不纯性心房纤颤(扑动)与左、右心房扩大的关系

目的 探讨不纯性心房纤颤(简称不纯性房颤)或不纯性心房扑动(简称不纯性房扑)与左、右心房扩大的关系.方法 在67例患者体表12导联心电图上V1导联以颤动波(扑动波)为主,当中夹以短暂的扑动波(颤动波)诊断为不纯性房颤(房扑).每个患者的左、右心房均经彩色超声心动图检查.结果 67例患者的双心房内径均在32 mm以上,无l例在30 mm以下.其中37例双房内径均在41 mm以上,61 mm以上左心房23例、右心房3例.在44例不纯性房颤中41～100 mm左心房40例、右心房22例.在23例不纯性房扑中,41～100 mm左心房21例、右心房9例,且无1例超过61 mm.结论 在不纯性房颤(房扑)中,左、右心房均增大,左房增大更多.     

高血压病患者左心房内径增大与左心室结构改变的关系探讨

本文研究了55例高血压病左心房内径增大患者左心房内径与左心室结构参数的关系.结果表明,左心房内径≥40mm组,左心室扩大/肥厚的发生率显著高于<40mm组(P<0.05);左心房内径与左心室内径及重量显著相关(P<0.01).提示高血压病患者左心房内径增大有伴随左心室结构改变的趋势,可能是高血压性心脏病的早期表现.     

心房颤动患者心房组织醛固酮和心房基质重构研究

目的 探讨心房颤动患者心房组织醛固酮水平和心房基质重构的相关关系。方法 入选行人工瓣膜置换术的风湿性心脏病患者25例,其中窦性心律者12例,慢性心房颤动者（房颤时程≥6月）13例。术前进行经胸超声心动图检查并留取有关资料,于手术时取左右心房侧壁组织,用放射免疫法测定心房组织醛固酮水平;用VG染色法对总胶原容量分数（CVF）半定量分析;RT-PCR检测Ⅰ型和Ⅲ型胶原mRNA表达改变。结果 与窦性心律者比较心房颤动组左房内径显著扩大（均P<0.01）;心房肌组织醛固酮［右房:(310.3±69.6) vs (154.5±35.8)pg/g,左房:(334.2±76.6) vs (166.5±38.6)pg/g,均P<0.01］、Ⅰ型胶原mRNA表达［右房:(1.95±0.22) vs (0.71±0.11),左房:(2.05±0.28) vs (0.74±0.16),均P<0.01］和CVF［右房:(13.0±1.9)％ vs (6.5±1.1)％,左房:(14.1±1.7)％ vs (6.7±1.2)％,均P<0.01］均明显增加;Ⅲ型胶原mRNA表达在房颤组和窦性心律组间无差异;上述指标在左、右心房之间无差异。Ⅰ型胶原mRNA与左心房直径（r＝0.885,P<0.01）、CVF和左心房直径（r＝0.845,P<0.01）均显著正相关;心房组织醛固酮水平与左心房内径（r＝0.814,P<0.01）和CVF（r＝0.885,P<0.01）均呈明显正相关。结论 心房组织醛固酮水平可能在心房颤动心房基质重构中起重要作用,并可能参与了心房颤动的发生和维持。     

