Echocardiographic criteria of normal left atrial size in adults.

Although the measurement of left atrial diameter (LAD) is a standard part of any echocardiographic examination, the normal range for adults has never been well established or correlated with body surface area (BSA) and sex. We studied 100 males and 100 females whose ages ranged from 15 to 70 years, with no evidence of mitral value disease or other form of heart disease which might cause left atrial enlargement. All measurements were obtained between the external surface of posterior aortic root (AR) and the internal surface of the left atrial wall and were recorded at ventricular end diastole (ED) as well as end systole (ES). The LAD at ED ranged from 9.5 to 29.5 mm with a mean of 19 mm +/- 5.0 S.D.; the diameter at ES ranged from 18.3 mm to 38.7 mm with a mean of 28.5 mm +/- 5.1 S.D. The mean LAD at ED was 20.7 mm +/- 4.8 S.D. in makes compared to the mean diameter of 18.3 +/- 4.9 S.D. in females which represents a significant difference (p less than 0.001). The LAD did not correlate with BSA. The left atrial dimension by ultrasound in these 200 normal patients was compared with the same measurement in 50 catheterized patients with mitral valve disease and proven left atrial enlargement. When absolute values of the left atrial dimension both at end systole and end diastole were determined by ultrasound, there was a clear separation between normal and abnormal (p less than 0.001).     

The relationship of pulmonary artery wedge pressure to the posterior aortic wall echocardiogram in patients free of obstructive mitral valve disease

Aortic wall echocardiograms were obtained simultaneously with pulmonary artery wedge pressures (PAWP) in 21 patients free of obstructive mitral valve disease. There was a significant (p < 0.001) negative correlation between the fraction of passive posterior aortic wall motion occurring in the first third of diastole (the atrial emptying index-AEI) and the pulmonary artery wedge pressure (r = ?0.91). The AEI for patients with normal PAWP (≤ 12mm. Hg) was 0.94 ± 0.06 (mean ± S.D.) compared with 0.61 ± 0.20 for those with abnormal PAWP (> 12 mm. Hg). No patient with a normal PAWP had an AEI < 0.80, and no patient with a PAWP > 18 mm. Hg had an AEI > 0.66. These data suggest that analogous to the reported use of the AEI to estimate severity of mitral obstruction, the index provides a noninvasive measure of left ventricular filling pressure when the mitral valve is normal.     

Influence of recipient atrial contraction on left ventricular filling dynamics of the transplanted heart assessed by Doppler echocardiography

Recipient atrial remnants retain electrical and mechanical activity after orthotopic cardiac transplantation. This study investigated the influence of recipient atrial contraction timing on Doppler ultrasound mitral flow velocity curves, isovolumic relaxation time, peak early mitral flow velocity (M1), mitral valve pressure half-time and peak mitral flow velocity due to atrial systole (M2). Clearly identifiable recipient atrial electrical activity (P waves) was present in 7 of 10 patients studied early postoperatively 2 to 6 months (mean 2.5) (early group) and in 20 of 24 patients seen 1 to 11 years (mean 3) after transplantation (late group). Median age and gender distribution were similar in both groups. For analysis of its influence on isovolumic relaxation time, pressure half-time and M1, recipient atrial contraction was classified by its position in the cardiac cycle as early systole, late systole or diastole. For analysis of M2, it was classified as early diastole, late diastole or systole. Compared with its occurrence in diastole, recipient atrial contraction in late systole was associated with a shorter isovolumic relaxation time, shorter pressure half-time and higher M1. In early systole it was associated with a longer pressure half-time and lower M1 than in diastole; isovolumic relaxation time was unchanged. Recipient atrial contraction in early diastole resulted in a lower M2 than in systole, whereas simultaneous contraction of recipient and donor atria in late diastole resulted in an increase in M2. These results indicate that the timing of recipient atrial contraction and relaxation significantly influences left ventricular filling dynamics.     

