不同年龄段房间隔缺损经皮介入术后右心重构差异

目的研究不同年龄段房间隔缺损（AsD）经皮介入术后右心形态重构差异。方法回顾性分析经导管介入治疗ASD91例患者的年龄、ASD大小,以及有无发生肺动脉高压（PAH）等资料,并对术前3d及术后3d、3个月、6-12个月做超声心动图随访。结果介入术后ASD患者右心均有恢复,但≥40岁组术后3d至12个月右心大小无进一步的缩小。结论40岁前对ASD纠治右心恢复较好。     

急性肺血管药物扩张试验在评价先天性心脏病合并重度肺动脉高压中的应用进展

<正>一、先天性心脏病合并重度肺动脉高压继发于左向右分流型先天性心脏病(CHD)的肺动脉高压(PAH)是一种进行性病变,主要表现为肺动脉压力和肺血管阻力的进行性升高,最终导致右心衰竭甚至死亡。这类肺动脉高压按其性质可分为动力性肺动脉高压和梗阻性肺动脉高压,CHD合     

小窝蛋白与先天性心脏病肺动脉丛样病变研究进展

<正>我国现有先天性心脏病(先心病)患者400余万,每年新增15～20万。左向右分流型先心病常常合并重度肺动脉高压(pulmonary arterial hypertension,PAH)和艾森蔓格综合征,部分患者在手术或介入治疗后PAH恢复正常     

高海拔地区经胸超声心动图在老年房间隔缺损封堵术中的应用价值

高海拔地区根据青海省不同海拔高度地区的调查,先心病患病率为5.66‰,海拔越高,发病率越高,房间隔缺损(ASD)在各种先心病中ASD发病率最高(约占37.42%),并发肺动脉高压早的常见的先天性心脏病。老年(≥60岁)ASD患者由于年龄大,长期处于心房水平左向右分流,加之高海拔缺氧,往往合并肺动脉高压及不同程度的心功能损害,同时全身脏器功能趋于减退。本文探讨经胸超声心动图(TTE)在ASD封堵术中的应用价值。     

手振50%葡萄糖溶液右心声学造影的临床应用

目的:总结各种心内、心外分流性疾病右心声学造影的不同表现,明确右心声学造影的临床价值。方法:回顾性分析我院2006~2014年期间行右心声学造影检查的102例受检者的超声表现。造影剂为9 ml 50%葡萄糖注射液与1ml空气混合形成的手振50%葡萄糖溶液。结果:检出分流性疾病49例,包括右向左或双向分流房间隔缺损8例、左向右分流房间隔缺损7例、卵圆孔未闭伴功能性右向左分流9例、动脉导管未闭合并肺动脉高压13例、肺动静脉瘘3例、永存左上腔静脉引流入冠状静脉窦8例、引流入左心房1例。结论:右心声学造影能够简便、有效地检出合并肺动脉高压患者心内、心外异常分流,提高先天性心脏病诊断的准确性,是一项重要且实用的辅助诊断方法。     

心内畸形修补同期行肺移植治疗埃森曼格综合征的进展

埃森曼格综合征(Eisenmenger syndrome,ES)是左向右分流型先天性心脏病发展到重度肺动脉高压,出现不可逆性肺动脉压力升高,导致血液通过心内或心外异常通路产生双向或反向分流的一种病理生理综合征。患者一旦产生ES,心内畸形即失去修补的手术机会,预后很差。     

波生坦治疗先天性心脏病合并肺动脉高压的研究进展

<正>肺动脉高压(pulmonary arterial hypertension,PAH)是一种少见的预后不良的疾病,以肺动脉压力和阻力增高为特征[1]。先天性心脏病(congenital heart disease,CHD,先心病)体-肺分流型是由于缺损部位大量左向右分流导致肺循环容量明显增加,肺血管处于高流量高压力状态,肺动脉压力阻力升高,引起PAH。     

