移植心冠状动脉增殖性心脏病的预防和监测

目的 观察心脏移植患者冠状动脉增殖性病变的发病情况。方法 对５例长期存活的心脏移植受者进行了观察。患者在心脏移植后使用祛脂药、血管紧张素转换酶抑制剂及硝酸酯类药,观察心电图ＳＴ－Ｔ改变、临床症状（如胸痛等）、血压、血糖、血脂,并行冠状动脉造影。结果 ５例患者术后各发生急性排斥反应１～３次,均出现心电图我个导联Ｔ波倒置及ＳＴ段轻度下移,１年后ＳＴ－Ｔ改变恢复正常,１例患者血糖长期升高,１例血脂升高,     

心脏移植后的移植心冠状动脉血管病与急性排斥反应一例

目的 探讨移植心冠状动脉血管病与急性排斥反应的早期诊断。方法 对1例扩张型心肌病患者施行同种原位心脏移植术。术后定期随访，观察项目有：临床表现，血液生化，标准十二导联心电图，超声心动图，心内膜心肌活检，冠状动脉造影术。结果 术后5-6个月，患者出现乏力，活动后胸闷，心悸，发热等全身或心脏非特异性症状，并有持续存在的窦性心动过速，左心室射血分数（EF）降低，右心房内径增大，室间隔增厚，持续三尖瓣返流，外周血白细胞持续升高，增加免疫抑制剂用量后症状好转或消失，术后9个月，冠状动脉造影显示典型的冠状动脉血管病改变，以左前降支及其中，远段分支血管弥漫性狭窄病变为甚，心内膜心肌活检显示典型的急性排斥反应改变（I-A型）。结论 心脏移植术后系列超声心动图和心电图检查可作为早期移植心冠状动脉血管病和急性排斥反应的无创性检测方法。心内膜心肌活检和冠状动脉造影为确诊手段。     

心脏移植长期存活患者冠状动脉病变一例

目的　探讨 1例心脏移植长期存活患者冠状动脉病变的原因、诊断和处理。方法　对1例心脏移植术后存活 8年的患者进行长期随访。结果　术后患者生活质量好 ,恢复正常工作 ;血液生化正常 ;心电图无心肌缺血改变 ;肱动脉内皮依赖性血管舒张功能正常 ;心内膜心肌活检未见急性排斥反应征象 ;同位素心肌显像提示左室壁心肌放射性分布进行性减低 ;冠状动脉造影显示左冠状动脉弥漫性狭窄、右冠状动脉近段有一局限性严重狭窄 (>90 % )、远端为轻度弥漫性狭窄 ,行右冠状动脉近段成形和支架植入 ,同位素心肌显像示左室壁心肌放射性分布明显改善。结论　慢性排斥反应可能是导致移植心冠状动脉病变的重要原因 ;定期行同位素心肌显像检查有助于了解心肌血液供应 ;严重的局限性冠状动脉病变可应用冠状动脉成形和支架植入予以治疗。     

存活十年以上同种原位心脏移植三例

目的总结同种原位心脏移植后患者获得长期存活的临床治疗经验和体会。方法为2例扩张性心肌病和1例慢性克山病患者施行心脏移植，术前患者的肺动脉压力为42-53mmHg（5．60-7．07kPa），肺血管阻力为5．6-7．0wood。供、受者体重相差10％～15％，HLA配型有3个抗原相同。供心采用含钾温血经冠状静脉窦连续逆行灌注。2例采用标准法心脏移植，1例采用全心法心脏移植，心房及大血管均采用外翻缝合法。术后应用环孢素A、硫唑嘌呤及皮质类固醇激素预防排斥反应。结果3例患者术后存活时间分别为13年10个月、12年及10年3个月，患者心功能NYHA分级为Ⅰ级，均恢复正常生活和工作。3例术后分别发生6、3、1次排斥反应，经治疗逆转。心电图检查显示，例1、例2有2个P波，例3为正常窦性心律。超声心动图显示，例1、例2有左、右心房增大，三尖瓣轻度返流，例3各心腔大小正常，无二尖瓣、三尖瓣返流。3例术后经449次冠状动脉造影，均未发现异常。结论选择合适的供、受者，保护好供心，采取恰当的术式和吻合技术，合理应用免疫抑制剂以及预防心脏移植物血管病，是关系心脏移植患者长期存活的重要因素。     

