62例小儿心脏瓣膜置换术

目的总结１９７５～１９９７年间６２例１４岁以下儿童人工心脏瓣膜置换术的经验,探讨儿童瓣膜置换的手术适应证、瓣膜选择和术后抗凝等问题。方法全组低温体外循环下行心脏瓣膜置换术,１７例使用生物瓣,４５例使用机械瓣。结果住院死亡１２例,晚期死亡１３例,术后失访４例,长期存活３３例;随访时间２～２５７个月,其中心功能Ⅰ级２８例,Ⅱ级５例,无１例因生长发育出现人工瓣膜相对狭窄。结论儿童人工心脏瓣膜置换术的死亡率高,宜慎重掌握适应证;儿童心脏瓣膜置换宜选择机械瓣     

"瓣中瓣"法二尖瓣置换术21例

目的 探讨保留全部二尖瓣结构置换二尖瓣的方法，即“瓣中瓣”方法的应用。方法 2002年1月至2005年2月，对21例二尖瓣病变患者采用“瓣中瓣”方法行二尖瓣置换术，术中保留全部二尖瓣结构，维持自然瓣下结构形态与位置，均采用2-0Prolene线进行连续缝合，将人工瓣膜置于二尖瓣口中央，同期行三尖瓣成形术15例。结果 全组均植入人工机械二尖瓣膜20枚和生物二尖瓣1枚，三尖瓣机械瓣2枚。主动脉阻断时间平均17．1min，体外循环时间平均38．1min。手术及体外循环停机顺利，无1例住院死亡和严重并发症发生。术后第7d，左心室舒张期末内径由76．1mm下降至60．1mm，左心房舒张期末内径由67mm下降至49ram，心胸比率由0．72下降至0．56，射血分数由0．47增至0．59。结论 采用“瓣中瓣”方法置换二尖瓣，保持了二尖瓣下装置的自然位置，操作简便，有利于对心肌的保护，并减少术后并发症的发生。     

人工瓣膜功能障碍的外科治疗

目的 总结41例人工心脏瓣膜功能障碍(PHVD)的临床特点、外科治疗方法 及围术期处理经验.方法 手术均在全麻低温体外循环下进行;1例采取股动脉插管左侧开胸,40例均经原切口,主动脉、上下腔静脉插管建立体外循环.38例行瓣膜置换术,使用机械瓣35枚(二尖瓣位23枚,主动脉瓣位11枚,三尖瓣位1枚),生物瓣6枚(二尖瓣位3枚、主动脉瓣位2枚、三尖瓣位1枚);2例行瓣膜角度矫正术;1例行异物清除术.急诊手术13例,择期手术28例.结果 全组气管插管5.1～243.0 h,平均63.3 h,中位时间15.3 h;气管切开5例.全组死亡6例,病死率14.6%,均发生于急诊手术后,死因为低心排血量综合征3例、多器官衰竭2例及恶性心律失常1例.并发症包括感染性心内膜炎、顽固性呃逆及切口感染各1例.结论 对急性PHVD,无论是生物瓣或机械瓣,均应立即进行急诊手术.对慢性PHVD亦应强调及早再次手术.     

心脏瓣膜病再次手术221例临床分析

目的总结既往有二尖瓣闭式扩张术、瓣膜成形术、瓣周漏及生物瓣失功能等的患者再次瓣膜手术的经验。方法自1998年1月至2005年8月,实施心脏瓣膜病再次手术221例,其中急症手术8例。其中二尖瓣闭式扩张后再狭窄105例,二尖瓣或主动脉瓣成形术后复发性瓣膜病变37例,瓣周漏29例,生物瓣衰败18例,其他瓣膜再发病变11例,人工瓣膜机械功能障碍9例,Ebstein畸形矫治术后三尖瓣关闭不全7例,人工瓣膜心内膜炎5例。再次手术方式包括二尖瓣置换、二尖瓣和主动脉瓣双瓣置换、主动脉瓣置换、三尖瓣置换。两次手术间隔时间1～21年。结果全组术后死亡19例,占8．6％。早期死亡主要原因为术后低心排综合征、恶性心律失常、多脏器功能衰竭与肾功能衰竭,其中急症手术8例中死亡3例,术前心功能Ⅳ级者手术死亡9例,病死率为14．5％（9／62例）。结论瓣膜病再次手术危险因素包括急症手术、术前心功能差、合并其他重要脏器功能不全、体外循环时间和主动脉阻断时间长等。针对这些因素积极防治,可以进一步降低这类患者手术病死率和并发症发生率。     