肺动脉压力正常及轻度增高的成年房间隔缺损患者心房水平隐性右向左分流探查

目的:探查正常及轻度肺动脉压力增高的成年房间隔缺损(ASD)患者的右向左分流发生情况。方法:17例中央型ASD患者,男8例,女9例,年龄18~66(47±16)岁,均经胸心脏超声(TTE)检查诊断ASD、心房水平血流分流方向及肺动脉压力。封堵治疗前在静息状态及(或)Valsalva动作时行经颅多普勒超声(TCD)发泡试验联合TTE右心声学造影检查。所有患者在介入封堵治疗前通过右心导管测定肺动脉压力,在封堵治疗后即刻及术后3d、1个月、3个月及6个月再次行TCD发泡试验联合TTE右心声学造影检查。结果:TTE证实房间隔缺损直径5~24mm,所有患者心房水平左向右单向分流。11例患者静息TCD发泡试验联合TTE右心声学造影出现心房水平存在右向左分流,6例静息状态下检查未提示存在右向左分流患者Valsalva动作后均出现右向左分流现象。封堵治疗前经右心导管检查测得肺动脉压力(18~41)/(5~11)mmHg(1mmHg=0.133kPa)。所有患者均成功进行介入封堵治疗。1例患者在封堵治疗术后3d、1个月、3个月存在少量右向左分流,术后6个月17例患者均未见心房水平分流存在。结论:正常及轻度肺动脉高压的ASD患者心房水平存在隐性右向左分流,介入封堵治疗后分流消失。TCD发泡试验联合TTE右心声学造影检查可准确判定心房水平右向左分流。     

高流动性组蛋白1、生长分化因子15和血栓调节蛋白与左向右分流先天性心脏病单纯性室间隔缺损继发肺动脉高压的相关性

目的探讨高流动性组蛋白1(HMGB1)、生长分化因子15(GDF-15)和血栓调节蛋白(TM)与左向右分流先天性心脏病单纯性室间隔缺损继发肺动脉高压(PAH)的相关性,并评价其诊断价值。方法选取左向右分流先天性心脏病单纯性室间隔缺损继发PAH患者80例为PAH组,左向右分流先天性心脏病单纯性室间隔缺损不继发PAH患者80例为对照组,酶联免疫吸附试验检测2组患者血清HMGB1、GDF-15和TM的表达量。肺动脉收缩压与体循环收缩压比值0.75的患者为重度PAH组,比较轻中度PAH患者与重度PAH患者HMGB1、GDF-15和TM的差异。超声心动图测量2组患者左心室舒张末期直径(LVEDD)、左心房直径(LA)、右心室直径(RV)、右心房直径(RA)、主肺动脉直径(PA)、左心室射血分数(LVEF)、左心室缩短分数(FS)、三尖瓣反流的峰值速度(TRV)水平,并分析其与HMGB1、GDF-15、TM的相关性。采用受试者工作特征(ROC)曲线分析HMGB1、GDF-15、TM对左向右分流先天性心脏病单纯性室间隔缺损继发PAH的诊断价值。结果 PAH组的HMGB1[(16.40±4.98)比(5.32±1.65)μg/L]、GDF-15[(1 473.4±181.5)比(1 214.8±153.9)μg/L]的表达量高于对照组,TM[(1.14±0.09)比(3.02±0.37)μg/L]的表达量低于对照组。重度PAH患者血清中HMGB1[(21.49±5.59)比(12.24±3.10)μg/L]、GDF-15[(1 592.2±203.4)比(1 350.8±168.9)μg/L]的表达量高于轻中度PAH患者,TM的表达量[(0.57±0.11)比(1.82±0.39)μg/L]低于轻中度PAH患者。PAH组的LA、RV、RA、PA、TRV高于对照组(P0.05)。RA与HMGB1呈正相关(P0.05),PA与GDF-15呈正相关(P0.05)。HMGB1、GDF-15、TM诊断左向右分流先天性心脏病单纯性室间隔缺损继发PAH的灵敏度分别为80%、70%、83%,特异度为80%、93%、80%;HMGB1、GDF-15、TM的截断值分别为9.031、1 306、2.728μg/L;HMGB1、GDF-15、TM联合对左向右分流先天性心脏病单纯性室间隔缺损继发PAH的灵敏度为90.0%,特异度为91.2%,符合率为90.6%。结论HMGB1、GDF-15、TM与PAH存在相关性,可作为联合诊断左向右分流先天性心脏病单纯性室间隔缺损继发PAH的潜在标志物。     

先天性心脏病与心律失常

先天性心脏病 (先心病 ) ,尤其是先心病患者矫正术后的心律失常并非少见 ,其原因可能是多方面的 ,包括先天性心血管畸形的血流动力学变化对心腔大小、心肌肥厚和特殊传导系统的影响 ,以及可能共存有特殊传导系统的先天性异常等。　　一、未经手术治疗的先天性心脏病心律失常　　先心病患者手术治疗前的心律失常可直接由心血管畸形引起 ,也可继发于进行性血流动力学变化。　　 1 房间隔缺损　　房间隔缺损 (房缺 )患者 ,长期的左向右分流加重右心负荷 ,导致右心房和右心室扩张 ,可出现各种心律失常 ,主要为房性心律失常 ,如房性早搏 (房早 )…     