心脏移植术后冠状动脉病变的相关因素分析

目的探讨心脏移植术后长期存活的患者冠状动脉病变的相关危险因素。方法回顾性分析32例心脏移植术后长期存活患者的临床资料,并对相关的临床因素进行评价,筛选出移植心冠状动脉病变的独立危险因素。结果高脂血症、热缺血时间、巨细胞病毒(CMV)抗体阳性、移植后时间及慢性排斥反应是移植心冠状动脉病变的危险因素,而年龄、高血压和糖尿病与移植心冠状动脉病变的相关性不明显;多元Losgitic回归分析,移植后时间和慢性排斥反应是移植心冠状动脉病变的独立危险因素(P<0.001,P=0.003)。结论心脏移植术后冠状动脉病变的实质是慢性排斥反应;与供心的热缺血时间、高脂血症及巨细胞病毒感染等相关。     

建立黑山羊陈旧性心肌梗死模型的新方法

目的建立能长期存活的山羊心肌梗死实验模型。方法16只黑山羊,体重15~24kg,3~6月龄,雌雄不拘。均行剑突下切口,倒V字形切开胸骨下段,于左冠状动脉前降支中下1/3用5-0prolene线8字缝合包绕伴行静脉,阻断5min,再间歇3min,重复两次进行缺血预适应,然后结扎左冠状动脉及伴行静脉,建立羊心肌梗死模型。描记心电图,于建模前及建模后1、3、6、12、24、48h抽血检测血清肌酸激酶同工酶(creatinekinase-MB,CK-MB)及脂肪酸结合蛋白;并于模型建立后6周行心电图、超声心动图、选择性左冠状动脉造影、透射电镜及心肌梗死面积测定。结果造模过程中无实验动物死亡,造模成功率为100%。CK-MB于建模后3h开始升高,12h达高峰;脂肪酸结合蛋白于建模后1h开始升高,12h达高峰。建模后结扎点下方心肌逐渐出现片状紫红色区域,心电监测仪提示、、V3导联明显ST段上抬及T波改变,建模后6周,相应导联均出现明显病理性Q波;心脏超声检查显示左心室腔明显扩大并见室壁瘤形成;选择性左冠状动脉造影检查见心尖区血管纤细,外形呈瘤样扩张。透射电镜见梗死区肌丝溶解、断裂,排列混乱,细胞器崩解聚集。心肌梗死面积为4.74±0.78cm2。结论黑山羊是建立心肌梗死模型较好的实验动物;经剑突下切口,倒V字形切开胸骨下端入路,结扎左冠状动脉前降支中下1/3,是建立能长期存活的陈旧性心肌梗死模型简便、安全可靠的方法。     

心脏移植患者血浆同型半胱氨酸含量的变化及临床意义

目的　了解心脏移植患者血浆同型半胱氨酸含量的变化及临床意义。方法　利用高压液相方法测定 1 4例心脏移植患者的血浆同型半胱氨酸的浓度 ;以肱动脉充血内径变化百分率为血管内皮功能的指标 ;同时对其中的 7例进行冠状动脉造影。采用单因素直线相关分析 ,观察心脏移植患者血浆同型半胱氨酸的浓度与血管内皮功能以及移植血管病变的关系。结果　心脏移植组患者的血浆同型半胱氨酸浓度明显高于健康对照组 [(1 3.4 7± 2 .78) μmol/Lvs (9.2 6± 3.5 7) μmol/L];肱动脉充血内径变化百分率明显低于对照组 [(8.2± 3.7) %vs(1 2 .5± 1 .6 ) %];直线相关分析 ,两者呈负相关 ,γ =- 0 .80 4 ;冠脉造影 2例出现单支冠状动脉病变 ,其血浆的同型半胱氨酸的浓度均升高。结论　心脏移植患者血浆同型半胱氨酸浓度的升高 ,与心脏移植患者血管内皮功能下降密切相关 ,可能与移植血管病变有关。     