生物瓣衰坏病人的再次瓣膜替换经验

总结２０例生物瓣衰坏病人的再次换瓣经验。第一次替换生物瓣时１９例为单纯二尖瓣替换，１例为二尖瓣、主动脉瓣双瓣替换。生物瓣在体内工作６～１２４年。二次手术前心功能ＩＩ级１例，ＩＩ级１２例，ＩＶ级７例。手术共替换２２枚机械瓣。手术死亡２例。作者指出对生物瓣替换术后的病人要定期复查，发现瓣膜有运动异常应及时再次手术换瓣，对心功能差的病人应作积极术前准备。分离心包内粘连不宜过多，提倡采用常温体外循环，持续温血灌注保护心肌；术后支持呼吸、循环功能，延长辅助呼吸时间也是十分必要的。     

三尖瓣替换术及早期结果

目的 探讨三尖瓣替换术（TVR）的手术适应证和人工瓣膜的选择。方法 1997年3月至2004年6月,共施行TVR42例,其中20例有心脏手术史。手术适应证：①自然瓣膜损毁无法修复（34例）;②进行性三尖瓣病变（2例）;③修复后残余的瓣膜功能不全仍严重影响心脏功能（6例）。合并下列情况时,积极选择TVR：肺血管阻力中、重度升高;手术后有残余的左心功能不全;有三尖瓣成形手术史。人工心脏瓣膜替换术包括：单纯TVR30例,主动脉瓣和二尖瓣加TVR8例,二尖瓣加TVR3例,主动脉瓣加TVR1例。三尖瓣位人工瓣使用双叶型机械瓣28枚,生物瓣14枚。其他合并的心脏手术包括：先天性心脏畸形修复10例,人工瓣周漏修补、黏液瘤切除、冠状动脉搭桥各1例。结果 全组手术病死率17％（7／42）,手术并发症发生率31％（13／42）。术后心功能（NYHA分级）：Ⅰ级21例,Ⅱ级10例,Ⅲ、Ⅳ级各1例。术后晚期死亡2例。结论 当三尖瓣的病变程度严重,修复把握不大,特别是伴有肺血管病变、左心功能不良、左心病变未能完全矫治时,应积极行TVR;人工瓣应选择双叶型和机械瓣或生物瓣,特别是后者。     

儿童心脏瓣膜置换手术及其疗效

目的探讨儿童心脏瓣膜置换手术及治疗效果。方法1990年1月至2002年12月，45例14岁以下儿童施行了心脏瓣膜置换手术。其中男26例，女19例。年龄3—14岁，平均10．8岁；≤10岁15例，10～14岁30例。包括先天性心脏瓣膜病32例，风湿性瓣膜病6例，心内膜炎3例，部分型房室管畸形修补术后二尖瓣关闭不全3例，室间隔缺损修补术后主动脉关闭不全1例。行二尖瓣置换23例，其中2例为矫正型大动脉转位行解剖位三尖瓣置换，主动脉瓣置换9例；二尖瓣与主动脉瓣双瓣置换4例；三尖瓣置换9例。5例使用生物瓣膜或同种主动脉瓣，余40例均采用机械瓣膜，包括进口双叶瓣34枚，进口单叶瓣3枚，国产单叶瓣7枚。结果本组手术死亡(术后30d内)2例，死亡率4．4％，均死于手术当日，1例因顽固性心律失常，1例术后低心输出量综合征。生存者随访8个月-12年，平均4．9年。4例晚期死亡，晚期死亡率9．3％。置入机械瓣膜者均采用华法林抗凝治疗，未发生血栓栓塞及抗凝相关并发症，病儿术后心功能均Ⅰ-Ⅱ级。结论儿童瓣膜病病人，大多数可以置入合适的成人型号人工瓣膜，保证其术后生长发育，减少二次手术。采用华法林进行抗凝治疗，经过平均4．5年随访，无血栓栓塞或抗凝有关的出血并发症发生，治疗效果较为满意。     

