A new Doppler echocardiography parameter of diastolic ventricular function

The evaluation of flow velocities in left ventricular inflow tract (LVIT) by Doppler echocardiography gives information about the diastolic ventricular function. In late diastole, shortly after the flow velocity of atrial contraction V(A), we notice in the left ventricular outflow tract (LVOT) a laminar flow velocity directed to the aortic valve. The purpose of this study was to compare this flow velocity V(A*) in the LVOT with the flow velocity of the atrial contraction V(A), and the flow velocity of early diastole V(E) in LVIT, to determine whether such comparison would provide information concerning diastolic function. We studied three groups: 39 patients with left ventricular hypertrophy (HY) (mean age 56 +/- 12 y, 77% male), 41 patients with coronary heart disease (KHK) (mean age 53 +/- 10 y, 85% male) and 41 healthy subjects (N) (mean age 50 +/- 16 y, 51% male); all three groups were studied by pulsed Doppler from apical 4 chamber view in LVOT for maximal velocity (Vmax-A*) and time velocity integral of A* (TVI-A*), and in LVIT for maximal velocity of early diastole (Vmax-E), maximal velocity of atrial contraction (Vmax-A), ratio Vmax-E/Vmax-A, and the time velocity integrals (TVI-E, TVI-A). A slight correlation between Vmax-A* and Vmax-A was found (r = .60), being nearly the same as for TVI-A* and TVI-A (r = .64).(ABSTRACT TRUNCATED AT 250 WORDS)     

Main systolic blood flow patterns in the left and right ventricular outflow tracts determined by Doppler echocardiography

The main blood flow velocity patterns in the LVOT and RVOT were recorded by pulsed Doppler echocardiography in 28 normal healthy cases, in two athletes, and in 85 patients with atrial septal defects, pulmonary regurgitation, tetralogy of Fallot, aortic regurgitation, mitral stenosis, aortic stenosis, mitral regurgitation, hypertrophic cardiomyopathy, ischemic heart disease, and pulmonary hypertension. Blood flow velocities were displayed using a graphic system to form a real time sonogram, using Fast Fourier Transformation. In the normal group, the blood flow velocity was 1.69 KHz in LVOT, and 1.71 KHz in RVOT. In AR and T/F but not MS, there was high blood flow velocity in the LVOT, and the peak of blood flow velocity was shifted to mid-to late systole. In ASD and VSD with a L-R shunt, high blood flow velocity occurred in the RVOT, and the peak velocity shifted to early systole. Pulmonary hypertension occasionally produced a W- or V-shaped curve. In normal subjects, a small "a" wave could be detected in the LVOT recording. The "a" wave began at point B on the AML tracer of the M-mode echocardiography, reached maximum velocity at point C, and returned to zero (baseline) at point C'. The "a" wave was coincident with the R wave of the ECG, and with the Ia of the phonocardiogram (PCG). The normal velocity of the "a" wave was 602 Hz, and the a/H ratio was 0.36. In cases of HCM and IHD, the "a" wave velocity and the a/H ratio correlated with the end diastolic pressure and the peak dP/dT. These data suggest that the Doppler blood flow patterns in the LVOT and RVOT can indicate volume overload in the right and left ventricles, and that the "a" wave velocity and a/H ratio can provide new information concerning cardiac performance.     

Validation of the accuracy of both right and left ventricular outflow volume determinations and semiautomated calculation of shunt volumes through atrial septal defects by digital color Doppler flow mapping in a chronic animal model.

