光氧化处理脱细胞牛心包构建组织工程心肌补片的实验研究

目的 探讨经染料介导光氧化处理的脱细胞牛心包构建组织工程心肌补片的可行性。方法 新鲜牛心包先脱细胞,再经光氧化法处理,消毒后种植雄性SD骨髓间充质干细胞(MSCs)。结扎雌性大鼠左冠状动脉前降支,制作心肌梗死模型,1周后将符合心肌梗死标准的大鼠随机分成3组,心肌梗死对照组(MI)、补片组(P)、种细胞补片组(P+C)分别进行干预。4周后,超声评价心功能;2周、4周取材行组织学和免疫组化检查。结果 脱细胞处理完全去除了牛心包组织中的细胞,光氧化处理使组织结构致密;种植的细胞在组织表面形成连续的细胞层。P+C组牛心包心肌补片降解程度、微血管密度在2周、4周时均较P组大。超声评价补片4周后大鼠心功能,P+C组左室射血分数(LVEF)、左室缩短分数(LVFS)均较MI组和P组大,与MI组的差异有统计学意义。结论 光氧化处理脱细胞牛心包构建的组织工程心肌补片可以延缓心功能恶化,该处理方法具有良好的应用潜力。     

大鼠室壁瘤左心室重建模型的建立

目的探讨建立大鼠室壁瘤左心室重建(LVR)动物模型的可行性。方法对35只成年雄性Sprague-Dawley(SD)大鼠实施左冠状动脉前降支结扎以制作心肌梗死后室壁瘤(LVA)模型,4周后,对符合入选标准的16只LVA模型实施LVR手术,作为实验组;另10只模型行开胸手术作为对照组,在术后3 d、2周、4周分别以超声心动图评价两组大鼠心功能情况,以直视摄片、Masson’s Trichrome染色评价室壁瘤切除的彻底程度。结果 LVA模型及LVR模型的死亡率分别为11.4%(4/35)及18.8%(3/16),建模成功率分别为74.3%(26/35)和81.3%(13/16)。直视摄片及Masson’s Trichrome染色提示补片完全替代心肌梗死瘢痕。超声心动图提示:行LVR手术的实验组动物的左心室收缩期末内径(LVESD)及左心室短轴缩短率(FS)在术后3 d即较对照组有所改善[术后3 d:LVESD(5.00±0.87)mm vs.(5.90±0.92)mm,P<0.05;FS(34.20%±6.80%)vs.(26.60%±6.12%),P<0.01],随着时间的推移,施行LVR手术的实验组大鼠比对照组更好地维持了左心形态及收缩功能[术后2周:左心室舒张期末内径(LVEDD)(7.60±0.56)mm vs.(8.50±1.08)mm,P<0.01;LVESD(5.10±0.65)mm vs.(6.69±0.89)mm,P<0.001;FS(31.90%±6.90%)vs.(21.10%±6.17%),P<0.001;术后4周:LVEDD(7.70±0.50)mm vs(.9.10±0.89)mm,P<0.001;LVESD(5.20±0.39)mm vs.(7.20±0.95)mm,P<0.001;FS(31.80%±2.40%)vs.(20.20%±4.17%),P<0.001]。结论大鼠LVR模型可作为组织工程心肌补片(EHT)研究中一种稳定、可靠、经济的初选模型。     

共价结合生长因子的胶原补片修补大鼠左心室室壁瘤的实验研究

目的 比较采用碳化二亚胺法(EDC法)处理共价结合不同生长因子的胶原补片修补大鼠左心室室壁瘤后的再血管化情况,及其对大鼠左心功能的影响.方法 直径5 mm的圆形胶原补片经EDC法处理作对照组,再分别结合血管内皮细胞生长因子(VEGF)或VEGF+碱性成纤维细胞生长因子(bFGF)后作实验组.成年雄性SD大鼠行左冠状动脉前降支结扎制作透壁心梗模型.4周后,心脏彩超筛选心梗面积占左心室前壁25％～ 35％者入选.随机分成3组,以不同补片行室璧瘤修补,对照组(8只),VEGF组(10只),VEGF+ bFGF组(10只).术后1周、2周、4周分别行心脏彩超监测左心功能,至实验终点取材,免疫荧光法检测补片边缘毛细血管(vWFⅧ染色)及成熟血管(SMA染色)的生成情况.结果 全组死亡比例15％(6/40只).修补1周后,3组动物心功能均明显改善;4周后,结合生长因子的两组心功能较对照组明显改善(对照组对VEGF组,P＜0.05;对照组对VEGF+ bFGF组,P＜0.01).组织学检查显示,两组结合有生长因子的毛细血管生成情况均较对照组明显改善(P ＜0.05);VEGF+bFGF组的再血管化较其他两组明显改善(P＜0.01).相关性分析显示,大鼠心功能参数(FS)与再血管化呈正相关(P=0.0297,r2=0.998).结论 EDC法可有效改善胶原补片的机械性能,共价结合生长因子后可显著增加补片内血管生成,再血管化有助于左心功能的维持.     

