thus, it is concluded that mean right atrial pressure and mean right ventricular pressure may be useful in distinguishing hemodynamically significant tachycardias, and in the future design of antitachycardia devices.     

Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial-Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy

HETTRICK, D.A., et al .: Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy. The role of atrial lead location in cardiovascular function in the presence of impaired ventricular dysfunction is unknown. We tested the hypothesis that left atrial (LA) and left ventricular (LV) hemodynamics are affected by alterations in AV delay and are influenced by atrial pacing site in dogs with dilated cardiomyopathy. Dogs   (n = 7)   were chronically paced at 220 beats/min for 3 weeks to produce cardiomyopathy and then instrumented for measurement of LA, LV end diastolic pressure (LVEDP) and mean arterial pressure (MAP), LA volume, LV short-axis diameter, and aortic and pulmonary venous blood flow. Hemodynamics were measured after instrumentation and during atrial overdrive pacing from the right atrial appendage (RAA), coronary sinus ostium (CSO) and lower LA lateral wall (LAW). The AV node was then ablated, and hemodynamics were compared during dual chamber AV pacing (right ventricular apex) from each atrial lead location at several AV delays between 20 and 350 ms. Atrial overdrive pacing from different sites did not alter hemodynamics. Cardiac output (CO), stroke volume, LVEDP, MAP and +dLVP/dt demonstrated significant (P < 0.05) variation with AV delay during dual chamber pacing. CO was higher during LAW pacing than RAA and CSO pacing (   2.3 ± 0.4   vs   2.1 ± 0.3   vs   2.0 ± 0.3 l/min   , respectively) at an AV delay of 120 ms. Also, MAP was higher in the LAW than RAA and CSO (   65 ± 9   vs   59 ± 9   vs   54 ± 11 mmHg   , respectively) at an AV delay of 350 ms. Atrial lead location affects indices of LV performance independent of AV delay during dual chamber pacing in dogs with cardiomyopathy. (PACE 2003; 26[Pt. I]:853–861)