感染性心内膜炎62例外科治疗分析

目的 总结感染性心内膜炎(infective endocarditis,IE)的外科治疗经验.方法 对我院62例IE患者行全麻体外循环下心内直视手术,术中清除感染病灶,行心内畸形纠正和瓣膜置换.结果 本组术中植入生物瓣12例,机械瓣49例,另单独行动脉导管未闭缝合术1例.术后死亡1例,为人工瓣感染心内膜炎后再次换瓣,死于感染性休克和心功能不全.其余患者经过抗炎治疗4～6周后体温平稳出院.术后随访1年,未有复发病例.结论 早期给予足量、有效的抗生素治疗,感染无法控制时及时手术治疗,完善的手术纠治是治疗成功的关键.     

心脏瓣膜二次手术患者再手术原因分析

目的分析心脏瓣膜术后行二次手术的主要原因,并评价体外循环下瓣膜二次手术的安全性。方法回顾性分析四川大学华西医院心脏大血管外科2010年1月至2015年1月期间体外循环下行二次瓣膜手术45患者的临床资料,其中男14例、女31例,平均年龄(51.21±8.36)岁。结果 45例患者共有3例术后死亡,手术死亡率6.67%。42例存活患者中位随访时间为36(4~68)个月,期间患者无死亡或再次手术。心脏瓣膜术后行再次瓣膜手术的主要原因包括未干预瓣膜出现病变、瓣周漏、血栓形成伴瓣膜功能障碍、机械瓣膜瓣叶开闭不良、生物瓣膜退行性病变、感染性心内膜炎、瓣膜成形术后病变。结论首次手术涉及二尖瓣病变患者应早期积极处理三尖瓣病变。体外循环下心脏瓣膜二次手术安全有效,心脏瓣膜术后应加强随访复诊,如再次出现瓣膜问题应积极手术干预。     

人工心脏瓣膜替换术后瓣周漏18例

人工心脏瓣膜替换术后瓣周漏是一种严重并发症。我们报告２２９２例植入２５７５枚人工心脏瓣膜，发生瓣周漏者１３例，发生率为０．５１％（１３／２５７５）。外院术后瓣周漏转入我院者５例。１５例中再次手术，单纯修补５例，重新换瓣１０例。本组死亡５例。另３例瓣周漏因心功能尚好，暂未手术。     

Tricuspid valve repair for tricuspid valve endocarditis: tricuspid valve "recycling"

Tricuspid valve endocarditis traditionally has been treated with either valve excision or valve replacement. To avoid implantation of foreign material in an infected field, we have applied the principles of mitral valve repair to 4 patients with tricuspid valve endocarditis. On preoperative echocardiography, all patients had 3 to 4+ tricuspid regurgitation, evidence of progressive right ventricular enlargement, and mobile vegetations. In each case, up to three quarters of the anterior leaflet was excised en bloc with infected chordae and papillary muscle heads. Surgical procedures included standard quadrangular resection, conversion to a bicuspid valve, and pericardial patch replacement of the anterior leaflet with mobilization of basal chordae to replace resected marginal chordae. On postoperative echocardiography, tricuspid regurgitation and right ventricular dimensions were reduced in 2 of 4 patients in spite of loss of leaflet tissue. All excised valve tissue demonstrated bacteria on Gram stain or culture. Nonetheless, all repaired valves were successfully sterilized without recurrent infections. Tricuspid valve repair can allow eradication of infection with potential for improving valve competency in complicated tricuspid valve endocarditis.     