Relation of filling pattern to diastolic function in severe left ventricular disease.

M mode and Doppler echocardiograms, apex cardiograms, and phonocardiograms were recorded in 50 patients with severe ventricular disease of varying aetiology to examine how left ventricular filling is disturbed by cavity dilatation. The size of the left ventricular cavity was increased in all with a mean (SD) transverse diameter of 7.2 (0.8) cm at end diastole and 6.3 (0.8) cm at end systole. All were in sinus rhythm and 35 had functional mitral regurgitation. In nine patients, in whom filling period was less than 170 ms, transmitral flow showed only a single peak, representing summation. In the remainder there was a strikingly bimodal distribution of filling pattern. In 12 the ventricle filled dominantly with atrial systole (A fillers). Isovolumic relaxation was long (75 (35) ms) and wall motion incoordinate; mitral regurgitation was present in only one. In most (29) the left ventricle filled predominantly during early diastole (E fillers). Mitral regurgitation, which was present in 26, was much more common than in the A fillers, while the isovolumic relaxation time (10 (24) ms) was much shorter and the normal phase relations between flow velocity and wall motion were lost. In 24 E fillers no atrial flow was detected. In four there was no evidence of any mechanical activity, suggesting "atrial failure". In 20, either the apex cardiogram or the mitral echogram showed an A wave, implying that atrial contraction had occurred but had failed to cause transmitral flow, showing that ventricular filling was fundamentally disturbed in late diastole. A series of discrete abnormalities of filling, beyond those shown by Doppler alone, could thus be detected in this apparently homogeneous patient group by a combination of non-invasive methods. The presence and nature of these abnormalities may shed light on underlying physiological disturbances.     

Relation of filling pattern to diastolic function in severe left ventricular disease

M mode and Doppler echocardiograms, apex cardiograms, and phonocardiograms were recorded in 50 patients with severe ventricular disease of varying aetiology to examine how left ventricular filling is disturbed by cavity dilatation. The size of the left ventricular cavity was increased in all with a mean (SD) transverse diameter of 7.2 (0.8) cm at end diastole and 6.3 (0.8) cm at end systole. All were in sinus rhythm and 35 had functional mitral regurgitation. In nine patients, in whom filling period was less than 170 ms, transmitral flow showed only a single peak, representing summation. In the remainder there was a strikingly bimodal distribution of filling pattern. In 12 the ventricle filled dominantly with atrial systole (A fillers). Isovolumic relaxation was long (75 (35) ms) and wall motion incoordinate; mitral regurgitation was present in only one. In most (29) the left ventricle filled predominantly during early diastole (E fillers). Mitral regurgitation, which was present in 26, was much more common than in the A fillers, while the isovolumic relaxation time (10 (24) ms) was much shorter and the normal phase relations between flow velocity and wall motion were lost. In 24 E fillers no atrial flow was detected. In four there was no evidence of any mechanical activity, suggesting "atrial failure". In 20, either the apex cardiogram or the mitral echogram showed an A wave, implying that atrial contraction had occurred but had failed to cause transmitral flow, showing that ventricular filling was fundamentally disturbed in late diastole. A series of discrete abnormalities of filling, beyond those shown by Doppler alone, could thus be detected in this apparently homogeneous patient group by a combination of non-invasive methods. The presence and nature of these abnormalities may shed light on underlying physiological disturbances.     