OBJECTIVES: The aim of the present study was to quantitate shunt flow volumes through atrial septal defects (ASDs) in a chronic animal model with surgically created ASDs using a new semiautomated color Doppler flow calculation method (ACM). BACKGROUND: Because pulsed Doppler is cumbersome and often inappropriate for color flow computation, new methods such as ACM are of interest. METHODS: In this study, 13 to 25 weeks after ASDs were surgically created in eight sheep, a total of 24 hemodynamic states were studied at a separate open chest experimental session. Electromagnetic (EM) flow probes and meters were used to provide reference flow volumes as the pulmonary and aortic flow volumes (Qp and Qs) and shunt flow volumes (Qp minus Qs). Epicardial echocardiographic studies were performed to image the left and right ventricular outflow tract (LVOT and RVOT) forward flow signals. The ACM method digitally integrated spatial and temporal color flow velocity data to provide stroke volumes. RESULTS Left ventricular outflow tract and RVOT flow volumes obtained by the ACM method agreed well with those obtained by the EM method (r = 0.96, mean difference = 0.78 +/- 1.7 ml for LVOT and r = 0.97, mean difference = -0.35 +/- 3.6 ml for RVOT). As a result, shunt flow volumes and Qp/Qs by the ACM method agreed well with those obtained by the EM method (r = 0.96, mean difference = -1.1 +/- 3.6 ml/beat for shunt volumes and r = 0.95, mean difference = -0.11 +/- 0.22 for Qp/Qs). CONCLUSIONS: This animal study, using strictly quantified shunt flow volumes, demonstrated that the ACM method can provide Qp/Qs and shunt measurements semiautomatically and noninvasively.     

组织多普勒评价右室不同部位起搏对左室收缩功能和同步性的影响

目的运用组织多普勒方法测量心脏机械活动的同步性,了解右室不同部位起搏后左心室同步性和收缩功能的即刻变化。方法选择拟行心内电生理检查的患者9例,排除器质性心脏病。在右室心尖部、右室低位室间隔、右室流出道游离壁和间隔部按随机的顺序行房室顺序起搏,采集彩色编码的组织多普勒图像进行下线分析。计算整体收缩振幅（global systolic contraction amplitude,GSCA）和16节段峰值收缩速度和位移达峰时间的标准差Ts-SD与Tdis-SD。结果右室流出道游离壁或间隔部起搏的GSCA显著高于右室心尖部或低位间隔起搏时,但低于基础状态（P〈0．05）。右室心尖部起搏与右室流出道间隔部起搏的节段收缩位移比较显示,右室心尖部起搏时左室侧壁、后壁和下壁的平均位移显著降低（P〈0．05）,余节段差异无统计学意义。右室心尖部或低位室间隔起搏时,组织位移曲线由正常时的单峰变为双峰或三峰,且舒张末期出现负相位移,组织速度曲线出现等容收缩峰增高。Tdis-SD和Ts-SD在右室各部位起搏时均较基础状态时显著降低（P〈0．01）,但各部位起搏之间的差异无统计学意义。结论右室起搏即刻导致左心室内收缩非同步现象和左心收缩功能的下降。右室流出道起搏较右室心尖部起搏和低位室间隔起搏对左室收缩功能的影响小,是一种较为理想的起搏部位。     

Substrate in the interventricular septum for left ventricular and right ventricular outflow tract tachycardia: ablation from the right side of the septum

Simultaneous epicardial and endocardial mapping demonstrated that in a substantial number of ventricular tachycardias (VTs) endocardial, intramural, and epicardial structures are involved in the substrate of the reentrant circuits. Both right and left ventricular breakthrough has also been described during VT originating in the interventricular septum. We report the case of a patient with a nonischemic left ventricular aneurysm presenting with a left ventricular outflow tract (LVOT) tachycardia and a right ventricular outflow tract (RVOT) tachycardia. Mapping from the anterior interventricular vein and the endocardium of the RVOT revealed mid-diastolic potentials at the epicardium of the LVOT and the endocardium of RVOT, where the criteria of central isthmus sites could be demonstrated. Ablation targeting an isolated late potential during sinus rhythm in RVOT eliminated both the LVOT tachycardia and the RVOT tachycardia. In this patient with a nonischemic left ventricular aneurysm, the substrate of a LVOT tachycardia and RVOT tachycardia is described, and successful catheter ablation of the right and left ventricular tachycardia from the septal wall of RVOT is reported.     

