Spatial dispersion of action potential duration restitution kinetics is associated with induction of ventricular tachycardia/fibrillation in humans

INTRODUCTION: Action potential duration restitution (APDR) plays a role in initiation and maintenance of ventricular tachycardia (VT)/ventricular fibrillation (VF). We hypothesized that the steeply sloped APDR and its spatial heterogeneity contribute to VT/VF inducibility in patients with ventricular arrhythmia. METHOD AND RESULTS: After programmed ventricular stimulation (PVS) for evaluation of clinically documented VT, patients (n = 20, 15 male, age 52.5 +/- 9.5 years) were divided into two groups: inducible sustained VT/VF (IVT, n = 10) and noninducible VT/VF (NVT, n = 10). Data were compared with the corresponding results obtained from normal controls (C, n = 10). Right ventricular (RV) monophasic action potential duration at 90% repolarization (APD90) and ventricular effective refractory period (VERP) in the right ventricular apex (RVA) and right ventricular outflow tract (RVOT) were determined. APDR was acquired by scanning diastole with premature ventricular beats during a pacing cycle length of 600 msec (S1-S2) in all patients and by rapid pacing at the cycle lengths that induced APD alternans in three patients. Maximal slopes (Smax) of the APDR curves and DeltaAPD90 (APD90 at S2 400 ms - APD90 at the shortest S2) were measured. VERP and APD90 at each RV site did not differ among the three groups. Smax obtained by S1-S2 (1.6 +/- 0.6) did not differ from Smax obtained by rapid pacing (1.2 +/- 0.7), with a significant correlation noted between these values (r = 0.92, P < 0.01). The IVT group had a higher spatial dispersion of Smax (Smax at RVOT - Smax at RVA) compared to the C group (P < 0.05), with no difference between the NVT group and the IVT or C groups. The IVT group had a higher spatial dispersion of DeltaAPD90 compared to the NVT and C groups (P < 0.01, respectively). Smax at the RVOT (2.7 +/- 1.9) was steeper than that at the RVA (1.9 +/- 1.2, P < 0.05). Inducibility of sustained VT/VF was greater at the RVOT (83.3%) than at the RVA (50.0%, P < 0.05). CONCLUSION: In patients with ventricular arrhythmia, VT/VF is highly inducible under conditions of greater spatial dispersion of ventricular refractoriness and APDR.     

Functional abnormalities in patients with permanent right ventricular pacing: the effect of sites of electrical stimulation

OBJECTIVES: We sought to evaluate the long-term effects of alternative right ventricular pacing sites on myocardial function and perfusion. BACKGROUND: Previous studies have demonstrated that asynchronous ventricular activation due to right ventricular apical (RVA) pacing alters regional myocardial perfusion and functions. METHODS: We randomized 24 patients with complete atrioventricular block to undergo permanent ventricular stimulation either at the RVA (n = 12) or right ventricular outflow (RVOT) (n = 12). All patients underwent dipyridamole thallium myocardial scintigraphy and radionuclide ventriculography at 6 and 18 months after pacemaker implantation. RESULTS: After pacing, the mean QRS duration was significantly longer during RVA pacing than during RVOT pacing (151 +/- 6 vs. 134 +/- 4 ms, p = 0.03). At six months, the incidence of myocardial perfusion defects (50% vs. 25%) and regional wall motion abnormalities (42% vs. 25%) and the left ventricular ejection fraction (LVEF) (55 +/- 3% vs. 55 +/- 1%) were similar during RVA pacing and RVOT pacing (p > 0.05). However, at 18 months, the incidence of myocardial perfusion defects (83% vs. 33%) and regional wall motion abnormalities (75% vs. 33%) were higher and LVEF (47 +/- 3 vs. 56 +/- 1%) was lower during RVA pacing than during RVOT pacing (all p < 0.05). Patients with RVA pacing had a significant increase in the incidence of myocardial perfusion defects (p < 0.05) and a decrease in LVEF (p < 0.01) between 6 and 18 months, but patients with RVOT pacing did not (p > 0.05). CONCLUSIONS: This study demonstrates that preserved synchronous ventricular activation with RVOT pacing prevents the long-term deleterious effects of RVA pacing on myocardial perfusion and function in patients implanted with a permanent pacemaker.     