重危瓣膜病变合并巨大心脏的外科治疗

目的:报道181例重危瓣膜病变合并巨大心脏的外科治疗体会。方法:回顾性分析181例瓣膜外科病例中合并巨大心脏临床资料,男性76例,女性105例,年龄15～57岁,平均(45.7±15.2)岁。分为2组:巨大左心房(GLA)组84例,左心房内径(LAD)70～150mm,平均(80.3±17.5)mm;巨大左心室(GLV)组97例,左心室舒张末内径(LVEDD)70～112mm,平均(79.4±12.7)mm。患者全部行瓣膜置换术,其中GLA组行主动脉瓣与二尖瓣双瓣膜置换术12例,二尖瓣置换术72例,同期行三尖瓣环缩成形术42例,左心房血栓清出13例;84例均作左心房折叠术。GLV组行主动脉瓣置换术38例,主动脉瓣与二尖瓣双瓣膜置换术27例,二尖瓣置换术32例,二尖瓣置换术均保留全部或部分瓣膜和瓣下结构,同期行三尖瓣环缩成形术18例,左心房血栓清出4例,左心房折叠术21例。结果:手术早期死亡率GLV组和GLA组分别为9.3%和6.0%,GLV组明显高于GLA组(P<0.05);死亡原因GLV组以室性心律紊乱为主(55.6%),明显高于GLA组(P<0.05);GLA组以呼吸衰竭为主。术后1个月超声心动图显示,GLA组LAD平均(60.1±12.1)mm,GLV组LVEDD平均(56.6±16.1)mm,较术前明显缩小(P<0.01)。心功能恢复良好。结论:瓣膜置换同期左心房折叠术有利于改善合并巨大左心房的术后恢复;保留二尖瓣瓣膜及瓣下结构有利于合并巨大左心室病例的恢复。     

The Impact of Catheter Ablation on the Dynamic Function of the Left Atrium in Patients with Atrial Fibrillation: Insights from Four‐Dimensional Computed Tomographic Images

Functional Evaluation of the LA by Dynamic CT. Introduction: Elucidating the functional properties and remodeling process of the entire left atrium (LA) is important not only for offering the mechanistic insight into atrial fibrillation (AF) but also for assessing the effectiveness of catheter ablation. Methods: We included 65 patients with paroxysmal AF and 29 controls. Baseline multidetector computed tomography (MDCT) was acquired in all subjects and a follow‐up MDCT was available in 48 patients after pulmonary vein and LA ablation. The 3‐dimensional images at atrial end‐diastole (ED) and end‐systole (ES) were analyzed. Results: The LA volume (ED: 61.11 ± 15.94 vs 54.12 ± 8.94 mL/m², P = 0.03; ES: 45.29 ± 17.64 vs 33.38 ± 7.78 mL/m², P < 0.001) was increased, and ejection fraction (EF) (26.93 ± 13.40 vs 38.09 ± 11.62%, P < 0.001) decreased in AF patients as compared to controls. After ablation, the ES LA volume (44.73 ± 14.93 vs 38.04 ± 11.51 mL/m², P = 0.04) decreased and the LA EF (25.04 ± 13.13 vs 30.82 ± 7.85%, P = 0.03) increased in patients without any AF recurrence. The wall motion (WM) analysis of the 18 segments of LA revealed increased motional magnitudes of entire LA except for the anterior roof. In contrast, the volume, EF, and WM of LA remained similar in patients with recurrence. Conclusion: Dilated LA with global hypokinesia was noted in AF patients. Improved LA transport function was demonstrated in patients without any recurrence after ablation. However, the anatomic and functional reverse remodeling was not significant in patients with AF recurrence. (J Cardiovasc Electrophysiol, Vol. 21, pp. 270–277, March 2010)     

Pulmonary vein blood flow velocity waveform--with special reference to pulmonary "systolic runoff" in patients with atrial septal defect

