房室折返性心动过速的重整现象

目的:探讨房室折返性心动过速(AVRT)的重整特点及对经典重整概念的质疑。方法:选择41例行射频消融治疗的顺向型AVRT患者,心动过速发作时,在心脏的不同部位进行S2刺激扫描,观察心动过速对S2刺激的重整反应。结果:28例(其中左侧房室旁路19/32例,右侧房室旁路9/9例)经高位右房AS2刺激可以使心动过速重整,39例(其中左侧房室旁路30/32例,右侧房室旁路9/9例)经右心室VS2刺激可以使心动过速重整。其中8例左侧旁路患者从左心房、左心室刺激均能发生重整。重整时,偶联间期与回归周期之和(即代偿间歇)与心动过速周长(CL)的关系有3种不同的表现。结论:重整与刺激部位到折返环的距离密切相关;代偿间歇不仅可以小于CL的2倍,也可以大于或等于CL的2倍。     

快频率依赖性室房逆传左侧隐匿性房室旁道参与的心动过速及射频导管消融

目的探讨快频率依赖性室房逆传特性左侧隐匿性房室旁道的电生理特点及射频消融。方法对8例心电图显示窄QRS波群心动过速的患者行电生理检查,分析房室、室房传导情况、心动过速特点、旁道定位,并行射频消融。结果8例患者均证实存在快频率依赖性室房逆传特性左侧隐匿性旁道,在较慢频率起搏右心室时旁道逆传发生阻滞,而以中等频率起搏时表现为间断旁道逆传,较快频率起搏时才表现为旁道1：1传导且均诱发了房室折返性心动过速,于快频率心室刺激下标测消融靶点,消融均获成功。结论左侧隐匿性房室旁道有时可发生快频率依赖性室房逆传现象,并伴发房室折返性心动过速,在射频消融中需注意分辨,以免漏诊。     

三磷酸腺苷对室房传导的电生理作用

目的　探讨三磷酸腺苷 (adenosine triphosphate,ATP)对房室结双径路参与的房室交界区折返性心动过速和旁路参与的房室折返性心动过速患者的室房传导的电生理作用。　方法　 39例房室交界区折返性心动过速和 6 7例房室折返性心动过速患者在右心室起搏 (频率 140次 / m in)时 ,经股静脉快速注射 ATP 2 0 mg,连续记录体表心电图和心内电图 ,观察室房传导变化。　结果　房室交界区折返性心动过速组 33例 (84.6 % )在注射 ATP后出现室房阻滞 ,其余 6例无变化。6 7例房室旁路患者在消融前 ,6 1例 (91% )室房传导无变化 ,另 6例出现室房阻滞 ,其中 2例具递减性传导 ;而在消融后 2 4例右心室起搏频率超过 16 0次 / m in,仍为 1∶ 1逆传 ,注射 ATP后 2 3例出现室房阻滞 ,仅 1例不受影响。　结论　 ATP对房室结及旁路的电生理作用不同 ,注射 ATP后出现室房阻滞对鉴别经房室结或旁路逆传有一定价值 ,是旁路消融成功的一个判别指标 ,但并不一定完全可靠     

射频消融阻断房室旁路后室房逆传的特点

以射频电流阻断90例预激综合征患者的房室旁路.62例(68.9%)于旁路消融后呈室房分离,28例(31.1%)呈室房递减性传导.室房分离与患者年龄、性别及旁路传导特性无关,但左或右游离壁旁路阻断 后室房分离者多于递减传导者,而间隔旁路阻断后差别不显著.3例复发均为室房递减传导者.本研究提示,心房激动长期经旁路下传致房室结功能废用性退化可能为室房分离的原因,旁路阻断后室房递减传导者应仔细检测以除外潜在的旁路逆传.     

室性心动过速合并室上性心动过速的射频消融

目的报道7例室性心动过速（VT）合并室上性心动过速（sVT）的射频消融。方法7例患者男6例,女1例,平均年龄（21±9）岁。阵发性心动过速病史（3．7±2．0）年。术中心房和心室刺激诱发VT和SVT,并进行消融。结果7例患者心房或心室刺激能反复诱发和终止VT合并SVT。法洛四联症矫治术后右心室VT合并三尖瓣环峡部依赖性心房扑动（AFL）1例,其余6例均为维拉帕米敏感性左心室特发性室速（ILVT）,分别合并AFL1例,左后间隔旁路参与的顺向型房室折返性心动过速（AVRT）1例,冠状静脉窦口慢旁路参与的顺向型AVRT1例,慢慢型房室结折返性心动过速（AVNRT）1例,左侧游离壁旁路参与的顺向型AVRT2例。7例患者的两种心动过速均成功消融,所有患者消融术后随访2年,无一例VT或SVT复发。结论VT合并SVT并不少见,消融术中应放置必需的心腔内电极导管,完成详细电生理检查,避免漏诊。一次消融应根除两种疾病。     