Doppler assessment of pulmonary hypertension induced by hypoxic breathing in subjects susceptible to high altitude pulmonary edema

To verify the abnormal pulmonary vascular response implicated in the pathogenesis of high altitude pulmonary edema (HAPE), we examined the hemodynamic responses to hypoxia in HAPE-susceptible subjects (HAPE-S) by means of both right heart catheterization and pulsed Doppler echocardiography. The HAPE-S were seven men and one woman with a history of HAPE. Six healthy volunteers who had repeated experiences of mountain climbing without any history of altitude-related problems served as control subjects. The HAPE-S showed much greater increase in pulmonary vascular resistance (PVR) than did the control subjects, resulting in a much higher level of pulmonary arterial pressure (Ppa) under acute hypoxia both of 15% O2 and 10% O2. We then evaluated the usefulness of pulsed Doppler echocardiography in the prediction of pulmonary hypertension. Acceleration time (AcT) and right ventricular ejection time (RVET) were measured from the flow velocity pattern in the right ventricular outflow tract. The ratio of AcT to RVET was correlated to invasively determined mean Ppa (Ppa) and PVR. The results were as follows: (1) AcT/RVET = 0.52 to 0.0047 (Ppa), r = -0.93, SEE = 0.017, p less than 0.001 (HAPE-S); (2) AcT/RVET = 0.55 to 0.0055 (Ppa), r = -0.70, SEE = 0.030, p less than 0.001 (HAPE-S); (4) AcT/RVET = 0.52 to 0.00077 (PVR), r = -0.91, SEE = 0.016, p less than 0.001 (control subjects). We conclude that HAPE-S have a constitutional abnormality in the pulmonary vascular response to hypoxia, which is a possible causative factor of HAPE, and that pulsed Doppler echocardiography may be supportive to assess the pulmonary vascular pressor response in the HAPE-S.     

Differences in the duration of total ejection between right and left ventricles in chronic pulmonary hypertension

Background: Chronic pulmonary hypertension (cPH) is known to delay pulmonic valve closure resulting in a closely split second heart sound. We decided to measure total duration of right (RV) and left ventricular (LV) outflow tract (RVOT and LVOT) spectral signals using pulsed Doppler to determine if this approach was useful in identifying this narrowing in auscultation that should then result in a shorter temporal difference between the ejection of both ventricles. Methods: Standard measures of RV and LV performance as well as Doppler data was collected from 85 patients divided into two groups according to their estimated pulmonary artery systolic pressure obtained at the time of their echocardiographic examination. Difference in ejection between the ventricles was defined as the difference in ejection time between RVOT and LVOT, measured in milliseconds. Results: Chronic PH patients had a shorter total duration between RVOT and LVOT ejection time (–15 ± 16 ms vs. 22 ± 14 ms; P < 0.0001) than individuals without PH. This difference in total duration between RVOT and LVOT ejection not only showed a significant negative correlation with both PASP (r =–0.65; P < 0.0001) but also with pulmonary vascular resistance (PVR; r =–0.60; P < 0.0001). Conclusions: Shorter duration between RVOT and LVOT ejection is likely to explain the closely split second heart sound in cPH patients. When accurate echocardiographic assessment of RV function in cPH patients remains problematic due to the unusual geometry of this cardiac chamber; Doppler measures can simplify patient identification and follow up. (Echocardiography 2011;28:509‐515     

Right and left ventricular outflow tract tachycardias: evidence for a common electrophysiologic mechanism

