动态心电图判断室性早搏起源部位的分析

目的探讨12导联同步动态心电图（AECG）对室性早搏起源部位的定位价值。方法选择我院经12导联同步AECG检查明确诊断有频发单源室性早搏的患者90例,分析12导联AECG及该患者常规12导联心电图上室性早搏QRS波群形态的差异,对其起源部位分别进行初步定位,并与心内电生理检查结果进行对照分析。结果室性早搏起源于右室共65例,其中起源于右室流出道55例（占61．11％）、右室心底部5例（占5．56％）、右束支2例（占2．22％）、其他3例（占3．33％）,起源于左室流出道20例（占22．22％）、左室心底部3例（占3．33％）、左束支2例（占2．22％）。结论根据12导联同步AECG的室性早搏QRS波群的形态可以初步判断其起源部位,指导室性早搏射频消融治疗方式的选择。     

Localization of the site of ventricular premature complexes by radionuclide angiographic phase imaging

To investigate whether gated radionuclide angiographic phase imaging is useful for visually displaying the origin of ventricular premature complexes (VPCs), 82 patients were studied by gating only VPCs. The VPC "origin" by the scintigraphic method was defined as the area of earliest phase and was compared with that predicted by 12-lead electrocardiographic criteria in all patients and to invasive electrophysiologic mapping in 10. Separating the right ventricle into 3 and the left ventricle into 4 segments, the phase imaging method and the electrocardiographic criteria agreed as to ventricle of VPC origin in 69 patients (84%) and segment of origin within each ventricle in 46 (56%). When baseline ventricular wall motion was analyzed, the 2 methods agreed to the ventricle of VPC origin in 31 of 33 patients (94%) with normal wall motion, 20 of 23 (87%) with segmental wall motion abnormalities and 19 of 26 (73%) with diffuse wall motion abnormalities. Agreement between the 2 methods as to specific segmental localization of the arrhythmia focus was noted in 21 of 33 patients (64%) with normal wall motion, 11 of 23 (48%) with segmental wall motion abnormalities and 12 of 26 (46%) with diffuse hypocontractility. In the 10 patients with endocardial mapping studies, the phase imaging technique confirmed the segment of VPC origin in all 10; the electrocardiographic method was accurate in 8. Thus, gated radionuclide angiographic phase imaging methods may be of value in noninvasively defining the origin of spontaneous VPCs. The visual format allows ready interpretation of the arrhythmia origin, and there may be an advantage to this approach over electrocardiographic morphometric criteria.     

Factors influencing late right ventricular ejection

Forward flow from the right ventricle into the pulmonary artery continues longer than contraction in the right ventricular free wall. The momentum of blood flow, contraction of other areas of the right ventricular free wall, and movement of the interventricular septum are possible mechanisms regulating late right ventricular ejection. In this study the changes in shortening in right ventricular free wall and in free wall to septum distance were measured using sonomicrometry. Right ventricular free wall shortening was studied in both outflow and inflow regions in hoop and apex to base axes. Pulmonary artery flow was simultaneously measured using an electromagnetic flowmeter. Right ventricular free wall in the hoop axis was motionless during late ejection. The inflow segment in the hoop axis stopped shortening before all other segments (p less than 0.01). Both outflow and inflow segments in the hoop axis lengthened after the end of shortening. Both shortening of the right ventricular free wall in the apex to base axis and decrease in free wall to septum distance were continued until the end of ejection (p less than 0.01). Compared with the right ventricular outflow segment, the inflow segment shortened for a longer duration. It is concluded that forward flow during late right ventricular ejection is associated with continued shortening of the free wall in the apex to base axis. However, the results of this study do not exclude the role of septal bulge into the right ventricle during late ejection.     