脱细胞牛心包羊肺动脉补片的实验研究

目的　评价脱细胞牛心包构建有活性的组织工程羊肺动脉补片的可行性。　方法　将新鲜牛心包采用酶 -去污剂联合脱细胞处理作为血管补片材料 ,从小尾寒羊颈外静脉分离血管内皮细胞和成肌纤维细胞进行传代扩增培养 ,然后分层种植到已消毒的脱细胞牛心包 ,体外培养 7d后 ,自体细胞 -脱细胞牛心包补片作为实验组 (n=5 )植入羊肺动脉 ,分别于 4周 ,6周 ,8周 ,12周和 2 4周取材 ;单纯脱细胞牛心包补片作为对照组 (n=3) ,于 4周 ,12周和 2 4周取材 ,对两组牛心包补片均进行大体观察和组织学检查 ;测定钙、胶原和弹性蛋白的含量。　结果　所有动物均存活 ,羊肺动脉补片内未见血栓 ,无明显动脉瘤样扩张 ,两组补片钙含量与正常肺动脉比较无明显差别。随补片植入时间的推移 ,弹性蛋白含量逐渐增加 ,与正常肺动脉弹性蛋白含量相似 ,显示进行性的组织重塑。　结论　自体细胞 -脱细胞牛心包羊肺动脉补片与单纯脱细胞牛心包补片在体内通过组织重塑在一定程度上均可形成有活性的血管壁组织。     

非体外及体外循环下左心室运动异常型室壁瘤切除术的临床疗效比较

目的比较非体外循环（off-pump）室壁瘤折叠术与体外循环（CPB）室壁瘤线形切除术治疗左心室运动异常型室壁瘤的临床疗效,以提高室壁瘤的治疗效果。方法2003年9月至2007年9月,手术治疗32例左心室前壁或心尖部运动异常型室壁瘤患者,其中男23例,女9例;年龄46～70岁,平均年龄63岁。根据手术中是否采用CPB,将32例患者分为两组,off-pump组（n=17）：室壁瘤范围占左心室的25%～37%,在off-pump下行室壁瘤折叠术;常规体外循环（on-pump）组（n=15）：室壁瘤范围占左心室的27%～40%,在常规CPB下行室壁瘤线形切除术。两组均同期行冠状动脉旁路移植术。术后采用超声心动图测定左心室容积及收缩功能等指标,并进行比较,以评价临床效果。结果两组均无手术死亡。off-pump组无围术期并发症,术后心功能分级（NYHA）较术前有明显改善（1.0±0.8级vs.2.9±0.3级,P=0.001）,左心室射血分数（LVEF）明显提高（41.0%±4.5%vs.36.4%±4.8%,P=0.035）,左心室收缩期末容积指数（LVESVI）明显减小（52.6±27.7ml/m^2vs.79.7±21.4ml/m^2,P=0.003）。随访17例,随访时间12～53个月,平均随访29个月,随访期间无死亡。1例患者术后1年因二尖瓣重度反流再次手术治疗,1例患者于术后3年发生充血性心力衰竭,LVEF31%,仍在观察中;其余患者临床效果良好。on-pump组围术期发生并发症3例（神经系统并发症2例、呼吸功能不全1例）,术后心功能分级较术前有明显改善（1.0±0.6级vs.3.1±0.9级,P=0.001）,LVEF较术前明显提高（42.3%±3.2%vs.35.6%±6.5%,P=0.023）,LVESVI较术前明显减小（49.3±22.6ml/m^2vs.81.3±25.0ml/m^2,P=0.003）。随访15例,随访时间12～60个月,平均随访35个月,随访期间无死亡,临床效果良好。两组间临床指标比较差异无统计学意义（P〉0.05）。结论在off-pump下行室壁瘤折叠术治疗左心室运动异常型室壁瘤,可有效地减少左心室容积,提高左心室?     

