影响经皮二尖瓣球囊成形术术后肺动脉压力正常化的相关因素研究

目的　探讨继发性肺小动脉病变对经皮二尖瓣球囊成形术 (PBMV)术后肺动脉高压正常化的影响。方法　对 5 2 3例二尖瓣狭窄合并肺动脉高压的患者 ,PBMV术前、后测定其肺动脉收缩压 (PASP)、左房收缩压 (LASP)等血流动力学指标 ,运用多因素logistic回归分析影响术后肺动脉压正常化的因素 ,并将患者分为重度肺动脉高压组 (A组 )和非重度肺动脉高压组 (B组 )进行比较分析。结果　A组患者的PASP由术前的 (89 6 9± 16 2 7)mmHg(1mmHg =0 133kPa)下降为术后的 (5 3 0 4±16 5 2 )mmHg ,B组患者的PASP值由术前的 (48 2 3± 11 4 7)mmHg降至术后的 (33 6 4± 9 0 1)mmHg。logistic回归表明 ,术前PASP水平高是影响术后肺动脉压正常化的显著因素。A组中术后肺动脉压力下降至正常的患者比例 (4 5 % )明显低于B组 (42 5 % ) ;与B组比较 ,A组患者无论在术前、术后LASP与PASP均缺乏良好的线性关系。结论　由于继发性肺小血管改变引起的“二级狭窄”是造成PBMV术后肺动脉压力不能恢复至正常的主要原因。     

68例二尖瓣狭窄合并轻度主动脉瓣关闭不全患者经皮球囊形成术后5年随访结果分析

目的评价经皮二尖瓣球囊形成术(PBMV)对二尖瓣狭窄合并轻度主动脉瓣关闭不全患者的安全性和有效性。方法对68例二尖瓣狭窄合并轻度主动脉瓣关闭不全患者行PBMV,术后随访5年,平均随访时间(5.4±1.2)年,内容包括心胸比率、超声心动图及心功能评价。结果PBMV术前、术后一周二尖瓣口面积(MVA)分别为(1.16±0.30)cm2与(2.21±0.52)cm2,术后MVA明显增加P＜0.001;术后5年MVA(2.07±0.43)cm2,较术后一周MVA减少,仍比术前大,P＜0.001;PBMV前、后左心室舒张末期内径为(4.26±0.50)cm,(4.58±0.44)cm,术后5年为(4.85±0.47)cm2,术后及5年随访与术前分别比较无显著性差异,P均大于0.05;PBMV术前后及5年随访主动脉瓣返流峰值压差分别为(60.00±35.54)mmHg,(58.51±38.71)mmHg,(62.44±34.67)mmHg,术后一周及5年与术前比较无显著性差异。术前后心胸比率分别为(0.56±0.06)、(0.55±0.05)与(0.54±0.06),术后心脏无显著扩大。PBMV术后心功能改善一个级别以上占91.2%,能维持Ⅰ～Ⅱ级心功能5年者占83.8%,5年总生存率98.5%。4例二尖瓣钙化,瓣下结构粘连纤维化严重的患者和3例合并中重度三尖瓣关闭不全患者,PBMV术后心功能无改善而转外科行瓣膜置换术,或加做三尖瓣环缩术,1例青年患者在随访过程中出现二尖瓣再狭窄而再次PBMV,1例心功能Ⅳ级患者PBMV术后出现重度二尖瓣关闭不全,行瓣膜置换术后死于难以纠正的心力衰竭。结论PBMV对二尖瓣狭窄合并轻度主动脉瓣关闭不全患者是可行的,术后并不加重主动脉瓣返流,也不使左室扩大。瓣膜钙化、瓣下粘连、纤维化严重或伴有中重度三尖瓣关闭不全、心胸比率大于0.60患者,是PBMV反指征。     

经皮球囊二尖瓣成形术前后一氧化氮、内皮素变化的研究

目的探讨风湿性心脏病二尖瓣狭窄患者经皮球囊二尖瓣成形术(PBMV)前后肺动脉及左心房血浆中内皮素(ET)、一氧化氮(NO)变化。方法选择符合行PBMV适应证的风湿性二尖瓣狭窄患者50例,PBMV术前及术后30min监测肺动脉压、左心房压,并同时取肺动脉血、左心房血分别用重氮法和放射免疫法测定NO和ET值及NO／ET值。结果PBMV术后,肺动脉压、左心房压明显下降,肺动脉平均压由((51．7±19．3)mmHg(1mmHg＝0．133kPa)降至(21．5±7．0)mmHg(P＜0．01),左心房平均压由(25．3±6．7)mmHg降至(13．2±9．7)mmHg(P＜0．01)。术前左心房血浆ET(51．1±10．6)pg/ml,NO(99．6±9．4)μmol／L,NO／ET=1．95±1．12;肺动脉血浆ET(131．1±19．3)pg/ml,NO(165．4±50)μ     