老年人器质性心脏病室性早搏的心电图特点

目的 探讨老年人器质性心脏病室性早搏的特点。方法 对照分析了132例老年人器质性心脏病组引起的室性早搏及94例老年非心脏病组（对照组）室性早搏的心电图特点。结果 老年心脏病组室性早搏起源于左室98例，起源于右室34例；对照组起源于左室20例，起源于右室74例。老年人心脏病组室性早搏QRS波振幅〈20mV者占67．4％，时限〉0．12s者占77．3％，有切迹或呈错折波占87．1％。与对照组比较有显著差异（P〈0．05）。结论 老年人心脏病室性早搏多起源于左室，QRS波振幅〈20mV，时限〉0．12s，形态有切迹或错折波。     

射频导管消融治疗的特发性室性心律失常心电图特征分析

目的：探讨不同起源的特发性室性期前收缩（PVCs）和（或）室性心动过速（VT）的心电图特征,提出鉴别流程。方法根据射频导管消融PVCs/VT有效靶点或心室最早激动点的X线胸片进行定位,分析不同起源PVCs/VT的12导联心电图QRS波群。结果828例接受导管消融,580例起源于右心室,248例起源于左心室,左、右心室起源者胸导联移行指数＜0的分别占97.58%及7.24%;左和右心室流出道起源者下壁导联多数呈R型,V1上,多数右心室流出道起源者呈rS型,右室间隔起源呈QS型,主动脉瓣上起源者常呈rS或RS型;下壁导联上,左前分支起源者常呈qR型,左后分支起源者常呈rS型。结论结合体表心电图胸导联移行指数、下壁导联和V1上的QRS波群特征可初步判断特发性PVCs/VT的起源部位。     

Utility of introducing ventricular premature complexes during reciprocating tachycardia in specifying the location of left free wall accessory pathways

The usefulness of the response to single and double ventricular premature complexes (VPCs) introduced during reciprocating tachycardia (RT) in predicting the location of a left free wall accessory pathway was studied in 55 patients with the Wolff-Parkinson-White syndrome. One VPC introduced from the right ventricle into narrow QRS RT when the His bundle was refractory resulted in retrograde atrial preexcitation in 25 of 55 (45%) patients, while 30 (55%) showed no preexcitation. Double VPCs produced retrograde atrial preexcitation in 9 of 26 patients not responding to a single VPC. No difference in RT cycle length, AH, HV or ventriculoatrial intervals was found between those patients who did or did not show retrograde atrial preexcitation. The response to single and double VPCs during RT was related to the location of the AP. The average distance of the AP from the crux determined by intraoperative epicardial mapping in the 41 patients who underwent surgery was 2.7 +/- 0.7 mapping units (left posterolateral region) in patients showing retrograde atrial preexcitation with a single VPC, 3.6 +/- 0.7 units (at the lateral left ventricular margin) in those responding to double VPCs and 4.3 +/- 0.8 units (beyond the LV margin) in those showing no response. Left bundle--branch block (LBBB) aberrancy during RT resulted in an average 60 +/- 14 ms prolongation of the ventriculoatrial interval in 40 patients, including 5 in whom LBBB was seen only after procainamide infusion. VPCs introduced into LBBB RT resulted in significant retrograde atrial preexcitation in 6 additional patients in whom no response during normal QRS RT was observed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Accelerated idioventricular rhythm of infundibular origin in patients with a concealed form of arrhythmogenic right ventricular dysplasia

Five apparently healthy people (aged 16-47) presented with recurrent episodes of accelerated idioventricular rhythm characterised by left bundle branch block and right axis deviation. Clinical history, physical findings, basic electrocardiogram, chest x ray, and blood tests were within normal limits in all. Holter monitoring, exercise stress test, and electrophysiological study (in three patients) showed that accelerated idioventricular rhythm was mainly bradycardia dependent, easily suppressed by effort and overdrive pacing, and originated from the outflow tract of the right ventricle. The mechanism could be enhanced automaticity. Data from cross sectional echocardiography (in all patients) and from haemodynamic evaluation (in three) identified structural or wall motion abnormalities of the right ventricle or both without appreciable dilatation of the ventricle. Biopsy specimens of the right ventricular endomyocardium showed fibrosis in one patient, fibrosis and fatty infiltration in the second, and pronounced fatty infiltration in the third. These results show that some patients with accelerated idioventricular rhythm have right ventricular abnormalities that are typical of the localised and concealed forms of arrhythmogenic right ventricular dysplasia.     

Accelerated idioventricular rhythm of infundibular origin in patients with a concealed form of arrhythmogenic right ventricular dysplasia.