实时三维超声评价左室室壁瘤外科治疗后左心室局部收缩功能的改变

目的利用实时三维超声（real-time three-dimensional echocardiography,RT-3DE）评估左心室室壁瘤（LVA）外科治疗后左心室局部收缩功能的改变。方法 2009年2月至2010年2月,北京阜外心血管病医院连续14例冠状动脉粥样硬化性心脏病合并左心室室壁瘤形成患者（LVA组）接受手术治疗。LVA组患者术前和术后4个月随访期间均行二维超声（2DE）、RT-3DE,通过Qlab软件分析计算获得左心室局部射血分数（EF）;同时测量12例正常人的左心室局部EF作为正常对照（对照组）。利用统计方法对比分析LVA组（术前、术后4个月）与对照组左心室局部EF。结果 LVA组患者术前左心室局部EF呈心尖部至基底部递增方向,与对照组方向相反;除下基底段、下侧基底段和前侧基底段外,其余14个节段较对照组显著降低（P〈0.05）。术后4个月左心室局部EF恢复从基底部至心尖部的方向递增,前基底段和侧壁节段的EF与对照组差异无统计学意义（P〉0.05）,其余节段的EF低于对照组（P〈0.05）。结论 RT-3DE是评估LVA患者左心室局部收缩功能的有效检查方法。LVA患者手术治疗后早期左心室局部收缩功能恢复正常递增方向,部分非室壁瘤节段收缩功能恢复。     

血管内皮生长因子基因转染骨髓间充质干细胞移植于梗塞心肌的实验研究

目的 探讨骨髓间充质干细胞（MSCs）移植联合血管内皮生长因子（VEGF）基因转染对大鼠梗塞心肌组织的修复重建、血管再生及梗塞后心功能的影响。方法 体外分离、培养、纯化SD大鼠的MSCs，以BrdU标记MSCs，腺病毒介导VEGF基因转染MSCs。建立大鼠急性心肌梗死模型4周后，随机分为4组（每组10只），分别行梗塞心肌内注射：转染VEGF基因的MSCs移植组（组Ⅰ）、单纯MSCs移植组（组Ⅱ）、单纯VEGF基因治疗组（组Ⅲ）和以注射无血清IMDM培养液为对照组（组Ⅳ）。移植4周后观察移植细胞的分化和新生血管的形成，并通过超声多普勒检测心功能变化。结果 组Ⅰ和组Ⅱ中，梗塞心肌处可见BrdU标记的移植细胞，cTnT染色阳性。超声心动图检查发现，组Ⅰ和组Ⅱ的左室射血分数（LVEF）的改善显著高于对照组（P均〈0．01），而组Ⅰ的LVEF改善程度要明显高于组Ⅱ；部分BrdU染色阳性的细胞可以分化成为内皮细胞，参与构成了梗塞区域的新生毛细血管。相对于对照组，组Ⅰ和组Ⅲ都有明显的血管新生（P均〈0．01）。结论 MSCs移植联合VEGF基因转染可以通过促进心肌再生和新生血管的形成来重建缺血心肌，显著改善心功能。     

牛心包纤维支架宿主细胞重建后体内移植实验

目的 初步探讨牛心包纤维支架宿主细胞重建后体内移植后内皮细胞抗切应力和抗钙化能力以及肌成纤维细胞迁移和自身修复能力。方法 （1）新鲜牛心包片经脱细胞、鞣制、改性后制成试片。（2）A组试片上依序种植宿主肌成纤维细胞和内皮细胞（EC），B组试片上不种植细胞，随后将两组试片分别移植于猪腹主动脉壁上。（3）2个月后对试片进行厚度、钙含量、扫描电镜及组织学检查。结果 （1）A组试片表面覆盖白色光滑组织；B组试片呈灰黄色。A组试片钙含量显著低于B组（P〈0．05），但仍显著高于新鲜牛心包（P〈0．05）。（2）A组试片显著厚于B组试片（P〈0．05）。（3）A组试片60％～70％的表面覆盖EC，裸露的胶原纤维间隙已消失，肌成纤维细胞已迁移至表层下支架的1／2～2／3；B组试片表面无细胞，浅层有少量的肌成纤维细胞生长，大部分胶原纤维间隙消失。结论 通过组织工程技术在体外实现完全内皮化、部分间质细胞化的牛心包纤维支架材料，有可能成为构建组织工程新型生物瓣膜的材料。     