Introduction: "Idiopathic" ventricular arrhythmias most often arise from the right ventricular outflow tract (RVOT), although arrhythmias from the left ventricular outflow tract (LVOT) are also observed. While previous work has elucidated the mechanism and electropharmacologic profile of RVOT arrhythmias, it is unclear whether those from the LVOT share these properties. The purpose of this study was to characterize the electropharmacologic properties of RVOT and LVOT arrhythmias.
Methods and Results: One hundred twenty-two consecutive patients  (61 male; 50.9 ± 15.2 years)  with outflow tract arrhythmias comprise this series, 100 (82%) with an RVOT origin, and 22 (18%) with an LVOT origin. The index arrhythmia was similar: sustained ventricular tachycardia (VT)  (RVOT = 28%, LVOT = 36%)  , nonsustained VT  (RVOT=40%, LVOT=23%)  , and premature ventricular complexes  (RVOT = 32%, LVOT = 41%) (P = 0.32)  . Cardiac magnetic resonance imaging and microvolt T-wave alternans results (normal/indeterminate) were also comparable. In addition, 41% with RVOT foci and 50% with LVOT foci were inducible for sustained VT (P = 0.48), and induction of VT was catecholamine dependent in a majority of patients in both groups (66% and 73%; RVOT and LVOT, respectively; P = 1.0). VT was sensitive to adenosine (88% and 78% in the RVOT and LVOT groups, respectively, P = 0.59) as well as blockade of the slow-inward calcium current (RVOT=70%, LVOT=80%; P = 1.00) in both groups.
Conclusions: Electrophysiologic and pharmacologic properties, including sensitivity to adenosine, are similar for RVOT and LVOT arrhythmias. Despite disparate sites of origin, these data suggest a common arrhythmogenic mechanism, consistent with cyclic AMP-mediated triggered activity. Based on these similarities, these arrhythmias should be considered as a single entity, and classified together as "outflow tract arrhythmias."     

Hypertrophic Cardiomyopathy with Right Ventricular Outflow Tract and Left Ventricular Intracavitary Obstruction

Obstruction of the right ventricular outflow tract (RVOT) is a rare finding in hypertrophic cardiomyopathy (HCM) patients unlike left ventricular outflow tract (LVOT) obstruction. Although there are guidelines that aid in clinical decision making in patients with LVOT obstruction, there are none addressing RVOT obstruction. As RVOT obstruction may pose serious clinical implications similar to LVOT obstruction, appropriate medical and surgical management is very important. A unique phenotype of HCM with RVOT obstruction in conjunction with left ventricle (LV) intracavitary obstruction is discussed.     

Left ventricular outflow tract tachycardia originating from the right coronary cusp: identification of location of origin by endocardial noncontact activation mapping from the right ventricular outflow tract

Idiopathic left ventricular outflow tract (LVOT) tachycardia has been shown to originate from a supravalvular site in some patients. Considerable attention recently has focused on identifying this variant of LVOT tachycardia on 12-lead ECG. We report the case of 15-year-old boy in whom a noncontact three-dimensional mapping electrode deployed in the right ventricular outflow tract (RVOT) assisted in identifying a supravalvular LVOT tachycardia. Observation of two early breakthrough sites in the RVOT and right ventricular septum suggested a right aortic cusp origin of the tachycardia. Pace mapping in the right aortic cusp identified a successful ablation site.     

Attempts at measuring pulmonary arterial pressure by means of Doppler echocardiography in patients with chronic lung disease

In 72 patients with severe chronic pulmonary or pulmonary vascular disease pulmonary arterial pressure was measured by means of right heart catheterization. Forty three patients had pulmonary hypertension, (32 +/- 11 mmHg) and 27 patients had normal pressure (14 +/- 3 mmHg). These patients were examined with continuous wave (CW) and pulsed wave (PW) Doppler echocardiography. The retrograde systolic tricuspid valve pressure gradient assessed with CW Doppler correlated with systolic pulmonary pressure (r = 0.92, p less than 0.001, SEE 7.7 mmHg) but was measurable in only 17 of the 70 patients. The flow velocity pattern in the right ventricular outflow tract could be recorded in 68 of the 70 patients. Acceleration time (AcT) from systolic flow onset to peak velocity correlated with mean pulmonary artery pressure (r = 0.72, p less than 0.001, SEE 8.3 mmHg). An AcT less than 90 msec had an 84% positive predictive value for pulmonary hypertension. Right ventricular isovolumic relaxation time could be measured in 59 of the 70 patients and correlated with systolic pulmonary artery pressure (r = 0.69, p less than 0.001, SEE 12.4 mmHg). No single Doppler method is at the same time easily applicable and accurate in prediction of pulmonary arterial pressure in patients with chronic lung diseases.     