三维标测指导下射频导管消融右心耳起源的局灶性房性心动过速

目的 报道应用三维标测指导射频导管消融起源于右心耳的局灶性房性心动过速(房速),并初步探讨其临床及心电学特征.方法 共6例患者(男性4例,女性2例,年龄(43±19)岁]临床诊断为窄QRS心动过速,其中3例曾行常规射频消融失败,4例左心房内径明显扩大.经电生理检查证实为房速.术中行EnSite-NavX激动标测或者Carto电解剖标测以明确局灶性房速并指出最早激动大致范围.在局部做精细标测找到心房最早激动处,于心动过速时应用盐水灌注导管放电消融,能量30～40 W,温度43℃.即刻成功指标为心动过速终止并不再被诱发.结果 6例心动过速平均心动周期为(343±53)ms.三维激动标测结果显示房速呈右心耳部位点状扩布,并且整个右心房激动时间占心动周期的27%±8%.成功消融靶点局部A波较体表心电图P波提前(52±13)ms.消融后行右心房心耳造影确认消融导管位置.6例右心耳房速均成功消融且未有并发症发生.随访3个月其中1例复发心动过速,经再次标测证实为三尖瓣前侧部局灶性房速并且成功消融.左心房扩大者心房内径较术前显著缩小[(41±6)mm对(36±6)mm,P＜0.05].结论 局灶性房速可起源于右心耳并可以成功消融.三维标测有助于靶点定位及消融成功.     

心房扩大与房性快速心律失常关系分析

目的为进一步探讨房性快速心律失常发病机理。方法采用多普勒超声心动图和动态心电图检查方法对１５０例心血管病人心房扩大和房性心律失常发生情况进行分析。结果左心房扩大为主者房性快速心律失常发生率（７１．９３％）显著高于右心房扩大为主者（２０．００％）和心房内径正常者（１４．２９％），Ｐ〈０．０１；心房内径扩大越明显，房性快速心律失常的发生率越市，性质越严重；即便是程度相同的左心房扩大者，二尖瓣狭窄为主的     

50例肺移植术后心房颤动分析

目的 研究肺移植术后心房颤动（房颤）的发生率与术前相关危险因素.方法 收集无锡市人民医院2002年至2009年50例肺移植患者的临床资料,根据住院期间是否出现房颤持续5 min以上分为房颤组和非房颤组,分析两组患者的超声心动图检查指标及术前一般临床资料.结果 术后13例患者（26.0%）发生房颤,房颤组术前左心房内径（37.38±6.79）mm大于非房颤组中术前左心房内径（32.70±7.22）mm,两者间差异有统计学意义（P＜0.05）.术前左心房内径≥40 mm的患者高于非房颤组[50.0%（8例）对23.5%（8例）,x2=5.329,P=0.021],房颤组与非房颤组在性别、年龄、肺移植种类、原发疾病、术前左心室舒张末内径、肺动脉收缩压、右心房内径、右心室内径、室间隔厚度、左心室后壁厚度、左心室舒张功能之间差异无统计学意义（P＞0.05）.COX分析发现术前左心房内径≥40 mm是肺移植术后发生房颤的独立危险因素,风险系数为4.622.结论 房颤是肺移植术后常见的心律失常,其发生率为26.0%,左心房扩大是肺移植患者术后发生房颤的独立危险因素.     