心肌细胞移植改善心肌梗死大鼠左心室收缩功能

目的探讨心肌细胞移植对心肌梗死大鼠的左心室收缩功能的改善作用。方法将65只雄性Wistar大鼠随机分为试验组、对照组和假手术组。试验组（n=25）和对照组（n=25）均结扎冠状动脉左前降支，建立慢性心肌梗死模型。4周后，试验组于心肌梗死区与正常心肌交界处移植新生鼠的心肌细胞；对照组采用与试验组同样方式注射细胞培养液基质；假手术组（n=15）开胸后不结扎冠状动脉，不进行细胞移植。心肌梗死后4周和细胞移植后4周，均采用组织多普勒技术结合二维超声心动图测量大鼠心脏的左室收缩末期容积（ESV）、舒张末期容积（EDV）、左室前壁舒张末期厚度（LVAWD）、左室射血分数（LVEF）及短轴缩短率（FS）、左室短轴乳头肌水平测量前壁和后壁心肌收缩期峰值速度（Sm）和峰值位移（TTs），心尖四腔观测量二尖瓣环平均Sm。用免疫组织化学技术检测试验组心肌移植细胞的存活情况。结果心肌细胞移植后4周，试验组与对照组相比，EDV和ESV均显著缩小（P〈0．01），LVAWD、LVEF、FS、左室前壁和后壁Sm、TTs及二尖瓣环平均Sm均显著增加（P〈0．01）。二尖瓣环平均Sm与左室射血分数呈正相关（r=0．87，P=0．001）。免疫组织化学检测显示试验组心肌疤痕区边缘有移植心肌阳性细胞存在。结论心肌细胞移植能显著改善心肌梗死大鼠左心室收缩功能，逆转左心室重构。     

不停跳下冠状动脉旁路移植加左心室室壁瘤闭式成形术46例

目的总结46例不停跳下冠状动脉旁路移植（冠脉搭桥）加左心室室壁瘤闭式成形术的手术经验。方法在非体外循环及不停跳下以1．0～1．5mg／kg体重肝素抗凝。明确室壁瘤基底位置及其长度以2-0Surgipro843缝线平行左心室长轴加毡片行间断褥式缝合，使瘤腔与左心室功能心腔隔离。45例同期行冠脉搭桥术。结果27例搭桥3根，12例搭桥2根，6例搭桥1根。39例应用左乳内动脉吻合于前降支，3例于转机不停跳下完成手术，2例行前降支内膜剥脱术，2例应用IABP。全组死亡1例。余者无术后心梗发生，10—14d治愈出院。结论不停跳下冠脉搭桥加左心室室壁瘤闭式成形术可有效消除左心室矛盾运动及无效心腔，加固薄弱心室壁，防止心脏破裂；减少恶性心律失常发生；避免体外循环并发症。     

人同种心包补片在法洛四联症分期手术中的应用

目的比较人同种心包补片和G ore-tex补片在法洛四联症(tetra logy of F a llot,TOF)分期手术中扩大右心室流出道(righ t ven tricu lar ou tflow tract,RVOT)的效果。方法28例已行一期手术再行分期手术的TOF患者,按不同的二期或三期手术时间分为两组,G ore-tex组:13例,以G ore-tex补片扩大RVOT;人同种心包补片组:15例,以深低温冷冻保存的人同种心包补片扩大RVOT。比较两组术后临床结果和随访结果。结果G ore-tex补片组术中死亡1例(7.7%),人同种心包补片组术后早期死亡1例(6.7%)。人同种心包补片组住ICU时间、呼吸机使用时间和心包腔引流量均少于G ore-tex补片组(P<0.01)。所有患者均获得随访,随访时间0.8~4.5年,超声心动图检查提示G ore-tex补片组患者术后RVOT水平残余梗阻的比率高于人同种心包补片组(P<0.01),胸部X线片未发现钙化影。结论人同种心包组织致密,缝合后不易渗血,止血方便;且具有良好的弹性和顺应性,有助于降低术后RVOT水平的残余梗阻发生,可作为补片材料在心脏外科手术中应用。     

Delayed left ventricular pseudoaneurysms after left ventricular aneurysm repairs with the CorRestore patch

We present two cases of left ventricular pseudoaneurysm that developed after left ventricular aneurysm repair with the CorRestore patch (Somanetics Corp, Troy, MI). Both patients underwent subsequent pseudoaneurysm repair with Dacron patches (Boston Scientific Corp, Natick, MA). We discuss the physiologic limitations of the CorRestore patch and the causes of pseudoaneurysms that arise after left ventricular aneurysm repair.     