Right ventricular outflow versus apical pacing in pacemaker patients with congestive heart failure and atrial fibrillation

INTRODUCTION: Prior studies suggest that right ventricular apical (RVA) pacing has deleterious effects. Whether the right ventricular outflow tract (RVOT) is a more optimal site for permanent pacing in patients with congestive heart failure (CHF) has not been established. METHODS AND RESULTS: We conducted a randomized, cross-over trial to determine whether quality of life (QOL) is better after 3 months of RVOT than RVA pacing in 103 pacemaker recipients with CHF, left ventricular (LV) systolic dysfunction (LV ejection fraction < or = 40%), and chronic atrial fibrillation (AF). An additional aim was to compare dual-site (RVOT + RVA, 31-ms delay) with single-site RVA and RVOT pacing. QRS duration was shorter during RVOT (167 +/- 45 ms) and dual-site (149 +/- 19 ms) than RVA pacing (180 +/- 58 ms, P < 0.0001). At 6 months, the RVOT group had higher (P = 0.01) role-emotional QOL subscale scores than the RVA group. At 9 months, there were no significant differences in QOL scores between RVOT and RVA groups. Comparing RVOT to RVA pacing within the same patient, mental health subscale scores were better (P = 0.03) during RVOT pacing. After 9 months of follow-up, LVEF was higher (P = 0.04) in those assigned to RVA rather than RVOT pacing between months 6 and 9. After 3 months of dual-site RV pacing, physical functioning was worse (P = 0.04) than during RVA pacing, mental health was worse (P = 0.02) than during RVOT pacing, and New York Heart Association (NYHA) functional class was slightly better (P = 0.03) than during RVOT pacing. There were no other significant differences between RVA, RVOT and dual-site RV pacing in QOL scores, NYHA class, distance walked in 6 minutes, LV ejection fraction, or mitral regurgitation. CONCLUSION: In patients with CHF, LV dysfunction, and chronic AF, RVOT and dual-site RV pacing shorten QRS duration but after 3 months do not consistently improve QOL or other clinical outcomes compared with RVA pacing.     

正常心室肌复极离散度初步研究

目的     

心脏选择性部位起搏的电和机械同步性研究的初步报告

目的观察心脏不同部位起搏时的电及机械同步性和血流动力学变化。方法14例患者分别于右室心尖（RVA）、希氏束部位（His）、右室高位流出道间隔部（RVOT）起搏,记录心输出量和心脏指数;比较不同部位起搏和自身心律时12导联体表心电图的QRS波宽度和方向,以评价电同步性;用全数字化超声诊断系统的向量速度显像评价机械同步性。结果心输出量和心脏指数在RVA起搏时较差,但差异无统计学意义（P〉0．05）。各部位起搏时QRS波的宽度：His为（124±5．3）ms,RVOT（144±7．1）ms,RVA（156±8．6）ms,均较自身心律（92±4．5）ms时宽（P〈0．01）;而His及RVOT均较RVA起搏时的QRS波时限窄,其差异有统计学意义（P〈0．01）。向量速度显像检查提示,RVOT起搏相对于RVA起搏有更好的机械同步性。结论RVOT可能较传统的RVA部位起搏好,同时手术操作容易。     