心房颤动患者右心结构及压力变化研究

目的回顾性分析心房颤动(AF)患者右心结构及压力的变化,并分析右心功能不全的危险因素。方法序贯收集2011年5月至2013年5月在北京协和医院心内科确诊AF的患者291例。所有入选对象左心收缩功能正常,并除外冠心病、心肌病、先天性心脏病、瓣膜性心脏病、原发性肺动脉高压及慢性肺病患者。记录患者基本资料、基础疾病、AF症状(EHRA评级)、体质指数、血生化指标、超声心动图参数。分析AF伴或不伴右心室收缩压升高、伴或不伴右心增大患者的临床资料。结果与右心室收缩压<30 mm Hg的AF患者比较,右心室收缩压≥30 mm Hg的AF患者合并糖尿病、高血压、EHRA>I级的比例较高(22.9%比13.2%,67.1%比49.0%,37.1%比19.2%,均为P<0.05),左心房内径相对较大[(44.0±6.8)mm比(40.5±5.4)mm,P<0.01];右心房增大与右心房正常的AF患者在右心室收缩压[(33.8±10.1)mm Hg比(27.6±9.2)mm Hg]、下腔静脉内径[(16.2±2.8)mm比(14.6±2.3)mm]、左心房内径[(45.4±5.6)mm比(39.1±5.3)mm]、右心室内径[(25.7±5.4)mm比(22.1±4.5)mm]、静息心率[(82.2±17.4)次/min比(77.2±15.7)次/min],以及CHADS2评分[(1.5±1.2)分比(1.1±1.1)分]、CHADS2-VASc评分[(2.6±1.5)分比(2.0±1.6)分]上差异均有统计学意义(均为P<0.05),且右心房增大的AF患者EHRA>Ⅰ级比例较高(34.5%比20.7%,P<0.05);右心室增大与右心室内径正常的AF患者下腔静脉内径[(16.8±3.7)mm比(15.2±2.3)mm]、左心房内径[(47.7±8.1)mm比(40.9±5.1)mm]、左心室射血分数(65.0%±8.5%比62.9%±7.1%)以及高血压比例(74.1%比54.0%)差异有统计学意义(均为P<0.05);左心房内径与右心室收缩压(RR=0.481)、右心室内径(RR=0.34)、右心房内径(RR=0.544)均呈显著正相关(均为P<0.01)。结论存在糖尿病、高血压,EHRA评分>Ⅰ级,已出现左心房增大及体循环容量负荷高(下腔静脉相对较宽)的AF患者更易出现右心功能不全征象。左心房内径增加可能是AF合并右心功能不全的有力证据。CHADS2/CHADS2-VASC评分较高、心室率偏快的AF患者应积极进行右心功能及结构评估,以早期发现右心功能不全。     

心肌梗死患者右心房基质金属蛋白酶表达水平的变化

目的 研究冠心病心肌梗死(MI)患者右心房组织基质金属蛋白酶(MMP)及其抑制剂(TIMP)的基因表达,探讨其与右心房结构重构的关系.方法 选取因冠心病接受冠状动脉旁路移植术(CABG)的患者40例,其中MI 22例,不稳定性心绞痛(UA)组18例,术前进行超声心动图检查.于开胸手术时取右心耳标本,分别进行免疫组织化学染色检查、荧光定量PCR方法检测标本中MMP-1、MMP-3、MMP-7、MMP-9及TIMP-1表达.结果 MI组左右心房内径及左心室内径均大于UA组[左心房内径:(40.8±4.2)mm比(33.1±5.1)mm,P<0.01;右心房内径:(44.1±6.8)mm比(28.8±6.0)mm,P<0.01;左心室内径:(48.9±6.0)mm比(39.7±7.1)mm,P<0.01],心房组织中MMP-3、MMP-9及TIMP-1基因表达高于UA组(MMP-3:0.39±0.18比0.28±0.07,P<0.05:MMP-9:0.81±0.21比0.55±0.20,P<0.01;TIMP-1:1.79±0.89比0.94±0.47,P<0.01),MMP-1、MMP-7基因表达有增加趋势,但差异无统计学意义.结论 冠心病心肌梗死患者右心房组织MMP及TIMP表达水平的升高与右心房重构相关.     

心房颤动致心动过速性心房心肌病的临床分析

目的探讨心房颤动(AF)引起双心房扩大的临床特征. 方法对20例AF伴双心房扩大病例的临床资料及随访结果,进行分析. 结果本组年龄52～93岁(平均75.5岁).20例AF患者安静时HR均＜85次/分钟,双心房扩大与AF相关,系AF致心房解剖重构.20例中,左心房内径4.2～5.7cm(平均4.9cm),右心房内径4.6～6.8cm(平均5.5cm).3例AF经药物复律后在随访中双心房恢复正常或明显缩小接近正常. 结论少数持续性AF可引起双心房扩大(解剖重构),成为心房心肌病,认识该病有重要临床意义.     