In order to evaluate the magnitude of pulmonary "systolic runoff", we studied the pulmonary vein blood flow velocity waveform by positioning a catheter-tip velocity-pressure transducer into the extraparenchymal pulmonary vein just distal to the left atrium. We recorded blood flow velocity and pressure simultaneously, and subsequently identified the zero blood flow velocity with blood flow velocity level of the pulmonary artery in diastole. Patients with atrial septal defect were used as subjects because of the technical ease although the altered hemodynamics were present. Two kinds of flow velocity waveforms were consistently demonstrated. One was a waveform of two peaks with the first peak in late systole and the second peak in early diastole (n = 9). The other was a waveform of one peak with a summit near the end of systole (n = 5). On the assumption that the blood flow velocity waveform obtained with this method is roughly equivalent to the flow volume waveform, we initiated the second study. The area encompassed between the actual flow velocity waveform and the line of zero flow velocity was divided into two compartments, i.e., ventricular systole (S) and diastole (D). The ratios of the area in systole to the sum of the areas in systole and diastole, i.e., (S)/[S) + (D], which are analogous to the pulmonary "systolic runoff", were 0.45 +/- 0.07 (mean +/- SD, n = 13). This suggests that about 40% of the right ventricular stroke volume flows into the pulmonary veins, the left atrium and a portion of the right atrium through the atrial septal defect during ventricular systole.     

Left atrial reverse remodeling and prevention of progression of atrial fibrillation with atrial resynchronization device therapy utilizing dual-site right atrial pacing in patients with atrial fibrillation refractory to antiarrhythmic drugs or catheter ablation

Introduction

Dual-site right atrial pacing (DAP) produces electrical atrial resynchronization but its long-term effect on the atrial mechanical function in patients with refractory atrial fibrillation (AF) has not been studied.

Methods

Drug-refractory paroxysmal (PAF) and persistent AF (PRAF) patients previously implanted with a dual-site right atrial pacemaker (DAP) with minimal ventricular pacing modes (AAIR or DDDR mode with long AV delay) were studied. Echocardiographic structural (left atrial diameter [LAD] and left ventricular [LV] end diastolic diameter [EDD], end systolic diameter [ESD]) and functional (ejection fraction [EF]) parameters were serially assessed prior to, after medium-term (n?=?39) and long-term (n?=?34) exposure to DAP.

Results

During medium-term follow-up (n?=?4.5 months), there was improvement in left atrial function. Mean peak A wave flow velocity increased with DAP as compared to baseline (75?±?19 vs. 63?±?23 cm/s, p?=?0.003). The long-term impact of DAP was studied with baseline findings being compared with last follow-up data with a mean interval of 37?±?25 (range 7–145) months. Mean LAD declined from 45?±?5 mm at baseline to 42?±?7 mm (p?=?0.003). Mean LVEF was unchanged from 52?±?9 % at baseline and 54?±?6 % at last follow-up (p?=?0.3). There was no significant change in LV dimensions with mean LVEDD being 51?±?6 mm at baseline and 53?±?5 mm at last follow-up (p?=?0.3). Mean LVESD also remained unchanged from 35?±?6 mm at baseline to 33?±?6 mm at last follow-up (p?=?0.47). During long-term follow-up, 30 patients (89 %) remained in sinus or atrial paced rhythm as assessed by device diagnostics at 3 years.

Conclusions

DAP can achieve long-term atrial reverse remodeling and preserve LV systolic function. DAP when added to antiarrhythmic drug (AAD) and/or catheter ablation (ABL) maintains long-term rhythm control and prevents AF progression in elderly refractory AF patients. Reverse remodeling with DAP may contribute to long-term rhythm control.     

Hemodynamic correlates of late diastolic posterior motion of the aortic root

Motion of the posterior aortic root on echocardiography is related to left atrial volume change. Early diastolic posterior motion of the aortic root reflects both LA emptying and filling and has been measured as the atrial emptying index. To study late diastolic motion of the aortic root, we measured the slope of posterior motion of the aortic root after left atrial systole (following the P wave of the ECG) in 25 subjects without heart disease (Group 1), in 15 patients with left ventricular hypertrophy due to pressure overload (Group 2), and in 10 patients (Group 3) with mitral stenosis. The aortic root slope measured (mean ± SEM) 58.0 ± 1.9 mm./sec. in Group 1, 50.6 ± 4.5 mm./sec. in Group 2 (NS vs 1) and 28.8 ± 4.5 mm./sec. in Group 3, (p < 0.01 vs 1 or 2).In 16 patients (four in Group 1 and 12 in Group 2) studied at catheterization, an inverse correlation (r = ?0.74, p < 0.01) was found between the aortic root slope (over a range of 30 to 73 mm./sec.) and left ventricular late diastolic chamber stiffness measured with simultaneous left ventricular echo and high-fidelity pressure recordings. No correlation was found between this slope and either left atrial size, total aortic root excursion, left ventricular pressure pre “A” wave, height of the A wave, end-diastolic pressure, or the atrial contribution to left ventricular filling. Therefore, the aortic root slope in late diastole is decreased in mitral stenosis, and in the absence of mitral stenosis, it appears to be related to late diastolic properties of the left ventricle.     