Effect of site of pacing on dispersion of refractoriness

The variation in dispersion of ventricular refractoriness with different sites of pacing was measured in 11 patients not taking antiarrhythmic drugs. Dispersion of refractoriness between 3 right ventricular sites was determined at constant paced cycle lengths (S1S1). Refractoriness to ventricular extrastimulation (S2) using atrial pacing vs "clinical" pacing (drive or S1 at the right ventricular apex) vs the conventional measurement of dispersion (S1 at the site of S2) was compared. Effective and functional refractory periods (ERP and FRP) were measured from electrograms at the site of application of S2. Dispersion of ERP was always wider using clinical pacing (65.4 +/- 26 ms [+/- standard deviation]) than atrial pacing or traditional drive (20.4 +/- 14 and 19.1 +/- 10 ms, p less than 0.0001). Similarly, dispersion of FRP was greater with clinical pacing (45.0 +/- 35 vs 21.8 +/- 14 and 17.3 +/- 13, p less than 0.011). In 2 patients with left bundle branch block these differences were most striking. Clinical pacing foreshortened FRP relative to ERP (FRP shorter than ERP by an average 12.5 ms at nonapical sites) but this did not induce tachycardias, perhaps because FRP was still longer than the shortest V1V2 achieved conventionally (FRP was longer at nonapical sites than at the apex using clinical pacing, p less than 0.05). With atrial pacing there is less dispersion of refractoriness than with clinical ventricular pacing, although this difference is not appreciated when dispersion is measured in the conventional manner.     

右室双部位起搏与双室同步起搏的急性血液动力学对比研究

比较右室双部位 (RV Bi)起搏和双室 (BiV)同步起搏对血液动力学的影响 ,并与右室心尖部 (RVA)、右室流出道 (RVOT)、左室基底部 (LVB)起搏相比较 ,明确双部位起搏是否优于单部位起搏。 15例患者中病窦综合征 8例、Ⅲ度房室阻滞 7例。分别行RVA、RVOT、LVB、RV Bi、BiV起搏 (VVI,6 0～ 90次 /分 ) ,测定心输出量 (CO)和心脏指数(CI)、肺毛细血管嵌顿压 (PCWP)和QRS波时限 (QRSd)。结果 :①与RVA起搏相比 ,RVOT、LVB、RV Bi、BiV起搏CI分别增加了 7.5 %、11.3%、15 .5 %和 17.2 % ,PCWP分别降低了 14.9%、10 .3%、2 1.7%和 2 0 .0 % (P均 <0 .0 1)。②RV Bi、BiV起搏较RVOT、LVB起搏的CO、CI增高而PCWP降低 (P均 <0 .0 5 )。③RV Bi与BiV起搏、RVOT与LVB起搏之间CO、CI和PCWP无显著差异。④RVOT、RV Bi、BiV起搏的QRSd(分别为 12 8± 11,111± 16 ,10 3± 13ms)较RVA起搏 (146± 18ms)时显著缩短 (P≤ 0 .0 0 1) ,而LVB起搏 (142± 15ms)与RVOT、RVA起搏时无显著差异。结论 :RV Bi起搏和BiV同步起搏的急性血液动力学效果无明显差异 ,但双部位起搏的效果明显优于单部位起搏 ;双部位起搏的QRSd也比单部位起搏明显缩短     

右心室心尖部起搏与右心室流出道起搏的临床研究

目的利用超声多普勒优化房室间期后,比较右心室心尖部（RVA）起搏与右心室流出道（RVOT）起搏对左、右心室间收缩同步性的差别。方法（1）共入选45例三度房室阻滞患者,其中男16例,女29例。RVA组31例,RVOT组14例,出院前进行程控。（2）将感知的房室间期（SAV）由70～170ms递增,每次递增20ms,分别行超声心动图检查,测定心肌做功指数（MPI）,将MPI最小时的SAV确定为最适SAV。比较不同起搏部位所测最适SAV的差异。（3）应用组织多普勒同步图（TSI）技术分别测量左、右心室侧壁基底部心肌收缩达峰时问,二者之差用ATs表示,代表室间不同步程度。比较不同起搏部位ATs的差异。结果（1）RVA与RVOT起搏的最适SAV分别为（80．0±9．8）ms对（92±18）ms,差异有统计学意义（P〈0．01）。（2）RVA与RVOT组室间隔与左心室侧壁收缩达峰时间差分别为（89．5±25．7）ms对（27．94-10．5）ms（P〈0．001）,左、右心室侧壁基底部收缩达峰时间之差分别为（88．3±23．4）ms对（29．54-16．7）ms,差异有统计学意义（P〈0．001）。结论与RVA起搏比较,RVOT起搏对心室收缩同步性影响较小,分析其效果与RVOT起搏部位有关。     