典型逆钟向心房扑动特征性扑动波的电解剖研究

目的 通过对典型逆钟向心房扑动(房扑)左右心房的电解剖标测,阐明其体表扑动波的产生机制.方法 2012年10月至2014年2月于南京医科大学第一附属医院住院患者中入选15例典型逆钟向房扑患者,平均年龄(60±14)岁,男性14例,女性1例.对15例患者进行心脏超声检查、电生理检查及三维标测系统指导下的双心房激动标测,观察体表扑动波的形成与左右心房心内膜激动模式的关系.结果 15例患者的平均左心室射血分数为(60.8±6.6)％,平均左心房内径为(39.0±3.4)mm,平均扑动周期为(220±24) ms,均完成房扑节律下右心房、左心房的电解剖重建.在下壁导联,可将体表扑动波分为3个部分:缓慢下降区,快速下降区及终末正向成分,分别对应心腔内右心房峡部、间隔由下而上和左心房激动及右心房游离壁由上而下的激动.左心房激动始于快速下降区,终于终末正向成分.结论 典型逆钟向房扑体表扑动波与其特殊的大折返激动组成部分一一对应,是其特征性激动模式的心电反映.左心房激动参与了扑动波中下降部分的形成.     

Electrophysiologic Characteristics of a Dilated Atrium in Patients with Paroxysmal Atrial Fibrillation and Atrial Flutter

This study investigated the difference of atrial electrophysiologic characteristics between a normal and dilated atrium and compared them among patients with paroxysmal atrial fibrillation and flutter. Twenty-seven patients with paroxysmal atrial fibrillation and 28 patients with paroxysmal atrial flutter were divided into four subgroups, according to the presence of a normal atrium or bilateral atrial enlargement. Thirty patients without atrial arrhythmia (20 patients with normal atrium and 10 patients with bilateral atrial enlargement) were included in control group. The atrial refractoriness in patients with a dilated atrium was longer than those with normal atrial size. In patients with paroxysmal atrial fibrillation and patients of control group, the P-wave duration and interatrial conduction velocity with or without atrial enlargement were similar. However, in patients with paroxysmal atrial flutter, P-A_PCS (86 ± 10 ms vs. 73 ± 9 ms, p < 0.05) and P-A_DCS (109 ± 9 ms vs. 95 ± 9 ms, p < 0.05) in patients with a dilated atrium were longer than in patients with a normal atrium. The patients with paroxysmal atrial fibrillation or atrial flutter all demonstrated longer P-wave duration and interatrial conduction time than control group. Among the groups with a normal atrium or a dilated atrium, atrial refractoriness in patients with paroxysmal atrial flutter was shorter than that in control group. Moreover, in the patients with a normal atrium, the potential minimal wavelength in control group (6.6 ± 1.7) was longer than that of paroxysmal atrial fibrillation (5.3 ± 1.1), or atrial flutter (5.0 ± 1.2). These findings suggest that atrial electrophysiologic characteristics of a dilated atrium were different from those of normal atrium, and these changes were different between paroxysmal atrial fibrillation and flutter. Multiple factors are considered to be related to the genesis of atrial tachyarrhythmias.     

正交心电图对左房肥大的诊断价值

目的探讨正交心电图对左心房肥大的诊断价值。方法观察以超声心动描记术诊断的144例左心房正常人和124例左心房增大患者的正交心电图并与常规心电图比较。结果正交心电图与左心房前后径有直线相关关系。正交心电图综合标准和简化标准诊断左房肥大的敏感性、准确性和阴性预测性分别为83.1%、82.1%、84.8%和79.8%、81.75%、82.6%(p>0.05),显著高于常规心电图的51.6%、71.3%、67.9%(p>0.01)。结论认为正交心电图简化标准操作简便,是一种较好的诊断左心房肥大的方法。     

心电图诊断左房增大价值的探讨

对窦性心律109例、持续性房颤313例的各种心脏疾病患者参照UCG检查,探讨ECG诊断左房增大的价值及左房增大与房颤的关系.P波诊断左房增大的3项指标(P波时间>110ms、P波切迹双峰间距≥40ms、PTFv_1<一30mm·ms)的敏感性较低(58%-71%),但特异性高(83%—94%),其中PTFv_1的诊断价值最大.ECG对诊断左房增大仍不失为有用方法.左房增大程度与并发房颤的比例在风心病有密切关系,但在非风心病则否.     