Ebstein's anomaly: repair based on functional analysis.

OBJECTIVE: 'Classical' repair of Ebstein's anomaly is usually performed with transverse plication of the atrialized chamber. However, the anterior leaflet has restricted motion which is an important factor of the tricuspid valve insufficiency. We studied the long term results of mobilization of the anterior leaflet associated with longitudinal plication of the right ventricule. METHODS: From 1980 to July 2002, 191 patients (mean age 24.4+/-15 years (1-65)) were operated on. Anterior leaflet function was assessed on pre-op echocardiography and on surgical examination. Conservative surgery was possible in 187 patients (98%) and included mobilization of the anterior leaflet, longitudinal plication of the right ventricle and prosthetic annuloplasty in adults. Bidirectional cavo-pulmonary shunt was associated in 60 patients. Four patients had valve replacement. RESULTS: Hospital mortality occurred in 18 patients: 9% (95%CL: 6-15%) due to right ventricle (RV) failure in nine patients. Mean follow-up was 6.4 years (0.07-22). Actuarial survival was 82% at 20 years. Tricuspid valve insufficiency was 1 or 2+ in 80% of the cases. Reoperation occurred in 8% (16 patients). A successful second repair was obtained in ten patients. Electron beam computerized tomography (20 patients) demonstrated improved left ventricle ejection fraction 56-66% (P<0.05). Supraventricular tachycardia and pre-excitation syndromes were reduced from 23 to 5%. CONCLUSION: Conservative surgery is indicated for all symptomatic patients. The incidence of valve repair is high when leaflet mobilization is performed. Valve replacement can be avoided in most cases. Functional and hemodynamic results are excellent.     

Surgical treatment of Ebstein's malformation: report of 108 cases

OBJECTIVE: To review retrospectively the experience of surgical treatment of Ebstein's malformation in 108 patients. METHODS: One hundred and eight patients with Ebsteins malformation underwent surgical correction, including tricuspid valve annuloplasty in 83 patients (73.4%) and tricuspid valve replacement in 30 (5 with redo-operation). Concomitant procedure included division of the abnormal accessory conduction pathway in 8 patients. RESULTS: The overall hospital mortality was 8.8%. The hospital mortality rate was 10.4% before 1990 and 5.5% after that time. There was a significant difference between the two periods (P < 0.05). The main causes of death were low cardiac output, arrhythmias and right heart failure. The mean follow-up time was 6.3 years. The heart function improved to be NYHA class I or II in 92% of the patients. CONCLUSIONS: Early surgical intervention is recommended for patients with Ebstein's malformation, especially for those with symptoms and cardiac enlargement. Tricuspid valve repair should be performed if anterior leaflet of the tricuspid valve well developed. However, tricuspid valve replacement is advocated if anterior leaflet is dysplastic or its origin displaced.     

Anesthesia for tricuspid valve replacement after heart transplantation

A 41 year old male patient had received heart transplantation in U.S. in 1993. When myocardial biopsy was performed in 1998, tendinous cords of the tricuspid valve were injured. Tricuspid regurgitation developed along with right heart insufficiency, and the patient was scheduled for tricuspid replacement. For induction of anesthesia, midazolam and fentanyl were used. After induction, both blood pressure and pulse rate were stable. During extracorporeal circulation, perfusion pressure was controlled at 70-80 mmHg, and the duration of cardio-pulmonary perfusion was about 90 minutes. For withdrawal from extracorporeal circulation, dopamine and dobutamine were used. The course was steady and normal after the withdrawal. In tricuspid valve replacement after heart transplantation, stabilized anesthetic course could be maintained using midazolam and fentanyl.     