间隙性逆传阻滞房室旁道参与的心动过速及射频消融

目的研究间隙性逆传阻滞房室旁道参与的心动过速特点及射频消融术。方法6例患者,男性3例,女性3例,年龄24~58岁,其中A型预激1例,B型预激1例,采用右室心尖部和左室S1S1及S1S2起搏分析室房传导情况、心动过速特点、旁道位置确定及射频消融。结果左前游离壁2例,左侧壁1例(A型预激),左后壁旁道2例,右侧三尖瓣环10点处1例(B型预激)。所有旁道具有1:1室房传导功能,6例患者均有间隙性旁道逆传阻滞,均呈2:1室房逆传阻滞。在右室起搏下或窦性心律下标测靶点,所有病例均消融成功。结论不论隐匿性或显性房室旁道均可发生间隙性室房逆传阻滞,电生理检查及射频消融过程中应注意分辨偶发室房逆传阻滞现象,以免漏诊。     

预激综合征合并完全性房室阻滞的诊断及治疗

目的 报道5例预激综合征合并完全性房室阻滞患者的诊断和治疗。方法 进行心内电生理检查和射频消融旁路。结果 电生理检查未诱发房室折返性心动过速，心房刺激时体表心电图的预激程度无变化。消融阻断旁路前传后，均示完全性房室阻滞。4例患者在消融术后植入永久性起搏器．随访中无心房颤动发作。1例患者放弃对旁路的消融治疗。结论 预激综合征合并完全性房室阻滞是射频消融的适应证。消融前对房室传导功能的评定十分重要。成功消融旁路后应植入永久性起搏器。     

射频消融术治疗室上性心动过速80例体会

用射频消融术治疗室上性心动过速80例.其中,房室折返性心动过速64例(65条旁路),56条左侧旁路中52条(92.9%)和9条右侧旁路中7条(77.8%)被阻断.14例房室结折返性心动过速(消融慢径)及2例房性心动过速和心房纤颤(消融房室结)均成功.比较初期30例和以后34例房室旁路病人的消融,显示了射频消融术开展过程中的学习曲线.此外,本文对预激综合征体表心电图旁路定位误差的原因,作了初步探讨.     

射频消融术治疗快速心律失常287例报告

报道射频消融术治疗２８７例快速心律失常，其中房室旁路折返性心动过速２１２例，共有旁路２１９条。１６７条左侧旁路，１６１条（９６．４％）被阻断，３例在常规逆行插入大头导管消融失败后，改用经房间隔穿刺法消融成功；５２条右侧旁路，４６条（８８．５％）被阻断，１例在心中静脉内消融成功。６５例房室结折返性心动过速，６４例（９８．５％）选择性消融慢径成功，无一例遗留房室传导阻滞的并发症。５例特发性室性心动过速消融成功。本组并发症５例，６例心动过速复发。     

下位法射频消融慢径路改良房室结治疗室上性心动过速23例

用下位法射频消融慢径路改良房室结治疗房室结折返性心动过速(AVNRT)18例,房室折返性心动过速(AVRT)5例.AVNRT中16例为慢—快型,1例快—慢型,1例慢—快型与快—慢型并存,18例慢径路全部阻断成功.AVRT中1例显性预激,4例隐性预激,有5例慢径路和3例房室旁路消融成功.射频放电时21例出现结性心律.无严重并发症出现.AVNRT病人中随仿1—15个月有1例复发,第二次射频成功.认为下位法射频消融阻断慢径路成功率高,并发症少.     

Iatrogenic left pulmonary artery to left atrium fistula

Trans‐catheter balloon angioplasty is a well‐established treatment modality for pulmonary artery (PA) stenosis in children with congenital heart disease. We report a case of an unusual complication where a fistula developed between the left PA and the left atrium during balloon angioplasty in a patient with history of tetralogy of Fallot. This was successfully treated with placement of a covered stent. © 2014 Wiley Periodicals, Inc.     