Five apparently healthy people (aged 16-47) presented with recurrent episodes of accelerated idioventricular rhythm characterised by left bundle branch block and right axis deviation. Clinical history, physical findings, basic electrocardiogram, chest x ray, and blood tests were within normal limits in all. Holter monitoring, exercise stress test, and electrophysiological study (in three patients) showed that accelerated idioventricular rhythm was mainly bradycardia dependent, easily suppressed by effort and overdrive pacing, and originated from the outflow tract of the right ventricle. The mechanism could be enhanced automaticity. Data from cross sectional echocardiography (in all patients) and from haemodynamic evaluation (in three) identified structural or wall motion abnormalities of the right ventricle or both without appreciable dilatation of the ventricle. Biopsy specimens of the right ventricular endomyocardium showed fibrosis in one patient, fibrosis and fatty infiltration in the second, and pronounced fatty infiltration in the third. These results show that some patients with accelerated idioventricular rhythm have right ventricular abnormalities that are typical of the localised and concealed forms of arrhythmogenic right ventricular dysplasia.     

Effects of catheter ablation of "asymptomatic" frequent ventricular premature complexes in patients with reduced (<48%) left ventricular ejection fraction

Frequent ventricular premature complexes (VPCs), particularly those without troublesome palpitations, are often regarded as a benign arrhythmia and are not treated other than with reassurance. However, VPCs can contribute to left ventricular (LV) dysfunction in the absence of symptoms. The present study was designed to investigate whether catheter ablation of VPCs can improve LV dysfunction in patients with and without troublesome palpitations. Of 80 consecutive patients who underwent catheter ablation of frequent VPCs, 24 (aged 60 ± 15 years) were found to have a reduced LV ejection fraction at baseline (<48%) and included in the present study. No important procedure-related complications occurred in these patients. During a median follow-up of 8 months, the VPC burden after ablation had decreased from 15 ± 6% to 1 ± 1% (p <0.001), and the left ventricular ejection fraction had increased from 32 ± 15% to 43 ± 14% (p <0.001). Ten patients (42%) had no palpitations before ablation. In the other 14 patients, the palpitations were improved or entirely resolved after ablation. No significant difference was found in the extent of LV ejection fraction improvement after ablation between patients with and without palpitations (+11 ± 12% vs +11 ± 11%, p = 0.941) or between patients with different locations of VPC origin. In conclusion, VPCs might not necessarily be associated with palpitations in many patients with LV dysfunction. Successful ablation of frequent VPCs in these "asymptomatic" patients is associated with an improvement in LV function similar to that observed in "symptomatic" patients.     

Clinical implication of surface morphology of ventricular premature contractions

VPC morphology was studied in the surface 12-lead ECGs (resting) in one hundred and thirty-six patients over a nine-month period (January–September, 1978). Seventy four (54%) of these had coronary artery disease proven by cardiac catheterization (61) or by evidence of acute transmural myocardial infarction (13) diagnosed by ECG and serum enzyme study. Twenty-three of the patients (17%) had other organic heart diseases documented by cardiac catheterization. The remaining thirty-nine (29%) were healthy individuals.Three common types of VPCs are recognized as right, left and septal in origin. There is no significant difference in the prevalence of these types in the presence of heart disease (right, 35%, left 31%, and septal 34%). However, if septal VPCs are considered along with left VPCs, these are twice as common as right VPCs. VPCs occurring in healthy individuals are overwhelmingly (74%) right ventricular in origin.In general, VPCs are most likely to occur in the presence of ventricular dyssynergy and multiple coronary arterial lesions.     