血管紧张素Ⅱ受体拮抗剂对原发性高血压患者左心室肥厚和舒张功能的影响

目的　应用超声心动图评价血管紧张素 1型受体 ( AT1 )拮抗剂对原发性高血压患者左心室肥厚和舒张功能的影响。方法　分别于 AT1 拮抗剂 (氯沙坦 )治疗前和治疗 6个月后 ,对 3 0例原发性高血压患者进行超声心动图检查。 M型超声心动图测量舒张末期左心室内径、室间隔和左心室后壁厚度 ,计算左心室重量指数 ;在心尖左心长轴切面上 ,用多普勒超声心动图测量二尖瓣口舒张早期峰值速度 E、舒张晚期峰值速度 A和 E峰减速时间 ,并计算E/A比值。结果　氯沙坦治疗 6个月后 ,左心室重量指数从 12 4± 2 1g/m2减低为 10 2± 2 2 g/m2 ( P<0 .0 0 1) ;E/A比值 ( 1.2 5± 0 .2 7)明显高于服用前 ( 0 .94± 0 .2 6,P<0 .0 0 1) ,E峰减速时间从 2 2 1± 3 2 ms下降到 180± 2 7ms( P<0 .0 0 1)。结论　 AT1 拮抗剂氯沙坦治疗 6个月使原发性高血压患者左心室肥厚得到消退 ,并改善了其舒张功能     

PtfV1与左心舒张期血流动力学参数的多元偏相关分析

研究38例单纯二尖瓣狭窄患者二尖瓣球囊扩张前后左室舒张期血流动力学参数的变化,发现 Ptfv_1分别与左房内径(LAD)高度负偏相关,与平均左房压(MLAP)及二尖瓣口面积(MVA)正偏相关(-0.9167.0.6551和0.8433,P 均<0.01)。标准偏回归系数显示诸参数对 Ptfv_1的相对贡献率分别为LAD45%,MLAP24%和 MVA31%。风湿性心脏病 Ptfv_1异常的机制是左房收缩超负荷或左房内径增大。     

Atrial fibrillation in congestive cardiomyopathy: Echocardiographic and hemodynamic correlates

Previous studies have suggested an unexpectedly low incidence of atrial fibrillation in patients with congestive cardiomyopathy. To further investigate the incidence of chronic atrial fibrillation in these patients and its relationship to left atrial dimension and pressure, we retrospectively examined M-mode echocardiographic and cardiac catheterization data from 54 patients with idiopathic (n = 29) and ischemic (n = 25) congestive cardiomyopathy. The incidence of atrial fibrillation (17%) was surprisingly low given the degree of left atrial enlargement (51 ± 5 mm; mean ± SD) and left atrial hypertension (19 ± 8 mm Hg). In addition, there were no significant differences in left atrial pressure or left atrial dimension between those congestive cardiomyopathy patients in sinus rhythm and those in atrial fibrillation, nor was there a higher incidence of secondary mitral regurgitation in patients in atrial fibrillation. Comparisons were also made between congestive cardiomyopathy patients and 21 patients with primary mitral valve disease and atrial fibrillation. Left atrial pressure was not significantly different between these groups. However, the mean left atrial dimension of the patients with mitral valve disease (56 ± 8 mm) was greater (P < 0.01) than that of patients with idiopathic (51 ± 6 mm) or ischemic (50 ± 4 mm) cardiomyopathy in sinus rhythm and also greater (P = 0.07) than left atrial dimension (51 ± 6 mm) of congestive cardiomyopathy patients in atrial fibrillation. Furthermore, massive enlargement of the left atrium (greater than 60 mm) was a common feature of mitral valve disease (33% incidence) but occurred only rarely in congestive car-diomyopathy (5% incidence). We conclude that while left atrial volume and pressure loads may be important contributors to the pathogenesis of atrial fibrillation, these factors are not sufficient to produce the arrhythmia in most patients with congestive cardiomyopathy. Other variables such as disease duration or the degree of atrial fibrosis or inflammation may also be important in determining which patients with left atrial enlargement will develop atrial fibrillation. Furthermore, massive left atrial enlargement (left atrial dimension > 60 mm) is rarely associated with ischemic or idiopathic congestive car-diomyopathy and suggests underlying primary mitral valve disease.     