心脏移植长期存活受者免疫抑制治疗经验总结

目的总结并分析4例存活时间在16年以上的心脏移植受者免疫抑制治疗经验。方法回顾性分析哈尔滨医科大学附属第二医院心外科1992年4月至2000年1月施行的4例原位心脏移植临床资料,重点分析受者免疫抑制治疗经过。4例供者均为脑死亡器官捐献,供心采用改良St.Thomas液保存。1例受者原发病为慢性克山病,3例为扩张性心肌病。3例受者采用标准法心脏移植,1例采用全心法心脏移植。术后均采用环孢素+糖皮质激素+硫唑嘌呤三联免疫抑制方案,免疫维持治疗单用环孢素。随访期间监测环孢素血药浓度、外周血白细胞计数及淋巴细胞功能,行心电图、X线胸片、超声心动图、冠状动脉造影、光学相干断层扫描(OCT)及心内膜下心肌活检等检查。若受者出现排斥反应则采用冲击治疗或改用其他免疫抑制剂。结果截至2016年6月,3例受者存活,1例受者死亡。3例存活受者存活时间分别为22年4个月、20年7个月和16年5个月,1例死亡受者术后18年6个月死于多器官功能衰竭。4例受者术后10年内分别发生排斥反应1~6次,采用冲击治疗后均恢复。3例存活受者术后第10年环孢素剂量调整为0.5~1.0 mg·kg~(-1)·d~(-1)。4例受者术后10年内冠状动脉造影检查均未发现冠状动脉血管病变。2009年5月,3例存活受者冠状动脉造影和OCT检查示1例受者冠状动脉仅见斑块浸润,自觉症状良好,该受者2015年5月冠状动脉造影及OCT检查结果示冠状动脉多处狭窄,遂行支架治疗,其余2例受者检查结果均正常。结论心脏移植术后及时、准确地诊断排斥反应,合理、正确地调整免疫抑制治疗方案,个体化免疫治疗用药和积极、有效控制并发症是受者长期存活的重要手段。     

变异型心绞痛心电图特征性改变与临床探讨

近年来较多的资料显示,伴有急性心肌缺血的多种临床情况均可引起缺血性J波。我们分析42例变异型心绞痛患者的心电图特征性改变（包括ST段抬高、T波高耸、缺血性J波、对应导联ST段下移等）,并与冠状动脉造影结果进行对照,现报道如下。     

心脏移植治疗终末期冠心病五例

目的总结心脏移植治疗终末期冠心病的体会。方法共有5例患者,1例为2次急性心肌梗死后行左心辅助泵植入术后25个月的患者,3例为急性心肌梗死后大面积无存活心肌、出现心力衰竭的患者,1例为经皮冠状动脉支架置入术和冠状动脉旁路移植术后仍反复发生心力衰竭的患者。均施行标准式原位心脏移植术。术前使用达利珠单抗诱导治疗1次,术后采用环孢素A、霉酚酸酯和泼尼松预防急性排斥反应。结果5例患者均痊愈出院,恢复正常的生活和工作,心功能均恢复至Ⅰ级;术后未发生严重的感染和急性排斥反应。结论心脏移植可作为治疗不适宜施行冠状动脉旁路移植术,或冠状动脉旁路移植术后效果较差的终末期冠心病患者的有效手段;选择合适的供心、良好的心肌保护、合理的抗排斥治疗方案,以及围手术期血压、血糖、血清胆固醇、尿酸的有效控制,是手术成功的关键。     

Successful treatment of acute dissection of the donor aorta after orthotopic heart transplantation.