Identification of factors associated with progression of left atrial enlargement in patients with atrial fibrillation

Left atrial (LA) enlargement frequently occurs in atrial fibrillation (AF) patients, and this enlargement is associated with the development of heart failure, thromboembolism, or atrial functional mitral regurgitation (AFMR). AF patients can develop LA enlargement over time, but its progression depends on the individual. So far, the factors that cause progressive LA enlargement in AF patients have thus not been elucidated, so that the aim of this study was to identify the factors associated with the progression of LA enlargement in AF patients. We studied 100 patients with persistent or permanent AF (aged: 67 ± 2 years, 40 females). Echocardiography was performed at baseline and 12 (5–30) months after follow-up. LA size was evaluated as the LA volume index which was calculated with the biplane modified Simpson's method from apical four-and two-chamber views, and then normalized to the body surface area (LAVI). The deterioration of AFMR after follow-up was defined as a deterioration in severity of mitral regurgitation (MR) by a grade of 1 or more. Multivariate regression analysis demonstrated that hypertension (p = .03) was an independently associated parameter of progressive LA enlargement, as was baseline LAVI. In addition, the Kaplan–Meier curve indicated that patients with hypertension tended to show greater deterioration of AFMR after follow-up than those without hypertension (log-rank p = .08). Hypertension proved to be strongly associated with progression of LA enlargement over time in patients with AF. Our findings provide new insights for better management of patients with AF to prevent the development of AFMR.     

Significance of echocardiographic left atrial enlargement in aortic stenosis

This study investigated the significance of echocardiographic left atrial enlargement as measured by the left atrial dimension corrected for body surface area in 24 patients with pure aortic stenosis established by cardiac catheterization. Echocardiographic evidence of left atrial enlargement occurred in 11 of 15 patients (73%) with an aortic valve area below 0.8 cm2 and in none of nine patients (0%) with an aortic valve area above 0.8 cm2, p less than 0.0025. All 11 patients (100%) with an enlarged left atrial dimension had an increased diastolic left ventricular dimension, whereas 1 of 13 patients (8%) with a normal left atrial dimension had an increased diastolic left ventricular dimension, p less than 0.00001. The 11 patients (100%) with an enlarged left atrial dimension had increased posterior left ventricular wall thickness, whereas 2 of 13 patients (13%) with a normal left atrial dimension had increased posterior left ventricular wall thickness (p less than 0.0005). These data lead one to conclude that in patients with pure aortic stenosis, echocardiographic evidence of left atrial enlargement as measured by an increased left atrial dimension corrected for body surface area should lead one to suspect severe aortic stenosis.     

P-wave morphology correlation with left atrial volumes assessed by 2-dimensional echocardiography

To correlate prespecified P-wave morphologies with echocardiographically derived left atrial volumes (LAVs), we studied a convenience sample of 71 patients with predominantly normal left ventricular systolic function (mean ejection fraction = 58.2% +/- 6.6%) who underwent concurrent 2-dimensional echocardiogram and 12-lead electrocardiogram. Left atrial volume was calculated from apical end-systolic images by the biplane method of disks and was indexed for body surface area (BSA). Electrocardiograms were assessed manually with calipers, measuring leading edge to leading edge. Patients included 34 men and 37 women with a mean age of 53 +/- 14 years. P-wave duration/PR-segment duration in lead II and depth and duration of terminal P wave in lead V1 (P terminal force) correlate poorly with LAV and provided only modest predictive power (area under receiver operating characteristic curve = 0.466-0.619 and r = 0.30-0.42, P = .014-.021). Total P-wave duration in lead II correlated moderately (r = 0.47, P < .001) and predicted LAV (LAV/BSA = 8.0 + 0.2 [P-wave duration in lead II]), as did P-wave area in lead II (r = 0.49, P < .001) (LAV/BSA = 18.6 + 1.7 [P-wave duration in lead II]). The 4 P-wave morphologies were found to be poorly sensitive but highly specific for left atrial enlargement.     