Relationship of left atrial appendage function to left ventricular function

BACKGROUND: The study was conducted to evaluate the relationship of left atrial appendage function to left ventricular function and to analyze, if left ventricular dysfunction predisposed to left atrial appendage thrombus formation even in the presence of sinus rhythm. METHODS AND RESULTS: The study was conducted in 78 patients with a mean age of 53+/-8.5 years, all of whom were in sinus rhythm. Transesophageal echocardiography was performed to record the left atrial appendage emptying and filling velocity and to look for the presence of spontaneous echo contrast and thrombus. Patients with severe left ventricular dysfunction (Group I--left ventricular ejection fraction < 35%) and patients with moderate left ventricular dysfunction (Group II--left ventricular ejection fraction 35-45%) had lower left atrial appendage emptying velocity (33.6+/-16 and 39.7+/-19.5 cm/s, respectively) and filling velocity (41+/-14.7 and 41+/-17 cm/s, respectively) when compared to patients with preserved systolic function (Group II--left ventricular ejection fraction >45%), who had emptying and filling velocity of 55+/-16 and 56+/-15 cm/s, respectively (p <0.05). Twelve out of 32 (38%) patients with severe left ventricular dysfunction (Group I) and 7 out of 25 (28%) patients with moderate left ventricular dysfunction (Group II) had presence of left atrial appendage thrombus as compared to none of the patients with preserved left ventricular ejection fraction (Group III) (p <0.001). CONCLUSIONS: Patients with left ventricular dysfunction also had left atrial appendage dysfunction as evidenced by lower emptying and filling velocities and had increased incidence of thrombus formation.     

Isolation of the left common carotid or left innominate artery

Isolation of the left common carotid or left innominate artery from the aortic arch is rare. A six week malformed infant with a right aortic arch had isolation of a left innominate artery and connection to the pulmonary artery by a left ductus arteriosus. A right ductus arteriosus had been ligated. Another infant with a right aortic arch and ostium primum atrial septal defect was shown to have an aberrant left subclavian artery arising from the lower descending aorta. The left common carotid artery filled retrogradely and drained into the pulmonary artery by a left ductus arteriosus. This abnormality has not been reported before.     

Two-dimensional echocardiographic and left ventriculographic evaluations of left ventricular diverticula

Twenty cases of left ventricular diverticula were gleaned from 4,300 consecutive angiocardiographic records (13 males and seven females whose age ranged from 17 to 78 years with a mean of 52 +/- 16 years). Their findings were compared with those of 16 patients with left ventricular aneurysms due to myocardial infarction. In only one patient was a diverticulum first detected by two-dimensional echocardiography before left ventriculography was performed. None of the patient had an associated midline thoracoabdominal defect. Five patients had premature ventricular beats, two of whom had ventricular tachycardia. Three patients complicated mitral valve prolapse and three atrial septal defect. Of the 20 patients, four each had two diverticula, as opposed to 16 others who each had a single diverticulum. The diameter of the diverticula ranged from eight to 70 mm. The sites of 14 diverticula were along the inferior wall; five in the anterior wall; four in the apex. Morphologically 15 diverticula were bulky outpouchings, six were tongue-like, and three hammocking. All diverticula exceeding 15 mm in diameter and originated near the mitral ring could always be detected in the short-axis view of two-dimensional echocardiography. However, those originating in the apex or of a tongue-like configuration could rarely by detected. Comparative two-dimensional echocardiographic analyses of 16 diverticula, 16 left ventricular aneurysms, and 16 normal left ventricular walls disclosed that the left ventricular aneurysmal wall had a higher echo intensity, but the diverticula had the same wall echo intensity as the normal left ventricular wall. Left ventricular end-diastolic wall thickness in an aneurysm (7.6 +/- 1.5 mm) was lower (p less than 0.01) than the normal left ventricular wall (11.1 +/- 1.3 mm), but it did not differ from the normal left ventricular wall in any case of diverticulum (10.2 +/- 1.5 mm). The percent wall thickening ratio in aneurysms (-3.6 +/- 10.7%) was lower (p less than 0.01) than the normal left ventricular wall (39.8 +/- 10.9%), but it did not differ from the normal left ventricular wall in diverticula (45.8 +/- 16.6%). Regional fractional shortening in the diverticula (41.3 +/- 9.2%) did not differ from that in the normal left ventricular wall (34.5 +/- 5.2%). In conclusion, a small diverticulum without a midline thoracoabdominal defect is not rare, and two-dimensional echocardiography is the diagnostic method of choice in many cases based on the echo features described above.     

Usefulness of left atrial abnormality for predicting left ventricular hypertrophy in the presence of left bundle branch block