特发性室性心动过速及室性期前收缩的射频消融治疗

目的探讨射频导管消融(radiofrequency catheter ablation,RFCA)治疗特发性室性心动过速(idiopathic ventricular tachycardia,IVT)和室性期前收缩(premature ventricualr contraction,PVC)可行性、必要性和疗效。方法回顾性分析16例IVT、PVC患者采用激动顺序标测和起搏标测法确定室性心动过速(ventricular tachycardia,VT)、PVC的起源部位并行RFCA治疗的资料。结果 3例IVT中2例起源于左室间隔部左后分支的蒲肯野系统,1例起源于右心室流出道(right ventricular outflow tract,RVOT)游离壁,同时合并另一种游离壁起源的PVC,3例消融均成功,1例复发。13例PVC中7例起源RVOT间隔部,3例起源于RVOT游离壁,1例同时存在两种形态PVC(分别起源于ROVT间隔部和游离壁),2例起源于左心室流出道,13例消融成功,1例复发。结论 RFCA治疗IVT及特定部位的PVC是安全、有效且成功率高的一种方法。     

心腔内超声心动图指导下经导管射频消融治疗左心室后乳头肌室性早搏

目的左心室后乳头肌起源的室性早搏（室早）因其体表心电图与左后分支参与的特发性室性心动过速（室速）一样,都表现为心电轴左偏,伴右束支阻滞合并左前分支阻滞,因此有相当一部分被误认为分支室早。为了明确二者起源点的异同,我们采用术中心腔内超声心动图（ICE）来实时监测消融靶点的确切解剖位置。方法选择3例频发室早患者（男2例,女1例）,平均24h室早30000多次,超声心动图均未见心脏结构异常。在三维电解剖系统（CartoXP）指导下,跨主动脉瓣逆行送入3．5mm冷盐水磁定位标测电极导管于左心室,以激动标测构建左心室内膜图。以室早时提前最多;起搏时能得到12／12导联一致的QRS波以及放电20S内室早逐渐减少和消失作为理想靶点标准。在理想靶点确认后,经ICE确认消融导管在左心室内的确切位置,并记录和分析其局部双极电位图。以既往消融成功的经典左后分支室速作为对照,比较两者之间心电图的异同,为以后的标测和消融提供真实可靠的参照。结果ICE证实该3例室早靶点均位于左心室后乳头肌根部或中段,其解剖位置与左心室特发性室速靶点明显不在同一位置,其消融位点较特发性室速更靠心尖部;其局部双极电位在窦性心律时偶尔也可记录到浦肯野电位,但在早搏时都不能记录到浦肯野电位,说明其为肌源性起源,而特发性室速靶点无论窦性心律下还是室速时均可记录到清晰的浦肯野电位;体表心电图尽管可鉴别的特征不多,但后乳头肌起源的室早较特发性室速胸前导联（V：～V。导联）QRS时限明显增宽（前者平均124ms,后者仅86ms）,R／S≤1移行也早于特发性室速（后乳头肌室早在V,导联移行为R／S≤1,特发性室速在V,导联才移行为R／S≤1）。消融10余小时后,室早复发。1个月时复查动态心电图,24h平均室早10000余次,二尖瓣功能未受到任何影响。结论通过实时ICE证实,后乳头肌室早无论起源位置、体表心电图形态还是局部靶点电图均与特发性室速有区别,这类室早消融效果较差,易复发。如何在增强消融强度、扩大消融范围和避免乳头肌损伤之间找到平衡点是该类室早消融的重点和难点。     

Radiofrequency catheter ablation of ventricular tachycardia originating in the left posterior and left anterior fascicles in a patient with prior myocardial infarction

A 61-year-old man with prior anteroseptal myocardial infarction (ejection fraction: 40%) presented with recurrent episodes of palpitations. Twelve-lead ECG during palpitations showed an incessant ventricular tachycardia (VT1) with right bundle branch block (RBBB) morphology and inferior axis. Electrophysiologic study revealed that the clinical VT originated from the anterolateral left ventricle. A Purkinje potential preceded onset of the QRS complex by 34 ms. Radiofrequency ablation guided by the Purkinje potential terminated the VT1. Another ventricular tachycardia (VT2) showing RBBB morphology with superior axis and originating from the posteroseptal left ventricle, was induced by programmed ventricular stimulation. A Purkinje potential preceded onset of the local ventricular potential by 120-130 ms in this VT. Radiofrequency ablation guided by the Purkinje potential terminated the VT2.     