High frame rate Doppler echocardiography in the rat: an evaluation of the method.

AIMS: In small animal models, two-dimensional (2D) and Doppler echocardiography should provide more information than M-mode, especially in animals with infarcted and distorted left ventricles, but has been limited by low frame rates and poor near field resolution. New, high frame rate echo-Doppler equipment with digital processing was tested for accuracy of measurements. METHODS AND RESULTS: Fourteen normal Wistar rats (232-328 g) were examined under halothane anaesthesia. Pulsed Doppler recordings from both left ventricular outflow tract(LVOT) and right ventricular outflow tract (RVOT) cor-responded well with simultaneous ultrasound transit time measurements of aortic flow (LVOT: v=0.99x+4.8, min R=0.93. Standard error of estimate (SEE)=8.3 ml x min(-1), and RVOT: v=0.97x -4.3. R=0.93. SEE =8.4 ml x min(-1). No systematic differences were observed over a flow range of 20-90 ml x min(-1). Left ventricular (LV) dimensions assessed by 2D parasternal long-axis and short-axis views were equal to M-mode measurements with LV diameter 6.6 + 0.44 mm, anterior wall 1.8 +/- 0.18 mm, and posterior wall 1.5 + 0.56 mm. Mean absolute difference 4.4-8.5%. Intra- and interobserver variability was 4.6 +/- 4.1% and 6.7 +/- 7.0% for Doppler measurements, and 4.3 +/- 3.8% and 3.8 +/- 4.6% for dimensions, respectively. CONCLUSION: High frame rate Doppler echocardiography provides accurate non-invasive measurements of cardiac structure and function in the rat.     

Right ventricular dysfunction due to right ventricular outflow tract patch

Doppler tissue imaging analysis was used to examine the relationship between right ventricular function and right ventricular outflow tract damage in 54 patients with repaired tetralogy of Fallot. The patients were divided into three groups: 16 in whom the right ventricular outflow tract was directly sutured (group DS), 23 who had transventricular patch repair (group TVP), and 15 who had transannular patch repair (group TAP). The control group consisted of 16 age-matched patients who underwent patch closure of a ventricular septal defect (group C). The Tei index was obtained from tricuspid and pulmonary Doppler flow velocities. The right ventricular Tei index was significantly greater in groups TVP and TAP than in group DS. Doppler tissue imaging analysis in groups TVP and TAP showed shorter myocardial systolic velocity, diastolic peak velocity, and atrial diastolic peak velocity, lower peak myocardial velocity and acceleration during isovolumic contraction, and prolonged isovolumic relaxation and contraction times compared to groups DS and C. Right ventricular dysfunction is due to the right ventricular outflow tract patch. Thus, the right ventricular outflow tract may be essential for right ventricular ejection and maintenance of right ventricular function.     

起源于左右心室流出道心动过速和早搏的射频导管消融治疗

目的 探讨射频导管消融（RFCA）治疗心室流出道特发性室性心动过速（室速）和室性早搏（室早）的临床效果、心电图及电生理特征。方法 58例患者中室速10例,室早48例。起源于右室流出道（RVOT）43例,左室流出道（LVOT）15例,其中起源于主动脉瓣上Valsalva左冠窦（LSV）12例。5例RVOT室速是在非接触标测系统Ensite3000指导下进行消融的。结果 （1）58例患者中55例成功,3例失败,9例复发。（2）其中1例患者术中出现急性心包压塞。（3）起源心室流出道的室速和室早具有典型的心电图特征,其中Ⅱ、Ⅲ、aVF导联单向R波是流出道室性心律失常的共同特点。（4）V1或V2导联的R波时限指数与R／S波幅指数可作为区别LSV与RVOT室速和室早的有效指标。结论 射频导管消融治疗心室流出道特发性室性心律失常是一种安全、有效的方法。非接触标测系统对于血流动力学不稳定的复杂性室性心律失常的标测与治疗具有重要的意义。     

Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy

OBJECTIVES: The purpose of this study was to determine whether the dynamic cause for mitral systolic anterior motion (SAM) is a Venturi or a flow drag (pushing) mechanism. BACKGROUND: In obstructive hypertrophic cardiomyopathy (HCM), if SAM were caused by the Venturi mechanism, high flow velocity in the left ventricular outflow tract (LVOT) should be found at the time of SAM onset. However, if the velocity was found to be normal, this would support an alternative mechanism. METHODS: We studied with echocardiography 25 patients with obstructive HCM who had a mean outflow tract gradient of 82 +/- 6 mm Hg. We compared mitral valve M-mode echocardiogram tracings with continuous wave (CW) and pulsed wave (PW) Doppler tracings recorded on the same study. A total of 98 M-mode, 159 CW, and 151 PW Doppler tracings were digitized and analyzed. For each patient we determined the LVOT CW velocity at the time of SAM onset. This was done by first determining the mean time interval from Q-wave to SAM onset from multiple M-mode tracings. Then, CW velocity in the outflow tract was measured at that same time interval following the Qwave. RESULTS: Systolic anterior motion began mean 71 +/- 5 ms after Q-wave onset. Mean CW Doppler velocity in the LVOT at SAM onset was 89 +/- 8 cm/s. In 68% of cases SAM began before onset of CW and PW Doppler LV ejection. CONCLUSIONS: Systolic anterior motion begins at normal LVOT velocity. At SAM onset, though Venturi forces are present in the outflow tract, their magnitude is much smaller than previously assumed; the Venturi mechanism cannot explain SAM. These velocity data, along with shape, orientation and temporal observations in patients, indicate that drag, the pushing force of flow, is the dominant hydrodynamic force that causes SAM.     

Non-invasive methods for determining the pulmonary blood pressure using ultrasonics in patients with chronic respiratory diseases

Ultrasound techniques and especially Doppler echocardiography offer several approaches to non-invasive assessment of pulmonary arterial pressure. The method based on the measurement of the velocity of the jets of tricuspid or pulmonary regurgitation is the most straightforward one, in most cases allowing for reliable quantitative assessment of pulmonary hypertension and thus should be applied as a method of choice whenever possible. Unfortunately, its application in patients with lung hyperinflation is limited by topographic factors. Short acceleration time of flow velocity in the right ventricular outflow tract (AcT less than 70-75 msec), especially accompanied by midsystolic deceleration occurring at end-expiration, is a strong evidence of severe pulmonary hypertension. Long AcT (above 115-120 msec) is virtually diagnostic of normal pulmonary arterial pressure. If high speed Doppler tracings of both pulmonary and tricuspid valve flow are available right ventricular isovolumic relaxation time may be used for estimation of pulmonary systolic pressure. However, the elaboration of the laboratory's own regression formula rather than application of Burstin nomogram seems more advisable in such cases. The future of non-invasive assessment of pulmonary hemodynamics will depend on the reliability to monitor acute and chronic changes not only in pulmonary arterial pressure, but also in flow and resistance. At present, echocardiography should be considered as a good screening test allowing also to stratify moderate and severe pulmonary hypertension. The exact assessment of pulmonary hemodynamics, especially in patients with chronic respiratory disease, when needed for important therapeutic decisions, should in most cases rely on right heart catheterization.     