Acute aortic dissection is one of the rare aortic complications that occur after orthotopic heart transplantation. We report the second case of successful surgical treatment of aortic dissection confined to the donor aorta in a recipient of an orthotopic cardiac allograft. A 68-year-old patient was admitted with chest pain and shortness of breath 7 years after orthotopic heart transplantation. He previously had undergone twice coronary artery bypass grafting. Echocardiography revealed acute dissection of the donor aorta. The patient underwent urgent Bentall procedure with a prosthetic conduit. The post-operative course was uneventful. The heart donor was a 40-year-old man with known arterial hypertension and who had received long-term ergotamine tartrate therapy for migraine. This case demonstrates that heart-transplant recipients with arterial hypertension and donor-related risk factors are prone to aortic complications and require careful follow-up.     

Combined coronary intervention in heart-transplant patient with rapidly accelerated cardiac allograft vasculopathy

A 46-year-old man accepted for heart transplantation due to persistent cardiac failure from dilated cardiomyopathy underwent a transplant in Germany on July 13, 1995. The donor heart was suspected of coronary artery disease at explantation, but he could wait no longer because of his rapidly deteriorating hemodynamics. Postoperative coronary angiography revealed 25% stenosis of the left descending artery. He showed several episodes of minimal or moderate rejection postoperatively, and coronary angiography 15 months postoperatively showed rapidly accelerated cardiac allograft vasculopathy demonstrating triple vessel disease with multiple lesions. Percutaneous transluminal coronary angioplasty was successful on 2 coronary vessels, but immediately recurrent stenosis and new lesions involving the left main trunk occurred 6 weeks thereafter. Since he was financially unable to afford a second heart transplantation, quadruple coronary artery bypass grafting was conducted October 25, 1996. A biventricular assist device was used when he could not be weaned from cardiopulmonary bypass. He died of multiple organ failure 3 days after surgery.     

Beating heart coronary artery bypass surgery after orthotopic heart transplantation

Beating-heart coronary artery bypass surgery was performed in a 52-year-old man with accelerated transplant coronary artery disease 10 years after orthotopic heart transplantation. Transplant coronary artery disease was first detected in the left circumflex coronary artery 9 years after transplantation. Rapid progression to triple vessel disease occurred within 1 year, and the patient developed worsening symptoms of shortness of breath and chest pain. He underwent off-pump "beating heart" left internal mammary artery to left anterior descending coronary artery bypass surgery. The circumflex coronary artery was not graftable due to diffuse and truncated small vessel disease. His postoperative course was uneventful and he was discharged on the fifth postoperative day. Coronary angiography 3 months after the surgery revealed a widely patent left internal mammary artery to left anterior descending artery bypass. He is alive and symptom free more than 1 year after his surgery.     

Incidence, progression and functional significance of cardiac allograft vasculopathy after heart transplantation