腔镜不停跳术对左心瓣膜置换术后远期三尖瓣重度反流疗效分析

目的 总结左侧心脏瓣膜置换术后远期出现孤立性重度三尖瓣关闭不全患者的腔镜辅助不停跳三尖瓣手术治疗经验。方法 11例心脏瓣膜疾病患者行左心瓣置换术后远期发生重度三尖瓣关闭不全并右心衰竭,8例出现心脏恶病质综合征及肝肾功能不全,予行再次三尖瓣手术,包括人工瓣环成形术2例,行三尖瓣置换术9例,其中置换生物瓣5例,双在叶机械瓣4例;在腔镜辅助下行心脏不停跳再次手术5例,常规再次心脏停搏手术6例。结果 2例围术期死亡,均为停跳组瓣膜置换病人。术后心包引流液量心脏不停跳组明显少于停跳组（P<0.05）。停跳组术后严重低心排血量综合征4例,不停跳组1例。两组术后1月复查超声心动图,右心房、室均明显缩小,三尖瓣无或少量反流,两组间无明显差异。获长期随访5例、随访时间25~86月、心功能Ⅱ级3例、Ⅲ级2例。结论 左心瓣膜置换术后远期孤立性重度三尖瓣关闭不全合并右心衰的再次手术死亡率高、合理掌握手术指征、手术时机、积极开展微创不停跳手术和良好的围术期治疗是手术成功的关键。对于终末期病例,手术死亡率高,应积极开展针对右心系统的心脏超声及磁共振检测指标,综合评估手术风险,常规换瓣手术指征需慎重,必要时可考虑微创经皮导管瓣膜植入术。     

应用彩色多普勒对二尖瓣置换术后三尖瓣功能的远期随访

目的应用彩色多普勒超声评价二尖瓣置换术后远期三尖瓣功能及形态变化。方法对接受二尖瓣置换术的903例病人术后三尖瓣功能进行了2～9年,平均(3.6±2.4)年的跟踪观察。所有病例术前均有不同程度的三尖瓣环扩大或关闭不全,其中未行三尖瓣成形术者201例;行Kay或改良DeVega成形术者686例;三尖瓣成形术同时加成形环者16例。结果未行三尖瓣成形术者术后2～3年有46例出现三尖瓣重度关闭不全;行Kay或改良DeVega成形术者,术后3～5年150例出现中重度三尖瓣关闭不全;三尖瓣成形术同时加成形环者仅1例术后2年出现三尖瓣轻-中度关闭不全。结论二尖瓣置换术后远期三尖瓣功能性关闭不全与三尖瓣环扩大、右心功能损害和严重肺动脉高压有关,三尖瓣环扩大是其重要的原因。对二尖瓣置换术者,手术中一旦发现有三尖瓣环扩大,即使无三尖瓣关闭不全,亦应行三尖瓣成形术,重度三尖瓣关闭不全、瓣环明显扩大者最好在环缩术的同时加成形环。     

风湿性心脏病左心瓣膜置换术后晚期重度三尖瓣关闭不全的外科治疗

目的 探讨风湿性心脏病(风心病)左心瓣膜置换术后晚期重度三尖瓣关闭不全(TR)的发生机制、手术指征、手术方法和疗效.方法 风心病左心瓣膜置换术后5～16年出现重度TR病人37例,均有不同程度的右心衰竭表现,左室射血分数(LVE)0.52±0.05,肺动脉收缩压(37.6±7.8)mm Hg.经右胸前外侧切口或正中切口再次手术行三尖瓣置换(TVR)25例,改良DeVega环缩术4例,带环成形术8例.结果 术后住院死亡4例,其中死于呼吸衰竭2例、多脏器功能衰竭和肾功能衰竭各1例.随访2个月～10年,死于右心衰竭3例,严重心律失常1例;生存的25例临床症状均有明显改善.结论 左心瓣膜置换术后晚期重度TR与肺动脉高压持续存在、风湿性三尖瓣病变、初次未作三尖瓣环缩术或方法不确实等有密切关系.左心功能良好、右室收缩功能无严重损害,无严重肺动脉高压是再次手术的指征,并主张尽早行TR纠正术.保留全瓣结构行三尖瓣置换有助于提高手术疗效.影响术后长期疗效仍是右室收缩功能.     