Assessment of right heart function in the athlete's heart

 It is known that the heart of an athlete has been physiologically adapted by prolonged training. There are a large number of echocardiographic studies which have focused on left ventricular wall thickness and dilatation, but there are few studies concerning right heart function in the athlete's heart. The aim of this study was to assess right heart function in elite athletes by conventional and new echocardiographic methods. The study population consisted of 36 elite highly-trained male athletes and 16 age-matched healthy sedentary controls. Right atrial, right ventricular, and inferior vena cava dimensions, and pulsed Doppler measurements of tricuspid inflow and right ventricular outflow were obtained, and systolic (preejection period, ejection time, preejection time/ejection time, QV peak, isovolumic contraction time) and diastolic (E peak, A peak, E/A ratio, decelaration time, isovolumic relexation time) function parameters were measured. The myocardial performance index was calculated as (isovolumetric contraction time + isovolumetric relaxation time)/ejection time. In addition, right ventricular systolic and diastolic functions were determined by Pulsed wave tissue Doppler imaging (S, E, and A velocities) at the lateral corners of the tricuspid annulus. The left ventricular mass index (P < 0.005), and right atrial (P < 0.001), right ventricular (P < 0.001), and inferior vena cava dimensions (P < 0.001) were significantly greater in athletes than in controls. Tricuspid E peak, A peak, E/A ratio, deceleration time, isovolumic relaxation time, preejection period, right ventricular ejection time, preejection time/ejection time, isovolumic contraction time, QV peak, and myocardial performance index were found to be similar in athletes and in controls (P > 0.05). Systolic, early diastolic, and late diastolic tissue Doppler imaging velocities were not significantly different in athletes and controls (P > 0.05). Left ventricular hypertrophy (LV mass index >134 g/m²) was found in 15 of the athletes. Right atrial dimension was greater in the athletes with left ventricular hypertrophy than in those without hypertrophy (P < 0.05). All right ventricular systolic and diastolic echocardiographic parameters were similar in athletes with and without left ventricular hypertrophy (P > 0.05). The results of this study indicate that right ventricular systolic and diastolic functions do not deteriorate in the athlete's heart despite significant chamber dilatation. They suggest that these changes are a normal physiologic adaptation to prolonged training. Received: November 28, 2001 / Accepted: March 8, 2002     

Update in carcinoid heart disease - the heart of the matter

Carcinoid heart disease (CHD) is a paraneoplastic cardiac manifestation occurring in patients with carcinoid syndrome (CS) and advanced neuroendocrine malignancy. In about 20–40% of patients with CS, chronic exposure to tumor-released circulating vasoactive peptides typically results in right-sided valvular fibrosis leading to valve dysfunction and right heart failure. CHD remains a significant cause of morbidity and mortality. The management of patients with CHD is complex, as both the systemic malignant disease and the heart involvement have to be addressed. Early diagnosis and timely surgical intervention in selected patients are of utmost importance and offer a survival benefit. In patients with advanced carcinoid heart disease, valve replacement surgery is the most effective option to alleviate cardiac symptoms and contribute to survival outcomes. A collaboration of a multidisciplinary team in centers with experience is required to provide optimal patient management. Here, we review the current literature regarding CHD presentation, pathophysiology, diagnostic tools, and available treatment strategies.

     

Apoptosis in heart failure and the senescent heart

The progressive loss of cardiac myocytes by apoptotic cell death has been discussed as an important pathogenic component in the failing myocardium as well in the aging heart. The degree to which apoptosis contributes to myocyte loss in these conditions, however, is a controversial issue. This review focuses on the regulation of apoptosis, evidence implicating apoptosis as a mechanism for the progression and development of heart failure, the role of apoptotic death in senescent cardiac dysfunction, as well as on the problems of detection of apoptosis.     

Malignant lymphoma in the donor heart after heart transplantation

A case of post-transplant lymphoproliferative disease (PTLD)with donor heart involvement is reported. The 49-year-old patientpresented with heart failure initially ascribed to acute graftrejection. The treatment with high doses of immunosuppressiveagents was unsuccessful and the outcome rapidly fatal. Thiscase suggests that cardiac failure occurring after high dosesof immunosuppressive therapy could be a sign of early PTLD inheart transplant recipients.