Posterior Ventricular Septal Rupture: An Anatomical Reconstruction

A bstract Rupture of the ventricular septum following posterior myocardial infarction is an uncommon, but lethal, injury that requires prompt repair. Surgical reconstruction can be complex, demanding, and unfamiliar. Conventional techniques, as described in the literature, are associated with a variety of potential pitfalls. An alternative method we have successfully used in our last four patients is presented in detail. The procedure uses two composite (felt/pericardium) patches: an internal patch to reconstruct the left ventricular geometry and an external patch to repair the subtotal infarctectomy. For maximal security, all suture lines sandwich myocardium between two continuous felt surfaces. Specific transition stitches are described, which reliably anchor the entire repair at the critical, but poorly visualized, areas where the ventricular septum makes its transition to left and right ventricular free walls. This technique offers immediate hemostasis and a more anatomical left ventricular geometry. The method also reduces the risk of systemic thromboembolism, residual VSD, and repair disruption.     

Peritoneal regeneration induced by an acellular bovine pericardial patch in the repair of abdominal wall defects

BACKGROUND: This study was to evaluate the feasibility of using an acellular bovine pericardium fixed with genipin (AGP) to repair an abdominal wall defect created in a rat model. MATERIALS AND METHODS: The glutaraldehyde-fixed acellular pericardium (AGA), the genipin-fixed cellular pericardium (GP), and a commercially available polypropylene mesh were used as controls. RESULTS: Gross examination at 3-month post-operatively revealed that dense adhesions to the visceral organs were observed for the polypropylene mesh and the AGA patch, while a filmy to dense adhesion was seen for the GP patch. In contrast, no adhesion to the visceral organs was observed for the AGP patch. Histologically, inflammatory cells were found mainly surrounding the GP patch. In contrast, host cells (inflammatory cells, fibroblasts, and neo-capillaries) were able to infiltrate into the AGA and AGP patches. Unlike the AGA patch, the AGP patch retrieved at 1-month post-operatively became well integrated with the host tissue near the suture line. Additionally, there were some mesothelial cells, identified by the van Gieson stain, observed on the AGP patch. At 3-month post-operatively, a neo-peritoneum was observed on the AGP patch. The neo-peritoneum consisted of organized vascularized connective tissues covered by an intact layer of mesothelial cells. The calcium contents of the polypropylene mesh and the AGA patch increased significantly at 3-month post-operatively, while those of the GP and AGP patches stayed minimal throughout the entire course of the study. CONCLUSIONS: The results obtained in the study revealed that the AGP patch effectively repaired abdominal wall defects in rats and successfully prevented the formation of post-surgical abdominal adhesions.     