Use of three-dimensional echocardiography for analysis of outflow obstruction in congenital heart disease

To evaluate the feasibility and accuracy of 3-dimensional (3D) echocardiography in analysis of left and right ventricular outflow tract (LVOT and RVOT) obstruction, 3D echocardiography was performed in 28 patients (age 4 months to 36 years) with outflow tract pathology. Type of lesion and relation to valves were assessed. Length and degree of obstruction were measured. Three-D data sets were adequate for reconstruction in 25 of 28 patients; 47 reconstructions were made. In 13 patients with LVOT obstruction, 3D echocardiography was used to study subvalvular details in 8, valvular in 13, and supravalvular in 1. Four of these 13 patients had complex subaortic obstruction. In 12 patients with RVOT lesions, 3D echocardiography was used to study subvalvular details in 11, valvular in 12, and supravalvular in 2. Three-dimensional reconstructions were suitable for analysis in 100% of subvalvular LVOT, 77% valvular LVOT, 100% supravalvular LVOT, 100% subvalvular RVOT, 50% valvular RVOT, and 50% supravalvular RVOT. Twenty patients underwent operation, and surgical findings served as morphologic control for thirty-four 3D reconstructions (LVOT 17, RVOT 17). Operative findings revealed an accuracy at subvalvular LVOT of 100%, valvular LVOT 90%, supravalvular LVOT 100%, subvalvular RVOT 100%, valvular RVOT 100%, and supravalvular RVOT 100%. Quantitative measurements could adequately be performed. Three-D echocardiography is feasible and accurate for analyzing both outflow tracts of the heart. Particularly, generation of nonconventional horizontal cross sections allows a good definition of extension and severity of lesions.     

右室心尖部起搏与右室流出道起搏对Ⅲ度房室传导阻滞患者疗效的对比研究

目的:比较右室心尖部起搏与右室流出道起搏对Ⅲ度房室传导阻滞患者心室间运动同步性及左室内运动同步性,以及对患者心功能的影响。方法:选取因Ⅲ度及高度房室传导阻滞患者置入双腔起搏器患者共38例。其中心室电极置入右室流出道者20例(RVOT组),置入右室心尖部18例(RVA组),超声心动图术前测量左室舒张末内径(LVEDD),左室收缩末内径(LVESD)、左室射血分数(LVEF)、E/A值、心室间激动延迟时间(IVMD)、室间隔与左心室后壁间收缩延迟时间(SPWMD)。术后1个月、12个月随访。结果:术后1个月,与RVOT组比较,RVA组IVMD、SPWMD明显延长[IVMD(39.83±6.01)∶(31.95±7.86)ms,P=0.02],[SP-WMD(97.83±20.81)∶(84.6±10.89)ms,P=0.023]。术后12个月,与ROVT组比较,RVA组LVEDD明显增大[(49.11±2.39)∶(47.4±1.96)mm,P=0.02],LVESD明显增大[(34.28±3.41)∶(32.5±1.5)mm,P=0.04];LVEF明显降低[(59.56±3.38)∶(62.8±2.14)%,...     

Left Ventricular Outflow Tract Tachycardia Including Ventricular Tachycardia from the Aortic Cusps and Epicardial Ventricular Tachycardia

Idiopathic outflow tract ventricular tachycardia (VT) can arise from the right (RVOT) or left ventricular outflow tract (LVOT). The electrocardiographic (ECG) pattern of RVOT VT is typical in most patients, showing a monomorphic left bundle branch block (LBBB) QRS morphology with an inferior axis. Radiofrequency catheter ablation can be performed with a high success rate and provides a curative therapeutic approach. However, not all VTs with LBBB and inferior axis can be ablated from the RVOT. It has become apparent that LVOT VTs including VT originating from the aortic sinus of Valsalva or epicardium represent underrecognized VT entities which are also amenable to successful catheter ablation. Twelve-lead ECG criteria can contribute to distinguish between sites of VT origin.LVOT arrhythmias represent an increasingly recognized VT entity which can be safely and successfully treated by catheter ablation. Identification of VT origin using ECG criteria and differentiation of LVOT versus RVOT origin is essential in the careful planning of the ablation strategy.     

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。