Acute Changes in Cardiac Synchrony and Output According to RV Pacing Sites in Koreans with Normal Cardiac Function

Introduction: The synchrony of the pacing heart can be affected by the right ventricular (RV) pacing site and is crucial to cardiac function in pacemaker recipients. We evaluated the acute changes in cardiac synchrony according to the RV pacing sites in normal systolic functioning subjects with normal QRS. Methods: We conducted this study with 30 patients with the pacing in the RV apex (RVA), RV septum (RVS), and RV outflow tract (RVOT) in a sequential manner . Transthoracic echocardiography was conducted at rest and during pacing in order to measure interventricular and intraventricular dyssynchrony in all patients. Results: QRS duration (148.1 ± 12.8 ms) of RVA pacing was significantly shorter than that of RVS pacing (154.4 ± 14.1 ms, P < 0.01) and RVOT pacing (160.6 ± 15.7 ms, P < 0.001). We noted no statistically significant difference in cardiac output according to the pacing sites. The interventricular dyssynchrony with M-mode and Doppler echocardiography in RVOT pacing was increased to an insignificant degree as compared with those with RVS pacing or RVA pacing. The intraventricular dyssynchrony with tissue Doppler echocardiography in RVA pacing was reduced significantly as compared with that of RVS pacing or RVOT (RVA = 60.3 ± 32.7 ms, RVS = 82.1 ± 33.8 ms, RVOT = 79.1 ± 33.3 ms; RVA vs RVS = P < 0.05, RVA vs RVOT = P < 0.01, RVS vs RVOT = P = NS). Conclusion: RVA pacing is superior to RVS and RVOT pacing with regard to intraventricular synchrony in normal systolic functioning subjects with normal QRS. Cardiac output at RVA pacing is not inferior to other sites.     

程序电刺激时心室复极离散度的研究

了解程序电刺激 (PES)时心室复极离散度的变化 ,探讨PES诱发室性快速心律失常 (VTA)的可能机制。采用单相动作电位 (MAP)标测技术测定 10例无器质性心脏病的阵发性室上性心动过速患者接受PES时的心室复极离散度。结果 :S1 S1 刺激 ( 5 0 0ms)时的动作电位时程 (APD)的离散度 (APDd)与窦性心律时无明显差异 ( 34± 10msvs38± 9ms ,P >0 .0 5 )。随S1 S2 间期缩短 ,各标测点S2 的APD逐渐缩短 ,且与S1 S2 间期呈正相关 ,但激动时间 (AT)及其离散度 (ATd)、APDd、复极时间离散度 (RTd)逐渐延长 ;S1 S2 间期缩短至有效不应期 (ERP) +30ms后 ,S2 的APDd、RTd大于窦性心律及S1 S1 刺激时 (APDd :5 1± 8msvs 38± 9ms或 34± 10ms,P <0 .0 5 ;RTd :39± 10msvs2 4± 7ms,P<0 .0 5 ) ,但ATd无明显增大。心室内各点有效不应期离散度为 31± 14ms,ERP APD平均为 0 .89± 0 .0 8。认为在无器质性心脏病者PES可使心室复极离散度增大 ,但不增加传导差异 ,不易诱发VTA     

Frequency-dependent effects of quinidine on the relationship between action potential duration and refractoriness in the canine heart in situ

To determine the normal relationship in vivo between action potential duration (APD) and effective refractory period (ERP) over a large range of steady-state cycle lengths (CLs) and to determine how a sodium channel-blocking agent, quinidine, affects this relationship, we developed a new contact electrode technique for simultaneous measurements of monophasic action potentials and refractoriness at a single site in the beating heart in situ. Recordings were made from left ventricular epicardium in open-chest dogs during steady-state pacing at CLs from 220 to 600 msec both before and after therapeutic intravenous administration of quinidine. During baseline both APD at 90% repolarization (APD90) and ERP were linearly correlated to CL with nearly identical slopes: y = 0.24x CL + 83.0 (r = 1.0; p less than .0001) for APD90 and y = 0.22x CL + 82.3 (r = 1.0; p less than .0001) for ERP. Expressed in percent repolarization, ERP coincided with a repolarization level of 79% to 83%, with no appreciable influence of CL on this relationship. Quinidine increased APD90 by a small but significant amount (8 to 12 msec), which was independent of CL. In contrast, the effect on ERP of quinidine exhibited marked frequency dependence (p less than .0002), producing progressively greater ERP increase at shorter CLs, as compared with both baseline ERP and concomitant APD90. The duration by which ERP exceeded APD90 reached 44 +/- 14 msec at a CL of 220 msec.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term cardiac memory in canine heart is associated with the evolution of a transmural repolarization gradient