超声心动图评价成人房间隔缺损封堵术后心脏结构和功能的变化

目的探讨超声心动图评价成人房间隔缺损(atrial septal defects,ASD)介入封堵术后心脏形态和功能变化。方法经超声心动图和心电图检查确诊为ASD并成功施行ASD封堵术的患者74例,年龄(35.63±12.74)岁,ASD直径为(16.29±5.11)mm。于封堵器堵闭术后24h、1个月、3个月、6个月和12个月进行经胸超声心动图追踪测量主动脉内径、左心室舒张末内径、左心室收缩末内径和右心室前后径,肺动脉内径和肺动脉瓣血流速度,右心房和右心室的上下径、主动脉瓣口血流速度、二尖瓣口血流速度、三尖瓣口血流速度和左心室射血分数,同时测量封堵器的直径和长度,并进行统计学分析。结果术后24h与术前相比,右心房内径、右心室内径、肺动脉内径、三尖瓣口血流速度和肺动脉瓣口血流速度均显著减少(P0.01);左心房内径、左心室内径、主动脉内径、二尖瓣口血流速度和主动脉瓣口血流速度均显著增加(P0.05);左心室射血分数无明显变化。房室大小和血流速度在术后24h内变化明显,在术后1个月后的随访中逐渐趋于稳定。结论封堵器介入封堵ASD,既纠正了解剖畸形,又改善了左心和右心系统的几何结构。     

An echocardiographic assessment of atrial mechanical behaviour

Relations between movement of the atrioventricular ring and changes in left atrial and ventricular dimensions were studied by echocardiography and compared with apexcardiography and Doppler mitral flow velocity traces in 20 healthy controls and in patients with left ventricular hypertrophy (n = 28) or dilatation (n = 16). During left ventricular systole the atrioventricular ring, a structure common to ventricle and atrium, moved towards the ventricular apex, thus increasing left atrial volume. This action matched pulmonary venous return because it was in phase with the transverse left atrial dimension measured from aortic root to posterior left atrial wall. During early diastole, the mitral ring moved rapidly towards the atrium as transmitral flow accelerated. This requires a force directed from ventricle to atrium, likely to be the result of elastic recoil arising from compression of the ventricular myocardium or stretching of the atrial myocardium during ventricular systole. Two additional mechanisms of ventricular filling with atrial systole were recognised: (a) an increase in ventricular volume as the atrioventricular ring moved upwards and (b) transverse left ventricular expansion by pressure driven transmitral flow. The former is undetectable by Doppler from the apex; it accounted for 10% of ventricular filling in the healthy controls, but for significantly less in those with ventricular dilatation. In left ventricular hypertrophy, left ventricular filling was maintained by both mechanisms compensating for the reduced increase in volume early in diastole. Interactions between the atrium and ventricle are functionally important during ventricular systole, early diastole, and in atrial systole. They are not included in the traditional separation of atrial function into reservoir, conduit, and pump functions.     