Differential Left Atrial Remodeling in LV Diastolic Dysfunction and Mitral Regurgitation

Objective: Chronic pressure and volume overload may cause different type of left atrial (LA) remodeling in left atrial enlargement (LAE) leading to different cardiovascular outcomes. These two different patterns of LA remodeling can be discriminated by LA eccentricity index (LAEi). The goal of our study was to evaluate an association between LAEi, LV diastolic dysfunction (LVDD), and mitral regurgitation (MR). Method: LAEi was calculated from 3D of left atrium (LA): anteroposterior (D1), superoinferior (D2), mediolateral (D3), and LAEi = D2×2/ (D1+D3). LAE was described as elongated left atrium (EA) if LAEi ≥ 1.27, and spherical left atrium (SA) if LAEi < 1.27. Results: A group of 501 patients (10.4%) with LAE were categorized into two subgroups; 232 (46.3%) with EA and 269 (53.7%) with SA based on LAEi. Among 108 patients (21.6%) with LVDD without MR, 102 had EA and only 6 had SA (P < 0.0001). The cohort of 155(30.1%) patients with MR without LVDD, only 8 had EA and143 had SA (P < 0.0001). Of the total group of 501 patients, 59 had persistent AF and in this subgroup only 10 patients had EA and 49 patients had SA (P < 0.0001). There was a statistically significant difference for AF rate between EA-patients with LVDD without MR and SA-patients with MR without LVDD (P < 0.001). Conclusions: LVDD may contribute to pressure overload LA remodeling in a way quite different from volume overload LA remodeling by MR. LAEi can discriminate two different LA morphologies with significantly different potential outcomes. It may identify patients associated with a higher rate of AF with a higher cardiovascular risk.     

Left atrial enlargement and NT-proBNP as predictors of sudden cardiac death in patients with heart failure

AIMS: The identification of valuable markers of sudden cardiac death (SCD) in patients with established HF remains a challenge. We sought to assess the value of clinical, echocardiographic and biochemical variables to predict SCD in a consecutive cohort of patients with heart failure (HF) due to systolic dysfunction. METHODS: A cohort of 494 patients with established HF had baseline echocardiographic and NT-proBNP measurements and were followed for 942+/-323 days. RESULTS: Fifty patients suffered SCD. Independent predictors of SCD were indexed LA size>26 mm/m2 (HR 2.8; 95% CI 1.5-5.0; p=0.0007), NT-proBNP>908 ng/L (HR 3.1; 95% CI 1.5-6.7; p=0.003), history of myocardial infarction (HR 2.3; 95% CI 1.3-4.1; p=0.007), peripheral oedema (HR 2.1; 95% CI 1.1-3.9; p=0.02), and diabetes mellitus (HR 1.9; 95% CI 1.1-3.3; p=0.03). NYHA functional class, left ventricular ejection fraction and glomerular filtration rate were not independent predictors of SCD in this cohort. Notably, the combination of both LA size>26 mm/m2 and NT-proBNP>908 ng/L increased the risk of SCD (HR 4.3; 95% CI 2.5-7.6; p<0.0001). At 36 months, risk of SCD in patients with indexed LA size26 mm/m2 and NT-proBNP>908 ng/L reached 25% (p<0.0001). CONCLUSIONS: Among HF patients, indexed LA size and NT-proBNP levels are more useful to stratify risk of SCD than other clinical, echocardiographic or biochemical variables. The combination of these two parameters should be considered for predicting SCD in patients with HF.