OBJECTIVE: The contribution of regional electrophysiologic heterogeneity to the T-wave changes of long-term cardiac memory (CM) is not known. We mapped activation and repolarization in dogs after induction of CM and in sham animals. METHODS AND RESULTS: CM was induced by three weeks of AV-sequential pacing at the anterior free wall of the left ventricle (LV), midway between apex and base in 5 dogs. In 4 sham controls a pacemaker was implanted but ventricular pacing was not performed. At 3 weeks, unipolar electrograms were recorded (98 epicardial, 120 intramural and endocardial electrodes) during atrial stimulation (cycle length 450 ms). Activation times (AT) and repolarization times (RT) were measured and activation recovery intervals (ARIs) calculated. CM was associated with 1) deeper T waves on ECG, with no change in QT interval; 2) longer activation time at the site of stimulation in CM (29.7+/-1.0, X+/-SEM) than sham (23.9+/-1.3 ms p<0.01); 3) an LV transmural gradient in repolarization time such that repolarization at the epicardium terminated 12.4+/-2.4 ms later than at the endocardium p<0.01), in contrast to no gradient in shams (2.7+/-4.2 ms); in memory dogs, the repolarization time gradient was greatest at sites around the pacing electrode varying from 13.1+/-2.3 ms to 25.5+/-3.8 ms; 4) more negative left ventricular potentials at the peak of the body surface T wave (-4.9+/-0.8 vs -2.2+/-0.4 mV; p<0.05) but no altered right ventricular epicardial T-wave potentials. ARIs did not differ between groups. Right ventricular activation was delayed but was not associated with altered repolarization because of compensatory shortening of the right ventricular ARIs. CONCLUSION: CM-induced T-wave changes are caused by evolution of transmural repolarization gradients manifested during atrial stimulation that are maximal near the site of ventricular pacing.     

Right ventricular apex versus right ventricular outflow tract pacing: prospective, randomised, long-term clinical and echocardiographic evaluation

INTRODUCTION: In patients treated with permanent pacing, the electrode is typically placed in the right ventricular apex (RVA). Published data indicate that such electrode placement leads to an unfavourable ventricular depolarization pattern, while right ventricular outflow tract (RVOT) pacing seems to be more physiological. AIM: To compare long-term effects of RVOT versus RVA pacing on clinical status, left ventricular (LV) function, and the degree of atrioventricular valve regurgitation. METHODS: Patients with indications for permanent pacing, admitted to hospital between 1996 and 1997, were randomised to receive RVA or RVOT pacing. In 2004 during a final control visit in 27 patients clinical status, echocardiographic parameters and QRS complex duration as well as NT-proBNP level were measured. Analysed parameters were compared between groups and in the case of data available during the perioperative period also their evolution in time was assessed. RESULTS: Out of 27 patients 14 were randomised to the RVA group and 13 to the RVOT group. No significant differences between groups were observed before the procedure with respect to age, gender, comorbidities or echocardiographic parameters. Mean duration of pacing did not differ significantly between the groups (89+/-9 months in RVA group vs 93+/-6 months in RVOT group, NS). In the RVA group significant LV ejection fraction decrease was observed (from 56+/-11% to 47+/-8%, p <0.05); in the RVOT group LV ejection fraction did not change (54+/-7% and 53+/-9%; NS). Progression of tricuspid valve regurgitation was also observed in the RVA group but not in the RVOT group. During the final visit NT-proBNP level was significantly higher in the RVA group: 1034+/-852 pg/ml vs 429+/-430 pg/ml (p <0.05). CONCLUSIONS: In patients with normal LV function permanent RVA pacing leads to LV systolic and diastolic function deterioration. RVOT pacing can reduce the unfavourable effect and can slow down cardiac remodelling caused by permanent RV pacing. Clinical and echocardiographic benefits observed in the RVOT group after 7 years of pacing are reflected by lower NT-proBNP levels in this group of patients.     