Simulated left ventricular aneurysm and aneurysm repair in swine

Patch reconstruction of left ventricular aneurysm may be superior to linear closure, but this hypothesis has not been tested experimentally. Accordingly, six anesthetized domestic pigs were instrumented to measure regional left ventricular wall thickening, stroke volume, systolic left ventricular pressure, and myocardial oxygen consumption. With total bypass and cardioplegia, a 6 by 8 cm Dacron patch was inserted into the anteroapical left ventricle. Simulations were as follows: left ventricular aneurysm, patch open; patch reconstruction, 50% patch plication; standard repair, ventriculotomy edges approximated. Global function, from stroke work (stroke volume x integral of left ventricular pressure)-left ventricular end-diastolic pressure curves, was depressed in all three simulations compared with control. A tendency for stroke work to be greater for standard repair than for left ventricular aneurysm and patch reconstruction at higher preloads was not statistically significant. Mechanical efficiency, from stroke work/myocardial oxygen consumption (joules per milliliter oxygen per beat), was 2.43 +/- 0.52 (mean +/- standard error of the mean) (control), 2.22 +/- 0.94 (standard repair), 1.27 +/- 0.39 (patch reconstruction), and 1.09 +/- 0.37 (left ventricular aneurysm) (no significant differences). Regional work was calculated as regional left ventricular wall thickening x integral of left ventricular pressure. The slope of the regional work-end-diastolic wall thickness relation decreased in the posterior wall 14.0 +/- 2.9 (control) versus 8.4 +/- 2.0 (left ventricular aneurysm), 6.9 +/- 1.4 (patch reconstruction), and 7.4 +/- 1.4 (standard repair) (p less than 0.05). In the anterior wall, contractility did not change significantly (7.4 +/- 1.2, control; 7.8 +/- 2.7, left ventricular aneurysm; 5.0 +/- 0.4, patch reconstruction; and 5.3 +/- 0.4, standard repair). Decreased end-diastolic wall thinning anteriorly suggested tethering. These results in the normal left ventricle suggest that patch ventriculoplasty is of no greater benefit than linear repair. Either repair may impede function of adjacent myocardium through restriction of regional diastolic lengthening.     

Pericardium as a thoracic aortic patch: glutaraldehyde-fixed and fresh autologous pericardium

The repair of complex coarctation of the aorta often requires an aortic patch. Prosthetic patches lack growth potential and are associated with an increased incidence of aneurysm formation opposite the patch. We compared buffered glutaraldehyde-fixed patches, used in six animals (group 1), and untreated autologous pericardial aortic patches, used in five animals (group 2). Weanling pigs underwent pericardial patch replacement of a 1 X 2-cm diamond-shaped segment of the lateral wall of the descending thoracic aorta at the level of the aortic isthmus. Six months following patch aortoplasty, the animals were killed and the in situ patch dimensions were measured and compared to the measurements obtained at implantation. The increases in length, recorded as mean percentage change +/- SEM, were 34.7 +/- 3.7% for group 1 and 102.8 +/- 20.3% for group 2 animals; the increases in width were 91.4 +/- 31.7% for group 1 and 192.4 +/- 31.4% for group 2. The percentage changes for both length and width were significantly different between groups (P less than 0.05). Pull strength testing of standard-size patch samples demonstrated no significant difference in tensile breaking load between groups: group 1 = 959 +/- 277 g, group 2 = 795 +/- 86 g. Thoracic aortography revealed no evidence of stenosis or aneurysmal dilation in either group. Autologous pericardium is resilient, strong, and readily available and has expansile potential that makes it an ideal aortic patch material. We conclude that glutaraldehyde fixation does not provide additional strength and limits graft expansile potential when compared to untreated pericardium.     

Spontaneous disappearance of a false aneurysm after iatrogenic ruptured ventricle

We report the case of a 64-year-old woman who had an atypical subendocardial aneurysm, a space between the internal patch, which was used for the repair of a left ventricular rupture after mitral valve replacement, and myocardium, which filled with blood during the diastole phase. During the follow-up period, the aneurysm spontaneously disappeared. This case endorses combining internal and external approaches to repair a left ventricular rupture after mitral valve replacement.     

A case report of successful repair for ruptured aneurysm of sinus of Valsalva (I VSD) with aortic regurgitation

A nineteen-year-old female who had history of infectious endocarditis underwent surgical repair for ruptured aneurysm of sinus of Valsalva with aortic regurgitation. Through aortotomy mild degree of prolapse of right coronary cusp and perforation of left coronary cusp sized 6 mm in diameter were recognized and the latter was thought to be the dominant lesion resulting in severe aortic regurgitation. Following direct closure of ruptured aneurysm and patch closure of ventricular septal defect, perforated left coronary cusp was repaired with autologous pericardium. Post operative course was uneventful and she is now doing well.     

Postinfarction Left Ventricular Free Wall Rupture: Original Management and Surgical Technique

A case of postinfarction left ventricular free wall rupture is successfully treated. Prompt diagnosis was provided by echocardiography and an emergency operation was carried out. Following sternotomy, hemodynamic stabilization was obtained by gradually evacuating blood from the pericardium, while the femoral vessels were cannulated and the extracorporeal circulation was established. An autologous glutaraldehyde stiffened pericardial patch was sealed over the infarcted area using fibrin glue and fixed with a running suture on the surrounding healthy myocardium.