BACKGROUND: Cardiac allograft vasculopathy after heart transplantation leads to an accelerated form of atherosclerosis with marked and often diffuse vessel wall changes that limit long-term survival. Previous studies showed contradictory results relating vessel wall changes to endothelial vasodilator response. METHODS: A total of 30 cardiac transplant recipients were studied 3, 12, and 24 months after heart transplantation. Coronary angiography was performed at rest, during supine bicycle ergometry, and after 1.6 mg sublingual nitroglycerin. Coronary cross-sectional area (biplane coronary angiography) and coronary artery wall changes (intravascular ultrasound) were assessed and extent of intimal changes correlated to vasodilator responses to nitroglycerine and bicycle ergometry. RESULTS: Intravascular ultrasound showed significant intimal thickening in 43, 64, and 58% of patients at 3, 12, and 24 months. Intimal thickening 3 months after transplantation was related to donor age (r=0.70, P<0.01) but did not predict progression of disease that manifested itself angiographically as a decrease in coronary cross-sectional area at 12 and 24 months (P<0.005) and significant coronary stenosis in 12% of patients after 24 months. Endothelium-independent vasodilatation after nitroglycerin (33+/-15, 44+/-20, and 43+/-24%) was normal. Endothelium-dependent, flow-induced vasodilatation during exercise was decreased (14+/-11, 18+/-14, and 16+/-17%) but did not correlate to intimal changes assessed by ultrasound. CONCLUSIONS: The study confirms the high incidence of intimal thickening after heart transplantation as assessed by intravascular ultrasound. Impaired exercise-induced vasodilatation suggests diminished bioavailability of endothelium-derived nitric oxide to physiological stimulation but the lack of relationship between coronary wall changes and this functional impairment suggests intermittent and presumably reversible endothelial injury in graft atherosclerosis.     

Combined coronary intervention in heart-transplant patient with rapidly accelerated cardiac allograft vasculopathy.

A 46-year-old man accepted for heart transplantation due to persistent cardiac failure from dilated cardiomyopathy underwent a transplant in Germany on July 13, 1995. The donor heart was suspected of coronary artery disease at explantation, but he could wait no longer because of his rapidly deteriorating hemodynamics. Postoperative coronary angiography revealed 25% stenosis of the left descending artery. He showed several episodes of minimal or moderate rejection postoperatively, and coronary angiography 15 months postoperatively showed rapidly accelerated cardiac allograft vasculopathy demonstrating triple vessel disease with multiple lesions. Percutaneous transluminal coronary angioplasty was successful on 2 coronary vessels, but immediately recurrent stenosis and new lesions involving the left main trunk occurred 6 weeks thereafter. Since he was financially unable to afford a second heart transplantation, quadruple coronary artery bypass grafting was conducted October 25, 1996. A biventricular assist device was used when he could not be weaned from cardiopulmonary bypass. He died of multiple organ failure 3 days after surgery.     

Infant orthotopic cardiac transplantation

Infant orthotopic cardiac transplantation has been recently applied to various forms of congenital heart disease with encouraging short-term results. Between June 1986 and September 1987 we evaluated 16 infants for orthotopic cardiac transplantation. Fourteen had hypoplastic left heart syndrome, one had endocardial fibroelastosis with aortic atresia, and one had anomalous pulmonary arterial origin of the left main coronary. Eight families accepted the treatment program and eight families refused (two because of associated anomalies and six on philosophical grounds). Of the eight patients who were candidates for orthotopic cardiac transplantation, one died 6 hours after diagnosis, one was allowed to die after 60 days because of acquired neurologic complications, and another had congenital cytomegalic virus infection. The remaining five patients (four with hypoplastic left heart syndrome, one with anomalous pulmonary arterial origin of the left main coronary) had orthotopic cardiac transplantation. The operation was performed with absorbable polydioxanone suture with deep hypothermia and circulatory arrest in four neonates for hypoplastic left heart syndrome (average time 47 minutes) and bicaval cannulation and continuous bypass in one 11-month-old infant for anomalous origin of the left main coronary. In-house retrieval was used in all. One neonate died of complications as a result of pretransplant donor heart dysfunction and size discrepancy, whereas the remaining three neonates and one infant survived and are home 23 months, 12 months, and 8 months (the patients with hypoplastic left heart syndrome) and 17 months (the patient with anomalous origin of the left main coronary) postoperatively. Triple-drug immunosuppression included cyclosporine, azathioprine, and prednisone. Rejection was diagnosed by clinical evaluation of child activity and monocyte cell cycle analysis from peripheral blood samples without myocardial biopsies. Routine echocardiograms, electrocardiograms, and chest x-ray films were not helpful. Six episodes of rejection were successfully treated in four patients. Twelve-month postoperative catherization in one patient (hypoplastic left heart syndrome) showed appropriate graft growth, no aortic or pulmonary anastomotic strictures, normal right and left ventricular function, and no coronary artery disease. We conclude that infant orthotopic cardiac transplantation is an acceptable procedure for severe forms of untreatable congenital heart disease. The excellent short-term results warrant continued application of orthotopic cardiac transplantation.     