Preferential conduction across the ventricular outflow septum in ventricular arrhythmias originating from the aortic sinus cusp.

OBJECTIVES: The purpose of this study was to examine the relationship between the origin and breakout site of idiopathic ventricular tachycardia (VT) or premature ventricular contractions (PVCs) originating from the myocardium around the ventricular outflow tract. BACKGROUND: The myocardial network around the ventricular outflow tract is not well known. METHODS: We studied 70 patients with idiopathic VT (n = 23) or PVCs (n = 47) with a left bundle branch block and inferior QRS axis morphology. Electroanatomical mapping was performed in both the right ventricular outflow tract (RVOT) and aortic sinus cusp (ASC) during VT or PVCs. RESULTS: The earliest ventricular activation (EVA) was recorded in the RVOT in 55 patients (group R) and in the ASC in 15 (group A). In all group R patients, the closest pace map and successful ablation were achieved at the EVA site. Although a successful ablation was achieved at the EVA site in all group A patients, the closest pace map was obtained at the EVA site in 8 and RVOT in 7 (with an excellent pace map in 4). The stimulus to QRS interval was 0 ms during pacing from the RVOT and 36 +/- 8 ms from the ASC. The distance between the EVA and perfect pace map sites in those 4 patients was 11.9 +/- 3.0 mm. CONCLUSIONS: Ventricular arrhythmias originating from the ASC often show preferential conduction to the RVOT, which may render pace mapping or some algorithms using the electrocardiographic characteristics less reliable. In some of those cases, an insulated myocardial fiber across the ventricular outflow septum may exist.     

Comparison of apical and infundabular pacing in patients with primary dilated or ischemic cardiomyopathy

Dual chamber pacing has been proposed as an alternative treatment to patients with cardiac failure refractory to optimal medical therapy. The influence of the site of ventricular pacing was studied in 15 patients with an average age of 68.7 +/- 8.7 years with dilated cardiomyopathies and an average left ventricular ejection fraction of 22.3 +/- 6.8%. Three temporary USCI electrodes were positioned in the right atrium, the right ventricular outflow tract (RVOT) and the right ventricular apex. The average duration of the QRS complexes and the haemodynamic parameters (PAP, PCP and cardiac index) were measured in sinus rhythm and during DDD apical, RVOT and simultaneous apical and RVOT pacing. The RVOT and simultaneous pacing significantly reduced the QRS duration (135 +/- 14 ms and 137 +/- 17 ms, p < 0.0001 respectively) compared with apical pacing (150 +/- 19 ms). The mean PAP and mean PCP remained unchanged in the different modes of pacing but the cardiac index increased significantly during RVOT pacing (2.99 +/- 0.67 l/min/m2) and simultaneous pacing (3 +/- 0.77 l/min/m2) compared with apical pacing (2.66 +/- 0.62 l/min/m2) (p < 0.001 and p < 0.01 respectively) and compared with sinus rhythm (2.62 +/- 0.7 l/min/m2) (p < 0.001 and p < 0.005 respectively). This study suggests that better results may be obtained with RVOT screw in lead than with the traditional right ventricular apical electrode.     