The objective of this study was to identify left atrial (LA) abnormality on the electrocardiogram and other related variables as predictors of left ventricular (LV) hypertrophy in the presence of left bundle branch block (LBBB). In the presence of complete LBBB, the diagnosis of electrocardiographic abnormalities is problematic and that of LV hypertrophy remains difficult. The usual electrocardiographic criteria applied for the diagnosis of LV hypertrophy may not be reliable in the presence of LBBB. Therefore, noninvasive criteria will help physicians diagnose LV hypertrophy with electrocardiography. LA abnormality on the electrocardiogram was assessed by 2 independent observers as predictor of LV hypertrophy in the presence of LBBB in 120 patients, and data were compared with those of 100 patients without LA abnormality. LV mass was calculated from echocardiographic data. Besides LA abnormality, the other variables studied for prediction of LV hypertrophy were gender, age, body surface area, body mass index, frontal axis, and QrS duration. Of the 6 criteria analyzed, the P terminal force was found to be the most common and consistent criterion to detect LA abnormality. LV hypertrophy was confirmed by echocardiographic determination of LV mass in both groups. Observers reliably differentiated between the hypertrophied and normal-sized left ventricle in the presence of LBBB by correlating LA abnormality with LV mass determined by echocardiography. Observer 1 detected LA abnormality in 89% and observer 2 in 84% of patients. False-positive results were present in 11% and 16%. The observer's recognition of LA abnormality in the present study was 91%. The 2 observers showed a sensitivity of 81% and 79% and a specificity of 91% and 88%, respectively, when diagnosis of LV hypertrophy was determined. LV mass increased significantly and was diagnostic of LV hypertrophy in 92% of patients with LA abnormality. In the remaining 11 patients (8%), the LA abnormality was of marginal abnormal magnitude. Each 0.01-mV/s increase in LA abnormality gave an increase of 30 g of LV mass. LV mass was increased in 86% of patients when corrected by body surface area. LV hypertrophy in the presence of LBBB on electrocardiography was found in only 13 patients (10%) when the 6 frequently used conventional criteria for diagnosis of LV hypertrophy by electrocardiography were used. Regression analysis revealed LA abnormality to be a strong independent predictor of increased LV mass. Multivariate analysis also revealed age, body mass index, body surface area, frontal axis, and QrS duration to be significant predictors of LV mass. This noninvasive study correlates LA abnormality by electrocardiogram and LV hypertrophy with echocardiography to conclude that LA abnormality was significantly diagnostic of LV hypertrophy in the presence of LBBB. Age, body mass index, body surface area, frontal axis, and QrS duration were also significant predictors of LV mass.     

Ratio of left atrial to left ventricular size: an anatomical marker of the diastolic left ventricular pressure-volume relationship

BACKGROUND: Classification of diastolic heart function is best defined by the degree of leftward and upward shift of the diastolic pressure-volume relationship (DPVR). Direct measurement of DPVR, however, requires invasive techniques. Increased left atrial (LA) size is a marker of left ventricular (LV) diastolic hypertension, and so, the LA/LV diameter ratio has the potential to mark the degree of upward and leftward shift in the LV-DPVR. We thus investigated the association of this novel marker with exposures known to induce diastolic dysfunction and with clinical evidence of diastolic dysfunction. METHODS AND RESULTS: Reports from 7,803 patients undergoing maximal exercise stress echocardiography were reviewed. Increased LA/LV diameter ratio predicted diminished exercise capacity (P < 0.001) in a multivariate regression analysis. Increased LA and decreased LV diameters were each independently associated with exercise capacity (P < 0.001, both). Increased LA/LV diameter ratio was associated with hypertension (P = 0.001), diabetes (P = 0.03) and with increased severity of LV hypertrophy (P< 0.001). Those with LA/LV diameter ratio > or = 1.0 were more likely to use loop diuretics, odds ratio = 2.5 [95% CI, 1.4, 4.5], compared to those with lower ratio values. CONCLUSIONS: Increased LA/LV diameter ratio was observed in subjects with hypertension, diabetes and LV hypertrophy. Increased ratio predicted worse exercise capacity and was associated with more frequent loop diuretic use. These data are consistent with the hypothesis that this ratio is a noninvasive marker of the LV-DPVR.     

Evaluation of left atrial remodelling following percutaneous left atrial appendage closure

Objectives The left atrial appendage (LAA) is known to play a reservoir role in left atrial (LA) hemodynamics. The physiologic consequences of its percutaneous occlusion have not been evaluated. We sought to evaluate the effect of percutaneous LA appendage closure (LAAC) on LA remodelling and cardiac hemodynamics. Methods: All patients referred for LAAC in our institution were enrolled. Cardiac computed tomography for LA volume measurement and transthoracic echocardiography (TTE) for left ventricular diastolic function and filling pressure assessment were performed at baseline and 3 months after closure. Results: Sixty-three patients (mean age 73 ? 9 years) underwent successful LAAC and remain clinically stable at 3 months without change in medical treatment except the introduction of an antiplatelet therapy. Mean LA volume, excluding the LAA did not change between baseline and follow-up (145 55 mL and 144 50 mL, p=0.30). Among diastolic function echographic parameters, the E/E’ ratio increased (7.9?2.1 vs 9.1?3.6; p=0,038), suggesting a trend toward an elevation of LV filling pressure. Conclusions: In this preliminary study, we showed no early significant LA remodelling after LAA occlusion in terms of volume change, but a trend toward an increase of LV filling pressure. Our results suggest potential changes in cardiac hemodynamics after LAA closure, suggesting to be cautious when performing this procedure in patients with heart failure. Additional studies with longer follow-up and invasive evaluations should be performed to better investigate this potential issue.