Acute cholecystits leading to ischemic ECG changes in a patient with no underlying cardiac disease

Although chest pain with ST-segment elevation is often indicative of cardiac ischemia, it has also been described with surgical conditions such as acute cholecystitis. We report the case of a 34-year-old Caucasian female who was referred with symptoms consistent with acute cholecystitis. An electrocardiogram (ECG) showed unexpected changes with inferolateral ST-segment elevation indicative of an inferolateral myocardial infarct. Further investigations and analysis of the results along with the clinical picture meant an acute cardiac event was excluded. Gallstones were seen on ultrasound and an inflamed gallbladder, consistent with acute cholecystitis, was confirmed at laparoscopic cholecystectomy. This led to the resolution of her symptoms and a return to the isoelectric baseline of the ST segments on the ECG. Five previous cases of cholecystitis induced ECG changes have been described in the literature. This case describes the youngest patient with no previous cardiac disease. We review the literature and suggest the pathophysiological mechanism to explain these findings. When the initial diagnostic interventions for chest pain with ST-segment elevation do not yield the expected results, an alternative diagnosis such as cholecystitis should be considered.     

The tako-tsubo syndrome: therapeutic stakes

The authors report the case of 2-old-caucasian women in the pre- and interhospital setting, who presented chest pain with ST segment elevation. Coronary angiography did not show any significant coronary lesion, ventriculography revealed typical aspect of tako-tsubo. It resolved in a short time, with normalisation of the left ventricule function. The tako-tsubo syndrome, or transient left ventricular apical ballooning syndrome, first described by Japanese physicians, is more and more frequently observed in caucasian patients. This cardiomyopathy associates an apical transient dysfunction without any significant coronary lesion. This syndrome is usually observed in elderly women, occurs frequently after acute emotional or physical stress. The clinical presentation looks like an acute coronary syndrome, with chest pain, electrocardiographic changes and moderate cardiac enzymes release. Coronary angiography shows no significant coronary disease and ventriculography a systolic dysfunction with akinesia of middle and apical segments, leading apical ballooning, and basale hyperkinesia. These abnormalities are transient, with quick favorable outcome. The aetiopathegenia is still uncertain. The differential diagnosis with an acute coronary syndrome with thrombosis is not yet possible. Clinical or biological criteria allowing early diagnosis would lead to optimize the therapeutic management.     

Cardiac assessment with thallium scanning prior to aortic aneurysm repair.

Coronary artery disease occurs commonly in patients with aortic aneurysms and is a major cause of morbidity and mortality. The role of screening and intervention for cardiac disease prior to aneurysm repair is controversial. The outcome after cardiac screening with thallium scanning and/or angiography in 102 consecutive patients undergoing aortic aneurysm repair was documented. Significant coronary artery disease was found in 34 (33%) patients and two patients had either coronary artery bypass or angioplasty prior to aneurysm repair. There was no cardiac mortality after aneurysm repair and the overall mortality on an intention-to-treat basis was 2%. There was good correlation between prior history of cardiac events, electrocardiography (ECG) and the results of screening with thallium scanning and angiography. There was no correlation between cardiac history, ECG and the incidence of cardiac events in the postoperative period. Significant coronary artery disease was found in 33% of patients without a cardiac history or abnormal ECG. Cardiac screening with thallium scanning confirmed a high incidence of significant coronary disease in patients with aortic aneurysm. In this study, cardiac intervention followed by expedient aneurysm repair in 20 patients was associated with zero mortality. The short-term benefit of such a policy is difficult to prove and its main advantage may be better long-term survival.