右心室流出道与右心室心尖部起搏对心室收缩同步性和心功能的影响

目的研究右心室流出道(right ventricular outflow tract,RVOT)间隔部和右心室心尖部(right ventricularapex,RVA)起搏对心脏收缩同步性、收缩功能的影响,探讨RVOT间隔部起搏的意义。方法 50例病态窦房结综合征患者分为RVOT组(n=25)和RVA组(n=25),起搏器置入1个月后通过调整房室间期使心室节律全部为起搏节律或房室结自身下传节律,观察起搏参数,并行超声心动图检查。结果RVOT组与RVA组电极导线植入时间、X线曝光时间比较,差异无统计学意义(P>0.05)。全部患者未出现植入并发症。两组随访1个月时起搏参数比较,差异无统计学意义(P>0.05)。RVOT组和RVA组起搏后的QRS波时限较前明显增宽,差异有统计学意义[RVOT组:(135±8)ms vs.(88±8)ms,P<0.001;RVA组:(154±8)ms vs.(90±6)ms,P<0.001]。RVA组起搏后QRS波时限较RVOT组增宽更为明显,差异有统计学意义(P<0.001)。两组起搏后室间机械延迟(interventricularmechanical delay,IVMD)和室间隔-左心室后壁收缩运动延迟时间(septal-to-posteriowall motion delay,SPWMD)较起搏前均显著增加,差异有统计学意义(P<0.001)。RVA组起搏后IVMD和SPWMD绝对值较RVOT组显著延长,差异有统计学意义[IVMD:(38±7)ms vs.(24±5)ms,P<0.001;SPWMD:(118±21)ms vs.(60±11)ms,P<0.001]。两组左心室舒张末内径及左心室射血分数比较,差异无统计学意义(P>0.05)。结论右心室起搏会造成心室收缩不同步,RVOT起搏对心室收缩不同步的影响较RVA起搏小,提示RVOT起搏是较为生理的起搏位点。     

High dispersion of ventricular repolarization after an implantable defibrillator shock predicts induction of ventricular fibrillation as well as unsuccessful defibrillation

OBJECTIVES: To test the hypothesis that post-shock dispersion of repolarization (PSDR) is higher in T wave shocks that induce ventricular fibrillation (VF) than in those that do not, as well as in implantable cardioverter defibrillator (ICD) defibrillation shocks which fail to terminate VF when compared with those that are successful. BACKGROUND: Ventricular fibrillation has been linked to the presence of dispersion of repolarization, which facilitates reentry. Most of the studies have been done in animals, and the mechanism underlying the generation and termination of VF in humans is speculative and remains to be determined. METHODS: Monophasic action potentials (MAPs) were recorded simultaneously from the right ventricular outflow tract (RVOT) and the right ventricular apex (RVA) in 27 patients who underwent implantation and testing of an ICD. T wave shocks were used to induce VF while the termination was attempted using internal defibrillator shocks. The post-shock repolarization time (PSRT) was measured in both the RVA and RVOT MAPs, and the difference between the two recordings was defined as the PSDR. The averages of PSDR were compared between the successful and unsuccessful inductions and terminations of VF. RESULTS: T wave shocks that induced VF generated a greater PSDR (93.4 +/- 85.1 ms) than the unsuccessful ones (45.1 +/- 55.9 ms, p < 0.001). On the other hand, shocks that failed to terminate VF were associated with a greater PSDR (59.9 +/- 41.2 ms) than shocks that terminated VF (21.1 +/- 20.1 ms), p < 0.001. CONCLUSIONS: A high PSDR following a T wave shock is associated with induction of VF; while following a defibrillating shock, it is associated with its failure and the continuation of VF. Conversely, a low PSDR is associated with failure of a T wave shock to induce VF and successful termination of VF by a defibrillating shock.     

Comparison of the Acute Hemodynamic Effect of Right Ventricular Apex,Outflow Tract,and Dual‐Site Right Ventricular Pacing