Ventricular premature contraction after repair of tetralogy of Fallot--the influence of postoperative factors, particularly the right ventricular regional wall motion

The presence and severity of ventricular premature contraction (VPC) in 35 patients with tetralogy of Fallot (TF) were studied, 5 to 10 years after intracardiac repair (ICR), using treadmill exercise testing and 24-hour ambulatory monitoring. VPCs were observed in 24 patients (68.6%). The patients were classified into two groups according to the types of VPCs: group A (23 patients) without VPCs or with VPCs of Lown's grade 1 and group B (12 patients) with VPCs of Lown's grade 2, 3 or 4. Group B patients were found to have significantly higher right to left ventricular peak-systolic pressure ratios and higher right ventricular peak systolic pressures than those of group A. But there were no significant differences between the two groups in operative age, the time lapse between ICR and evaluation, the duration of exercise and so on. Group B patients also showed significantly decreased right ventricular regional wall motions in the right ventricular outflow tracts (ROTs), indicating akinetic or paradoxical movements than group A patients. It is thought that postoperative right ventricular hypertension and the akinetic or paradoxical wall movement of the ROT may have some effect on the genesis of postoperative VPCs after repair of TF.     

Idiopathic left ventricular tachycardia: assessment and treatment

Idiopathic left ventricular tachycardia (VT) has been classified into three subgroups according to mechanism: verapamil-sensitive, adenosine-sensitive, and propranolol-sensitive types. VT can be categorized also into left fascicular VT and left outflow tract VT. Although the mechanism of fascicular VT is verapamil-sensitive reentry, the mechanism of left outflow tract VT is not homogeneous. Fascicular VT can be classified into three subtypes: (1) left posterior fascicular VT with a right bundle branch block (RBBB) and superior axis configuration (common form); (2) left anterior fascicular VT with RBBB and right-axis deviation configuration (uncommon form); and (3) upper septal fascicular VT with a narrow QRS and normal axis configuration (rare form). Posterior and anterior fascicular VT can be successfully ablated at the mid-septum guided by a diastolic Purkinje potential or at the VT exit site guided by a fused presystolic Purkinjepotential. Upper septal fascicular VT also can be ablated at the site indicated by a diastolic Purkinje potential. The mechanism of left ventricular outflow tract VT is most likely adenosine-sensitive triggered activity. This VT can be classified into three subtypes according to the location where catheter ablation is successful, i.e., (1) endocardial origin; (2) coronary cusp origin; and (3) epicardial origin. The R-wave duration and R/S-wave amplitude in V1/V2 can be used to differentiate coronary cusp VT from other types of outflow tract VT. Recognition of the characteristics of the various forms of this group of arrhythmias should facilitate appropriate diagnosis and therapy.     

Assessment of abnormal left ventricular systolic blood flow in atrial fibrillation

In atrial fibrillation, it is known that hemodynamics vary according to the preceding R-R intervals. However, the informations of blood flow dynamics have not been available because of the methodological limitations. In this study, blood flow dynamics of atrial fibrillation were assessed using pulsed Doppler echocardiography. The subjects were 160 consecutive patients with atrial fibrillation and without left ventricular asynergy. Using a commercially-available pulsed Doppler instrument (Aloka SSD-910), blood flow patterns in the left ventricle were investigated from the apical long-axis view. The results were as follows: 1. In 22 of the 160 cases (14%), systolic blood flow in the central or apical region of the left ventricle directed towards the apex (termed "back flow"). 2. In the cardiac cycle with "back flow", the preceding R-R interval was shorter; whereas it was longer when "back flow" was absent (591 +/- 103 vs 817 +/- 179 msec, p less than 0.01). Moreover, when a long R-R interval (PPI) followed by a short R-R interval (PI) was observed (greater PPI/PI ratios), the next beat showed distinct "back flow". 3. Left ventricular ejection fraction decreased significantly in patients with "back flow" compared to those without it (42 +/- 15 vs 66 +/- 12%, p less than 0.01). 4. On left ventriculography, the motion of the base of the heart was preserved; however, with "back flow", the motion of the apical area was abnormal, extending towards the apex along the longitudinal axis. 5. Left ventricular ejection flow at the outflow tract disappeared in 13 of the 22 cases with "back flow" in cardiac cycles with short preceding R-R intervals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of left ventricular filling profile during preceding control beats on the occurrence of pulse deficit caused by ventricular premature contractions

