Objective: To study the kinetics and distribution of smooth muscle cell (SMC) proliferation, phe-notypic modulation, and various extracellular matrix (ECM) components accumulation during vein graft remodeling. Methods...Objective: To study the kinetics and distribution of smooth muscle cell (SMC) proliferation, phe-notypic modulation, and various extracellular matrix (ECM) components accumulation during vein graft remodeling. Methods: Normal vein and vein graft in carotid arteries were examined on d 4, d 7, d 14, d 60 and d180 after bypass grafting with immunohistochemical markers of cellular proliferation (proliferating cell nuclear antigen, PCNA), cytoskeletal protein production (a-actin SMC), myosin heavy chain (MHO iso-forms, ECM proteins, and histochemistry (hematoxylin eosin and Elastica-van Gieson stain). Results: Normal veins demonstrated an extremely low level of cellular proliferation and expressed as adult phenotype SM-Cs in media. After bypass grafting, medial SMCs in the graft appeared to be damaged and began to proliferate on d 4, and subsequently migrated and formed the neointima on d 7. Thereafter, the neointima thickened throughout the 180-day period of the experiment, although the neointimal SMC proliferation decreased after d 14. Meanwhile SMCs underwent a distinct phenotypic change from normal adult type to embryonic type. On d 60, embryonic phenotype SMCs began to return to the adult phenotype, but remain to be present in the neointima for as long as 180 d. ECM components including type I collagen, heparin sulfate proteoglucan (HSPG), and dermatan sulfate proteoglcan (decorin) were detected within the neointima on d 7. Thereafter, the accumulation of ECM increased progressively with time. On d 180, a large amount of ECM components were found in the neointima. HSPG mainly accumulated in the superficial and cellular region of the neointima , decorin, on other hand, located in hypocellular area deep in neointima. Type I collagen scatted in both regions. The elastic fibers became rich and arranged continuously in the neointima. Conclusion: The neointima of vein graft was initially formed by proliferation of the embryonic-type SMCs and then thickened infinitely due to ECM accumulation. Prolonged existence of the embryonic-type SMCs in the neointima may contribute to ECM accumulation and increase in the neointima thickness infinitely, which may predispose accelerated stenosis in the vein graft.展开更多
目的二尖瓣成形术被广泛应用于先天性及继发性二尖瓣病变的手术治疗中。文中探讨二尖瓣成形术后并发机械性溶血的机制及治疗策略。方法回顾性分析2010年8月至2018年6月解放军南部战区总医院行二尖瓣成形术(含房室管畸形病例)451例患者...目的二尖瓣成形术被广泛应用于先天性及继发性二尖瓣病变的手术治疗中。文中探讨二尖瓣成形术后并发机械性溶血的机制及治疗策略。方法回顾性分析2010年8月至2018年6月解放军南部战区总医院行二尖瓣成形术(含房室管畸形病例)451例患者临床资料。其中16例(3.5%)术后出现机械性溶血(血红蛋白尿、黄疸、贫血),心脏超声检查显示二尖瓣少量返流3例、中量返流9例、大量返流4例,其中12例二尖瓣返流束为高流速(Vmax>4m/s)。根据溶血治疗策略将患者分为2组:再手术组(n=10)确诊溶血后1周内接受再次二尖瓣成形术;保守治疗组(n=6)予以血液透析、输血、利尿、碱化尿液、护肝、口服美托洛尔等对症治疗。所有患者接受随访2～36个月,平均(16.0±7.5)个月,对比患者术后心脏超声结果、溶血症状改善程度、心功能水平等。结果两组术后均无死亡病例。再手术组全部患者症状迅速消退,痊愈出院;保守治疗组4例患者因治疗效果不佳于术后3～11周接受再次手术治疗(行二尖瓣成形1例、二尖瓣机械瓣膜置换3例),术后痊愈出院,另外2例患者长期保守治疗。接受再次手术患者心功能维持在I～II级,复查心脏超声显示二尖瓣微量返流10例,少-中量返流3例,无机械性溶血复发;2例长期保守治疗患者,轻中度贫血,尿胆原1+～2+,二尖瓣返流中量,心功能II级,处于亚临床溶血状态。再手术组患者治疗1周后血红蛋白水平、总胆红素水平、二尖瓣返流量均显著优于保守治疗组,差异有统计学意义(P<0.05);再手术组的再次干预发生情况(0 vs 66.7%)及溶血/亚临床溶血发生情况(0 vs 100%)均显著低于保守治疗组,差异有统计学意义(P<0.05)。结论机械性溶血多发生在二尖瓣成形术后早期,超声可发现具有高剪切力的二尖瓣残余返流,可结合临床血管内溶血症状进行诊断。手术是影响溶血的重要因素。术后出现溶血基本可判定手术失败,应尽早再次行二尖瓣成形手术是最佳选择,保守治疗通常效果不佳。展开更多