An echocardiographic assessment of atrial mechanical behaviour.

Relations between movement of the atrioventricular ring and changes in left atrial and ventricular dimensions were studied by echocardiography and compared with apexcardiography and Doppler mitral flow velocity traces in 20 healthy controls and in patients with left ventricular hypertrophy (n = 28) or dilatation (n = 16). During left ventricular systole the atrioventricular ring, a structure common to ventricle and atrium, moved towards the ventricular apex, thus increasing left atrial volume. This action matched pulmonary venous return because it was in phase with the transverse left atrial dimension measured from aortic root to posterior left atrial wall. During early diastole, the mitral ring moved rapidly towards the atrium as transmitral flow accelerated. This requires a force directed from ventricle to atrium, likely to be the result of elastic recoil arising from compression of the ventricular myocardium or stretching of the atrial myocardium during ventricular systole. Two additional mechanisms of ventricular filling with atrial systole were recognised: (a) an increase in ventricular volume as the atrioventricular ring moved upwards and (b) transverse left ventricular expansion by pressure driven transmitral flow. The former is undetectable by Doppler from the apex; it accounted for 10% of ventricular filling in the healthy controls, but for significantly less in those with ventricular dilatation. In left ventricular hypertrophy, left ventricular filling was maintained by both mechanisms compensating for the reduced increase in volume early in diastole. Interactions between the atrium and ventricle are functionally important during ventricular systole, early diastole, and in atrial systole. They are not included in the traditional separation of atrial function into reservoir, conduit, and pump functions.     

Echocardiographic characteristics and causal mechanism of physiologic mitral regurgitation in young normal subjects

Background: It has become evident that mitral regurgitation (MR) is not uncommon in healthy subjects, and Doppler color flow mapping is a technique that imparts important information relevant to its detection. Hypothesis: Using transthoracic echocardiography, this study evaluated the mechanism of physiologic MR in young normal subjects using transthoracic echocardiography. Methods: The study population consisted of 48 young normal subjects (mean 21 ± 5 years) with MR (physiologic MR group), 40 age-matched young normal subjects (mean 20 ± 5 years) without MR (control group), 45 patients (mean 41 ± 15 years) with mitral valve prolapse with MR (MVP group), and 27 patients (mean 59 ± 13 years) with ruptured chordae tendineae (rupture group). Results: Men were predominant in the rupture group, whereas there were no significant gender differences in the other three groups. Left ventricular end-diastolic dimension and left atrial systolic dimension were slightly smaller in the physiologic MR group than in the control group, but were significantly smaller than those in the MVP and rupture groups. The ratio of the maximum anteroposterior diameter to the maximum transverse diameter on chest radiography and the ratio of the short- to long-axis diameter of the left ventricular cavity at end diastole, determined from two-dimensional short-axis echocardiogram, were significantly lower in the physiologic MR group than in the other three groups. Mitral regurgitation occurred more frequently at the posteromedial commissural site in the physiologic MR and MVP groups, whereas there was no preference for location in the rupture group. Early systolic MR was often observed in the physiologic MR group, whereas pansystolic MR was common in the MVP and rupture groups. Conclusion: As a causal mechanism for physiologic MR detected in young normal subjects, “flattening” of the thorax during growth may cause morphologic abnormalities of the left atrial and ventricular cavities, resulting in spatial imbalance of the mitral complex and resulting in malcoaptation of the valve.     