This study was designed to investigate whether the left ventricularfilling profile during preceding control beats significantlyaffects the pulse deficit caused by ventricular premature contractions(VPCs). The study group consisted of 18 patients (10 men, eightwomen, 15–85 years old) who underwent electrophysiologicalcatheterization because of sinus bradycardia. Using a temporarypacing lead inserted in the right ventricular apex, isolatedVPCs with various coupling intervals were produced by electricalstimulation of the right ventricle. During the production ofthe VPCs, the mitral filling flow velocity using pulsed waveDoppler echocardiography, the femoral arterial pressure curveand the electrocardiogram were simultaneously recorded. Theright ventricle was siimulated 800, 750, 700, 650, 600, 550,500, 450 and 400 ms after the triggered control beat QRS complex.Pulse pressures during VPCs gradually decreased in relationto the shortening of the extra-systolic beat coupling interval.The longest coupling interval for each subject, which causedcomplete abolition of the pressure pulse during the VPC, wasdefined as the pulse deficit coupling interval. The early tolate diastolic velocity–time integral ratio (E_i/A_i ratio)of the mitral filling flow velocity during the control beatswhich precede the VPC was obtained as an index expressing theleft ventricular filling profile. The E_i/A_i ratio of the mitralfilling flow velocity ranged from 0.7 to 4.5 (1.8 ± 1.0).The pulse deficit coupling interval ranged from 440 to 640 ms(510 ± 60 ms). A significant negative correlation wasobserved between the E_i/A_i ratio and the pulse deficit couplinginterval (r = –0.69, P<0.01). A significant positivecorrelation was also observed between the age and the pulsedeficit coupling interval (r = 0.63, P<0.01). The findingsare consistent with the concept that pulse deficit by VPCs mayeasily occur in patients with reduced left ventricular fillingduring the early diastole.     

Right ventricular enlargement mimicking electrocardiographic left ventricular pacing

Electrocardiographic right bundle branch block morphology during cardiac pacing is occasionally the result of accidental placement of pacemaker or defibrillator leads into the left ventricle. Inadvertent lead placement in the left heart is associated with a risk of systemic embolism. Previous authors have attempted to define safe (right ventricular origin) and unsafe (left ventricular origin) patterns of right bundle branch block during pacing. We report a case of a patient with severe dilated cardiomyopathy and a correctly positioned pacemaker-defibrillator lead in the right ventricular apex, who meets electrocardiographic criteria for lead implantation into the left ventricle.     

Morphologic features of right ventricular ectopic beats

A study of the morphologic features of right ventricular ectopic beats produced by stimulating the endocardium of the right ventricle with a nonpacing catheter tip, and a comparison of these features with the patterns of classic left bundle branch block, afforded the following clues: (1) a wide (> 0.04 second) r wave in lead V₁; (2) a QS or rS complex deeper in lead V₄ than in V₁; and (3) right axis deviation in the frontal plane occurring commonly in right ventricular ectopic beats and rarely in left bundle branch block.

Artificially paced right ventricular beats shared the first 2 characteristics (wide r wave in lead V₁ and deep QS or rS complex in lead V₄) with the ectopic beats produced at catheterizatton but, unlike them, displayed an invariable left axis deviation.

Application of these findings to the clinical tracing may be helpful in discriminating between right ventricular ectopic beats and aberration of the left bundle branch block type.     

Idiopathic recurrent sustained ventricular tachycardia in children and adolescents

The electrophysiologic characteristics of recurrent sustained ventricular tachycardia were studied in seven pediatrie patients. The mechanisms of the ventricular tachycardia were evaluated using programmed electrical stimulation. Ventricular tachycardia could be reproducibly initiated in two patients and terminated in one patient in the basal state. It could be initiated in one additional patient and terminated in two additional patients after administration of a type IB drug. In four patients, ventricular tachycardia could not be initiated or terminated by programmed electrical stimulation. The site of origin of the ventricular tachycardia determined by catheter endocardial mapping was the right ventricular outflow tract in four patients, the interventricular septum in two patients and the inferior left ventricle in one patient. The ventricular tachycardia more frequently had an automatic than a reentrant mechanism, and originated more often in the right than in the left ventricle; it was not frequently associated with structural heart disease in this group of patients.