Background: We studied the acute effect of pacing at the right ventricular outflow tract (RVOT), right ventricular apex (RVA) and simultaneous RVA and RVOT—dual‐site right ventricular pacing (DuRV) in random order on systolic function using impedance cardiography. Methods: Seventy‐three patients (46 males), aged 52–89 years (mean 71.4 years) subjected to routine dual chamber pacemaker implantation with symptomatic chronic II or atrioventricular block, were included to the study. Results: DuRV pacing resulted in significantly higher cardiac index (CI) in comparison to RVOT and RVA and CI at RVOT was higher than at RVA pacing (2.46 vs 2.35 vs 2.28; P < 0.001). In patients with ejection fraction >50% significantly higher CI was observed during DuRV pacing when compared to RVOT and RVA pacing and there was no difference of CI between RVOT and RVA pacing (2.53 vs 2.41 vs 2.37; P < 0.001). In patients with ejection fraction <50%, DuRV and RVOT pacing resulted in significantly higher CI in comparison to RVA pacing while no difference in CI was observed between RVOT and DuRV pacing (2.28 vs 2.21 vs 2.09; P < 0.001). Conclusion: Dual‐site right ventricular pacing in comparison to RVA pacing improved cardiac systolic function. RVOT appeared to be more advantageous than RVA pacing in patients with impaired, but not in those with preserved left ventricular function. No clear hemodynamic benefit of DuRV in comparison to RVOT pacing in patients with impaired systolic function was observed. Ann Noninvasive Electrocardiol 2010;15(4):353‐359     

Dispersion of the monophasic action potential duration in patients with polymorphic ventricular tachycardia.

The mechanism of polymorphic ventricular tachycardia (PMVT) remains unclear. To investigate the electrophysiologic mechanism of PMVT, monophasic action potentials (MAPs) were recorded with a contact electrode technique from right ventricular sites during sinus rhythm and right ventricular pacing. MAPs were obtained from 6 patients with PMVT (PMVT group) and 11 patients without PMVT (control group). The duration from the onset of the upstroke to 90% repolarization of the MAP (MAPD90) during right ventricular pacing at both pacing cycle lengths of 600 and 400 ms was significantly longer in the PMVT group than in the control group (332+/-60 ms vs 279+/-33 ms [P < .005] and 276+/-32 ms vs 229+/-23 ms [P < .0001], respectively). Dispersion of the MAPD90 in sinus rhythm was significantly larger in the PMVT group than in the control group (52.5+/-34.6 ms vs 26.1+/-12.0 ms [P < .005]), and dispersion of the MAPD90 during right ventricular pacing at both pacing cycle lengths of 600 and 400 ms was also significantly larger in the PMVT group than in the control group (86.0+/-44.2 ms vs 37.4+/-28.6 ms [P < .005], and 48.8+/-19.3 ms vs 27.1+/-7.1 ms [P < .05], respectively). Dispersion of repolarization time (activation time plus MAPD90) at a pacing cycle length of 600 ms was longer in the PMVT group than in the control group (104.3+/-38.9 ms vs 49.4+/-31.2 ms [P < .05]). These results suggest that the patients with PMVT have a greater regional dispersion of ventricular repolarization time and that the heterogeneity of ventricular repolarization may play an important role in the genesis of PMVT.     

Resetting of ventricular tachycardia with electrocardiographic fusion: incidence and significance

The incidence and significance of fusion of the QRS complex during resetting of sustained ventricular tachycardias (VTs) was determined in 53 VTs induced by programmed stimulation in 46 patients with prior myocardial infarction. All 53 VTs were reset with one or two extrastimuli delivered at the right ventricular apex (RVA); 29 (54.7%) demonstrated fusion of the VT QRS complex coincident with the extrastimulus resetting the VT. Activation time at the RVA during VT (measured from the onset of the VT QRS complex to the first rapid deflection of the RVA electrogram) was longer in VT reset with fusion compared with those without fusion (91 +/- 30 vs 33 +/- 32 msec; p less than .001). A right bundle branch block VT QRS morphology and a rightward and inferior axis were more common in VT reset with electrocardiographic (ECG) fusion. Additionally, the shortest return cycle following the extrastimulus resetting the VT was shorter in VT reset with ECG fusion compared with those without (327 +/- 66 vs 423 +/- 84 msec; p less than .001). Fusion of the endocardial electrogram recorded at the site of VT origin was noted in 11 of 15 VTs that were reset while a recording catheter was positioned at this site, including all eight VTs with evidence of surface ECG fusion and three of seven VTs without fusion. Seventeen VTs were reset from the right ventricular outflow tract as well as the RVA; eight demonstrated QRS fusion at both sites, five from the right ventricular outflow tract only, and four from neither site.(ABSTRACT TRUNCATED AT 250 WORDS)