文摘目的采用自体肺动脉补片矫治主动脉缩窄伴弓发育不良已取得较好的早中期效果。文中评估采用该术式的中远期疗效及可靠性。方法回顾性分析2009年5月至2017年5月期间广州军区总医院心血管外科中心收治的42例主动脉弓缩窄(Co A)伴主动脉弓发育不良患儿临床资料。按手术年龄分为高龄组(>1岁)和低龄组(≤1岁),比较2组患儿手术前后缩窄段压差、肺动脉压力及主动脉变化。结果本组患儿术后并发症8例,无围手术期死亡。随访4~106个月,平均(40.0±15.5)个月,期间无患儿死亡。主动脉缩窄处平均压差(11.9±6.4)mm Hg,5例缩窄处压差>25 mm Hg。患儿术后早期及远期随访主动脉缩窄处压差及肺动脉平均压均显著低于术前(P<0.05),远期随访主动脉弓部Z值较术前均明显增大(P<0.05),且远期随访横弓近端Z值明显大于术前[(-0.64±0.44)vs(-1.27±0.66),P<0.05]。相比于低龄组,高龄组患儿术前及近期随访具有较高的肺动脉压力(P<0.05),且高龄组患儿术中体外循环时间、主动脉阻断时间较长(P<0.05),术后呼吸机辅助时间、ICU时间及住院天数均延长(P<0.05);但远期随访低龄组患儿主动脉缩窄处压差较高(P<0.05),且主动脉横弓近端Z值及峡部Z值较低(P<0.05);两组患儿术中选择性脑灌注时间比较的差异无统计学意义(P>0.05)。结论主动脉缩窄伴弓发育不良患儿应尽早手术。采用自体肺动脉补片主动脉成形术是较理想的手术方式,可以获得较好的中远期效果。
文摘Objective: To study the kinetics and distribution of smooth muscle cell (SMC) proliferation, phe-notypic modulation, and various extracellular matrix (ECM) components accumulation during vein graft remodeling. Methods: Normal vein and vein graft in carotid arteries were examined on d 4, d 7, d 14, d 60 and d180 after bypass grafting with immunohistochemical markers of cellular proliferation (proliferating cell nuclear antigen, PCNA), cytoskeletal protein production (a-actin SMC), myosin heavy chain (MHO iso-forms, ECM proteins, and histochemistry (hematoxylin eosin and Elastica-van Gieson stain). Results: Normal veins demonstrated an extremely low level of cellular proliferation and expressed as adult phenotype SM-Cs in media. After bypass grafting, medial SMCs in the graft appeared to be damaged and began to proliferate on d 4, and subsequently migrated and formed the neointima on d 7. Thereafter, the neointima thickened throughout the 180-day period of the experiment, although the neointimal SMC proliferation decreased after d 14. Meanwhile SMCs underwent a distinct phenotypic change from normal adult type to embryonic type. On d 60, embryonic phenotype SMCs began to return to the adult phenotype, but remain to be present in the neointima for as long as 180 d. ECM components including type I collagen, heparin sulfate proteoglucan (HSPG), and dermatan sulfate proteoglcan (decorin) were detected within the neointima on d 7. Thereafter, the accumulation of ECM increased progressively with time. On d 180, a large amount of ECM components were found in the neointima. HSPG mainly accumulated in the superficial and cellular region of the neointima , decorin, on other hand, located in hypocellular area deep in neointima. Type I collagen scatted in both regions. The elastic fibers became rich and arranged continuously in the neointima. Conclusion: The neointima of vein graft was initially formed by proliferation of the embryonic-type SMCs and then thickened infinitely due to ECM accumulation. Prolonged existence of the embryonic-type SMCs in the neointima may contribute to ECM accumulation and increase in the neointima thickness infinitely, which may predispose accelerated stenosis in the vein graft.
文摘目的二尖瓣成形术被广泛应用于先天性及继发性二尖瓣病变的手术治疗中。文中探讨二尖瓣成形术后并发机械性溶血的机制及治疗策略。方法回顾性分析2010年8月至2018年6月解放军南部战区总医院行二尖瓣成形术(含房室管畸形病例)451例患者临床资料。其中16例(3.5%)术后出现机械性溶血(血红蛋白尿、黄疸、贫血),心脏超声检查显示二尖瓣少量返流3例、中量返流9例、大量返流4例,其中12例二尖瓣返流束为高流速(Vmax>4m/s)。根据溶血治疗策略将患者分为2组:再手术组(n=10)确诊溶血后1周内接受再次二尖瓣成形术;保守治疗组(n=6)予以血液透析、输血、利尿、碱化尿液、护肝、口服美托洛尔等对症治疗。所有患者接受随访2～36个月,平均(16.0±7.5)个月,对比患者术后心脏超声结果、溶血症状改善程度、心功能水平等。结果两组术后均无死亡病例。再手术组全部患者症状迅速消退,痊愈出院;保守治疗组4例患者因治疗效果不佳于术后3～11周接受再次手术治疗(行二尖瓣成形1例、二尖瓣机械瓣膜置换3例),术后痊愈出院,另外2例患者长期保守治疗。接受再次手术患者心功能维持在I～II级,复查心脏超声显示二尖瓣微量返流10例,少-中量返流3例,无机械性溶血复发;2例长期保守治疗患者,轻中度贫血,尿胆原1+～2+,二尖瓣返流中量,心功能II级,处于亚临床溶血状态。再手术组患者治疗1周后血红蛋白水平、总胆红素水平、二尖瓣返流量均显著优于保守治疗组,差异有统计学意义(P<0.05);再手术组的再次干预发生情况(0 vs 66.7%)及溶血/亚临床溶血发生情况(0 vs 100%)均显著低于保守治疗组,差异有统计学意义(P<0.05)。结论机械性溶血多发生在二尖瓣成形术后早期,超声可发现具有高剪切力的二尖瓣残余返流,可结合临床血管内溶血症状进行诊断。手术是影响溶血的重要因素。术后出现溶血基本可判定手术失败,应尽早再次行二尖瓣成形手术是最佳选择,保守治疗通常效果不佳。