Role of the septal leaflet in tricuspid valve closure. Consideration for treatment of complete atrioventricular canal.

A septal leaflet of the tricuspid valve is thought to work differently from other anterior and posterior leaflets. We studied its role in valve closure in dogs by means of a dynamic area meter. During the control state, the tricuspid valve orifice area increased twice in diastole coincidentally with either atrial systole or rapid ventricular filling. We observed several findings after the septal leaflet resection: (1) two peak area patterns of the tricuspid valve orifice in diastole, (2) no elevation of right atrial pressure on ventricular systole (there was no V wave), (3) no tricuspid valve regurgitation on right ventriculography. These findings suggest that a complete valve closure occurred without the septal leaflet in regular sinus rhythm. An elevation of the right ventricular pressure produced by pulmonary artery stenosis without septal leaflet, however, easily caused tricuspid valve regurgitation in contrast to the same pressure of the right ventricle with the normal tricuspid valve. The right ventricular pacing caused severe valve regurgitation without the septal leaflet. Results indicate that in the repair of the complete atrioventricular canal defect and other tricuspid valve lesions, the septal leaflet of the tricuspid valve rarely requires attention. An atrioventricular block should be avoided, however, because electrical cardiac pacing on the right ventricle causes severe valve regurgitation without the septal leaflet.     

Advanced mitral-tricuspid disease with severe right ventricular dysfunction: the double-staged approach

Tricuspid valve surgery in the presence of severe right ventricular dysfunction and pulmonary hypertension secondary to mitral valve stenosis is associated with poor early outcomes. We report the case of a young patient, presenting with severe chronic mitral-tricuspid disease responsible for long-lasting pulmonary hypertension and altered right ventricular function, who initially underwent mitral valve replacement and 7 days later the correction of her tricuspid insufficiency. This 2-staged approach permitted progressive reduction of pulmonary pressure and partial right ventricular remodeling before closing the systolic release valve of the right ventricle represented by tricuspid regurgitation.     

Severe tricuspid regurgitation late after aortic and mitral double valve replacement; report of a case

A 59-year-old man had undergone aortic and mitral valve replacement (DVR) for rheumatic aortic and mitral valve stenosis 15 years ago. At that time, echocardiography did not detect tricuspid regurgitation (TR), and catheterization data showed right atrial pressure v wave of 8 mmHg and pulmonary artery pressure of 27/12 (17) mmHg. One year after DVR, hepatomegaly and jugular venous dilatation appeared, and after 5 years edema of both legs became apparent. After 7 years, chest X-ray showed an increase of cardio-thoracic ratio, and for the first time, echocardiography detected mild TR. Fifteen years after DVR, severe general fatigue, shortness of breath and hepatomegaly could not be controlled with medication. Catheterization data showed right atrial pressure v wave of 23 mmHg and pulmonary artery pressure of 28/13 (17) mmHg. Right ventriculography showed progression of severe TR. Tricuspid valve replacement (TVR) was performed using a St. Jude Medical 31 M mechanical valve under natural cooling and heart beating. The tricuspid valve was only slightly thickened and no subvalvular abnormalities were seen other than a severely dilated tricuspid annulus. Postoperative course was uneventful and he was discharged 44 days after the TVR. He is currently doing well 6 years after the TVR. All terms, he did not have pulmonary hypertension or left-side heart problems. We suspect that the cause of TR was not secondary, and was included in the category of isolated TR. If the left heart is completely treated, as in this case, it is important to follow-up for signs of right heart failure, before TR is detected.