经皮二尖瓣球囊扩张术394例随访结果

目的　观察经皮二尖瓣球囊扩张术(PBMV)治疗风湿性心脏病(风心病)二尖瓣狭窄的中、远期疗效。方法　采用Inoue单球囊对680例风心病二尖瓣狭窄者行PBMV术治疗,其中394例进行了随访。平均随访时间(36±14)个月。结果　二尖瓣平均跨瓣压差由(18.2±6.8)mmHg降至(7.2±3.8)mmHg,瓣口面积由(1.04±0.21)cm2增至(1.98±0.55)cm2,左房内径由(44±8)mm降至(38±6)mm;8例出现明显再狭窄,其中5例再次PBMV术,3例行瓣膜置换术。结论　随访结果证实,PBMV治疗风心病二尖瓣狭窄的中、远期效果良好,瓣膜条件特别是瓣下病变的程度是影响中、远期疗效的重要因素。     

部分联合瓣膜病患者经皮球囊二尖瓣成形术远期疗效观察

目的:观察部分风湿性心脏病二尖瓣狭窄合并轻度关闭不全或(和)轻度主动脉瓣病变患者经皮球囊二尖瓣成形术(PBMV)的远期疗效.方法:126例二尖瓣狭窄合并轻度关闭不全或(和)轻度主动脉瓣病变的患者,全部采用改良Inoue法行PBMV,术中采用逐步递增扩张法扩张二尖瓣,术后进行远期随访.结果:126例患者PBMV成功121例(成功率为96.0%).术后110例患者完成了远期随访,平均随访78±31(36～118)个月.术后近期和远期随访期间患者左心房平均压、左心房内径、二尖瓣瓣口面积、跨瓣压差及肺动脉收缩压均较术前明显改善,差异均有统计学意义(P均＜0.05),且远期随访结果与近期随访结果均相似,差异均无统计学意义(P>0.05).远期随访期间,大多数患者临床症状、心功能及生活质量亦明显改善.结论:对于部分二尖瓣狭窄合并轻度关闭不全或(和)轻度主动脉瓣病变的患者,只要合理选择适应证,恰当而谨慎地进行围手术期的各项工作,亦可安全地施行PBMV,其近期和远期疗效皆佳.     

经皮球囊二尖瓣成形术长期临床疗效的评价

目的评价经皮球囊二尖瓣成形术(PBMV)的长期临床疗效. 方法采用改良In-oue方法对143例风湿性二尖瓣狭窄患者行PBMV治疗,并对其中140例患者进行了术后长期随访. 结果与术前相比,术后二尖瓣口面积(MVA)增大[(1.03±0.55)cm2对(2.03±0.37)cm2],二尖瓣跨瓣压差(MVG)降低[(18.1±4.8)mmHg对(4.1±2.3)mmHg],左心房内径(LAD)减小[(4.67±1.10)cm对(4.13±0.59)cm],P＜0.001.平均随访(90±24)个月时MVA(1.73±0.48)cm2,MVG(6.5±3.4)mmHg,LAD(4.21±0.82)cm.29例患者发生了再狭窄,再狭窄率为20.7%. 结论PBMV术后长期临床疗效良好.     

二尖瓣狭窄并中度反流的经皮二尖瓣球囊扩张术42例及随访观察

目的　探讨二尖瓣狭窄 (MS)并中度反流 (MR)患者经皮二尖瓣球囊扩张术 (PBMV)近远期疗效。方法　采用Inoue单球囊对 42例风心病二尖瓣狭窄并中度反流患者行PAMV治疗。结果　二尖瓣口面积由 (0 92± 0 2 2 )cm2 增至 (1 94± 0 2 5 )cm2 (P <0 0 1) ;二尖瓣跨瓣压差由 (2 7± 1 0 1)kPa降至 (1 0 2± 0 5 6 )kPa(P <0 0 1) ;心功能由 (2 6 1± 0 2 2 )级改善至 (1 42± 0 46 )级 (P <0 0 1) ;左室最大前后径无明显变化 (P >0 0 5 )。 2例患者二尖瓣反流较术前加重。随访 37例患者 (18± 4)个月 ,二尖瓣口面积、左室最大前后径及心功能与术后比较 ,均无明显变化 (P >0 0 5 )。结论　掌握好病例选择 ,严格把握球囊扩张尺度 ,风心病二尖瓣狭窄并中度反流患者PBMV近、远期疗效满意     