Peak early diastolic mitral annulus velocity by tissue Doppler imaging adds independent and incremental prognostic value

OBJECTIVES: The aim of this study was to ascertain if left ventricular mitral annulus velocities measured by tissue Doppler imaging (TDI) are more powerful predictors of outcome compared with clinical data and standard Doppler-echocardiographic parameters. BACKGROUND: Tissue Doppler imaging of basal or mitral annulus velocities provides rapid assessment of ventricular long axis function. But it is not known if TDI-derived velocities in systole and diastole add incremental value and are superior to the standard Doppler-echocardiographic measurements as a predictor of outcome. METHODS: The study population consisted of 518 subjects, 353 with cardiac disease and 165 normal subjects who had full Doppler two-dimensional-echocardiographic studies with measurement of mitral inflow velocities in early and late diastole, E-wave deceleration time (DT), peak systolic mitral annular velocity (Sm) early and late diastolic mitral annular velocity (Em and Am) by TDI, early diastolic flow propagation velocity, and standard chamber dimensions. All subjects were followed up for two years. The end point was cardiac death. RESULTS: Tissue Doppler imaging mitral annulus systolic and diastolic velocities were all significantly lower in the non-survivors (all p < 0.05) as was DT (p = 0.024). In the Cox model the best predictors of mortality were Em, Sm, Am, left ventricular ejection fraction, left ventricular mass, and left atrial diameter in systole (LADs). By backward stepwise analysis Em and LADs were the strongest predictors. After forcing the TDI measurements into the covariate model with clinical and mitral DT <0.16 s, Em provided significant incremental value for predicting cardiac mortality (p = 0.004). CONCLUSIONS: Mitral annulus velocity measured by TDI in early diastole gives incremental predictive power for cardiac mortality compared to clinical data and standard echocardiographic measurements. This easily available measurement adds significant value in the clinical management of cardiac patients.     

心脏再同步化治疗慢性心力衰竭伴持续性心房颤动的疗效观察

目的评价心脏再同步化治疗(CRT)慢性心力衰竭(心衰)合并持续性心房颤动(房颤)患者的临床疗效。方法选择慢性心衰患者23例,其中13例窦性心律患者及4例房颤患者(房颤CRT患者)接受双心室起搏治疗,另6例房颤患者(药物治疗患者)继续服用抗心衰药物治疗。术后3个月进行随访,观察患者的心功能分级(NYHA),6 min步行距离,超声心动图测定各房室腔内径大小、LVEF、二尖瓣反流以及速度向量成像超声评价同步性参数的变化。结果 17例患者三腔起搏器置入术均取得成功。术后3个月随访,房颤CRT患者心功能分级[(3.00±0.00)级vs(2.25±0.50)级]、左心房内径[(52.75±3.50)mm vs (45.25±3.50)mm,P<0.05]、LVEF[(36.25±4.79)% vs (42.00±5.16)%]及二尖瓣反流(3.25±0.50 vs 1.50±0.58,P<0.01)较术前均有明显改善,速度向量成像超声结果显示,室内不同步较术前有明显改善。与药物治疗患者比较,房颤CRT患者LVEF、左心房内径、二尖瓣反流明显改善。结论对于慢性心衰合并持续性房颤患者,在有效控制心室率的基础上行CRT明显优于药物保守治疗,与窦性心律患者一样可以改善心功能。     

AAISafeR起搏模式自身对照研究

目的分析患者置入具有AAISafeR功能的Symphony2450起搏器后,短期内心脏结构和功能改变的特点及其与心室起搏百分比之间的关系。方法共入选22例患者,采用随机、单盲、自身前后交叉对照原则,观察同一患者在不同起搏模式下(AAISafeR和DDD)左房内径(LAD)、左室舒张末径(LVEDV)、左室收缩末径(LVESV)及左室射血分数(LVEF)的变化。结果不同起搏模式分别观察3个月后,LAD缩小(38.5±5.7mmvs39.7±4.5mm,P<0.05),但LVEDV、LVESV及LVEF变化不大。与DDD模式相比,AAISafeR模式下心室起搏、感知百分比有显著性差异(分别为67.49%±13.09%,43.89%±12.28%vs45.23%±11.15%,64.88%±15.08%,P均<0.05)。结论AAISafeR模式可有效减少心室起搏的百分比,较高比例的心室起搏百分比短期内(3个月)可影响心腔结构的重塑,但尚未引起心室功能的改变。