经皮球囊二尖瓣成形术长期临床疗效的评价

目的:评价经皮球囊二尖瓣成形术(PBMV)的长期临床疗效。方法:采用改良In-oue方法对143例风湿性二尖瓣狭窄患者行PBMV治疗,并对其中140例患者进行了术后长期随访。结果:与术前相比,术后二尖瓣口面积(MVA)增大[(1.03±0.55)cm~2对(2.03±0.37)cm~2],二尖瓣跨瓣压差(MVG)降低[(18.1±4.8)mmHg对(4.1±2.3)mmHg],左心房内径(LAD)减小[(4.67±1.10)cm对(4.13±0.59)cm],P<0.001。平均随访(90±24)个月时MVA(1.73±0.48)cm~2,MVG(6.5±3.4)mmHg,LAD(4.21±0.82)cm。29例患者发生了再狭窄,再狭窄率为20.7％。结论:PBMV术后长期临床疗效良好。     

经皮球囊二尖瓣并三尖瓣成形术及远期疗效观察

目的：对风湿性二尖瓣狭窄合并三尖瓣狭窄患者行经皮球囊成形术,观察其远期疗效。方法：对8例患者行经皮球囊二尖瓣并三尖瓣成形术并长期随访。结果：8例患者术后进行长达6.2±3.9(2.0～10.5)年的随访,患者术后即刻及远期随访的临床症状及血流动力学指标均较术前明显改善,有极显著性差异(P＜0.01),而远期随访与术后即刻相近似(P＞0.05)；且无严重并发症及再狭窄发生。结论：风湿性二尖瓣狭窄合并三尖瓣狭窄患者,行经皮球囊成形术后,术后即刻及远期疗效均好,值得临床推广。     

左向右分流型先天性心脏病即室间隔缺损介入封堵治疗肺动脉压力的变化规律

目的探讨成功介入封堵治疗的左向右分流型先天性心脏病即室间隔缺损(VSD)在封堵前、封堵后即刻、随访期间肺动脉压力的变化规律。方法选取675例成功施行介入封堵治疗的VSD患者,根据肺动脉压力大小分为正常肺动脉压力组、轻度肺高压组、中度肺高压组。经导管测定术前及术后即刻肺动脉收缩压(PASP)及肺动脉平均压(PAMP),并通过超声心动图测定VSD患者术后3 d、1、3、6个月的PASP与PAMP。结果 1正常肺动脉压力组:PASP和PAMP在术后即刻及随访期间均无统计学差异。2轻度肺高压组:PASP在术后即刻后无明显变化,术后6个月PASP与术前及术后即刻比较均显著下降(P0.05)。PAMP在术后即刻升高,但是该升高在术后得到抑制,术后1、6个月与术后即刻比较显著降低(P0.05)。3中度肺高压组:PASP及PAMP在术后即刻较术前均显著降低(P0.05),两者在随访期较术前进行性降低(P0.05);PASP在术后1、3、6个月较术后即刻降低(P0.05)。4PASP和PAMP超声和心导管测值均呈显著正相关。结论经导管封堵治疗能明显降低VSD合并轻、中度肺动脉高压患者肺动脉压力,近、中期疗效确切。     

Mitral Regurgitation After Percutaneous Mitral Valvotomy

Mitral regurgitation (MR) after percutaneous mitral balloon valvotomy (PMV) is commonly an end point and may be a significant complication. Some increase in MR occurs in more than half of patients undergoing PMV. An increase > 2 grades occurs in 3%–1.5% of patients, and < 5% have severe MR as a complication. MR is a significant predictor for late cardiac events and preexisting MR before PMV is also associated with poor late outcome. Mild increases in MR are due to stretching of the annulus, excess commissural tearing, or papillary muscle trauma. Mild MR frequently disappears at follow-up and rarely increases. Risk factors for development of MR have varied among multiple studies. Balloon oversizing and entrapment/tearing of chordae by the balloon(s) are mechanical factors. Most predictors are related to the pathologic anatomy of the mitral valve. Older age, a larger end-systolic volume index, and lower ejection fraction may be independent predictors of progression of MR. Subvalvular disease and valve thickening have also been identified as predictors. A recently described "scoring" system for predicting MR considers the distribution of anterior and posterior leaflet thickening, extent of commissural calcification/fibrosis, and degree of subvalvular disease. "Even" calcification/thickening produces a "lower" or "better" score than "uneven" distribution. Bicommissural calcification and thickening and shortening of chordae all predict bad outcome. Thus careful echocardio-graphic evaluation of mitral valve pathoanatomy pre-PMV can identify most predictors of the development of MR.     

Mitral Stenosis and Mitral Incompetence due to Libman-Sacks Endocarditis with Mitral Valve Replacement

Abstract: A patient is described with recurrent severe left heart failure induced by combined mitral stenosis and incompetence secondary to Libman-Sacks endocarditis. Marked improvement followed mitral valve replacement with a 29 mm St. Jude Medical Bi-Leaflet prosthesis. There was no evidence of rheumatic valve disease either macroscopically at operation or on histological examination of the excised valve .     

Peak Mitral Inflow Velocity Predicts Mitral Regurgitation Severity

Objectives. Mitral regurgitation (MR) is a common echocardiographic finding; however, there is no simple accurate method for quantification. The aim of this study was to develop an easily measured screening variable for hemodynamically significant MR.Background. The added regurgitant volume in MR increases the left atrial to left ventricular gradient, which then increases the peak mitral inflow or the peak E wave velocity. Our hypothesis was that peak E wave velocity and the E/A ratio increase in proportion to MR severity.Methods. We performed a retrospective analysis of 102 consecutive patients with varying grades of MR seen in the Adult Echocardiography Laboratory at the University of California, San Francisco. Peak E wave velocity, peak A wave velocity, E/A ratio and E wave deceleration time were measured in all patients. The reference standard for MR was qualitative echocardiographic evaluation by an expert and quantitation of regurgitant fraction using two-dimensional and Doppler echocardiography.Results. Peak E wave velocity was seen to increase in proportion to MR severity, with a significant difference between the different groups (F = 37, p < 0.0001). Peak E wave velocity correlated with regurgitant fraction (r = 0.52, p < 0.001). Furthermore, an E wave velocity >1.2 m/s identified 24 of 27 patients with severe MR (sensitivity 86%, specificity 86%, positive predictive value 75%). An A wave dominant pattern excluded the presence of severe MR. The E/A ratio also increased in proportion to MR severity. Peak A wave velocity and E wave deceleration time showed no correlation with MR severity.Conclusions. Peak E wave velocity is easy to obtain and is therefore widely applicable in clinical practice as a screening tool for evaluating MR severity.     

Management of Mitral Regurgitation Due to Mitral Prolapse

Opinion statement Notable advances have been made in the treatment of mitral regurgitation, especially the advances resulting from prolapse of the mitral valve with or without a flail leaflet. Prosthetic mitral valve replacement results in a high incidence of postoperative left ventricular systolic dysfunction. Recognition of the importance of the subvalvular apparatus for preserving contractile function has fostered development of new repair techniques that preserve native valve tissue and reduce or eliminate postoperative systolic dysfunction and the need for anticoagulation. Vasoactive medications have a very limited role in the management of patients with primary mitral regurgitation. Better screening tools enable detection of early ventricular decompensation, and appropriate operative interventions continue to significantly reduce the morbidity and mortality associated with mitral regurgitation. Mortality associated with ischemic mitral regurgitation resulting from annular ring dilatation or structural damage associated with rupture of a papillary muscle continues to be high, and the simplest and most expeditious operative intervention is emphasized.     

Mitral Regurgitation

Mitral regurgitation (MR) is increasingly prevalent and poses an important public health problem. There are several mechanisms through which MR can occur. Primary (organic) MR is due to intrinsic valvular disease, whereas secondary (functional) MR is due to disruption of an otherwise normal mitral apparatus because of abnormal ventricular geometry. Identification of the causative mechanism is important as this will dictate management strategy and may influence subsequent outcome. Careful assessment of MR severity is important with the use of quantitative measures. There is currently no effective medical treatment for chronic MR. Careful follow-up is paramount in the management of MR to accomplish timely surgical intervention. Mitral valve repair is preferable to valve replacement. In chronic primary MR, conventional timing of surgery is based upon appearance of symptoms and hemodynamic consequences of chronic volume overload. Optimal timing of surgery for asymptomatic patients with chronic severe MR remains controversial although there is an increasing trend toward earlier surgery. In recent years there have been significant advances in percutaneous valve interventions for MR. Although initial results are promising, longer term evaluation will answer questions concerning efficacy, durability, and safety of these interventions.