水蛭和丹参对血管成形术后平滑肌细胞增殖影响的实验研究

目的：探讨腔内血管成形术（ＴＡ）后再狭窄的预防方法。方法：将６０支髂动脉（３０只家兔）随机分为３组（每组２０支髂动脉）：水蛭组、丹参组和对照组，造成实验性动脉粥样硬化狭窄并进行ＴＡ后，水蛭组每天饲喂２ｇ水蛭粉和普通饲料，丹参组每天饲喂２ｇ丹参粉和普通饲料，对照组每天只饲喂普通饲料，３０天后，进行血管造影和病理形态学检查。结果：（１）水蛭组髂动脉内膜厚度（４０．１±９．８μｍ）显著小于丹参组（４８．     

紫杉醇药物涂层支架治疗左前降支病变临床研究

目的：探讨紫杉醇药物涂层支架（PES）治疗冠状动脉左前降支（LAD）病变的即刻疗效及预后。方法：2003年2月～2005年3月在本院造影证实连续LAD单支病变患者94例，共107处病变，按常规行经皮冠状动脉成形术加支架置入术，分析患者临床、X线影像学特征及手术成功率，并行随访。结果：94例患者中，29例置入PES，65例置入金属裸支架（BMS），手术成功率100％。病变弥漫性30例（31．9％），位于近段52例（55．3％），中段12例（12．8％）。全部患者均完成术后6个月的随访并行造影复查。PES组术后6个月时造影复查2例（6，9％）发生再狭窄；BMS组1例1个月内因急性前壁心梗死亡，6个月时造影复查21例（32．3％）发生再狭窄。结论：PES置入治疗冠状动脉LAD病变安全有效，术后心源性猝死及非Q波性心肌梗死发生率与置入BMS者相似，支架内再狭窄发生率明显降低，因再狭窄需冠脉搭桥率也显著降低，术后6个月再狭窄率与文献报道冠脉搭桥术相近。     

冠状动脉血管成形术后再狭窄的研究现状

经皮冠状动脉腔内成形术是目前冠心痛的重要治疗手段，而术后再狭窄的发生严重影响病人的远期疗效与生活质量。本文介绍了再狭窄的发生机制，并从药物、机械、涂层支架、放射及基因方面对再狭窄的防治研究现状进行了综述分析。     

血管紧张素转换酶抑制剂抑制大鼠损伤动脉内膜肥厚的机制

目的：研究血管紧张素转换酶抑制剂（ACEI）抑制大鼠颈总动脉损伤后内膜肥厚的机制。方法：Wistar大鼠20只，制备颈总动脉球囊导管损伤模型，实验组给予ACEI，对照组仅给予溶剂。测定2和5d动脉中膜血小板衍生生长因子B（PDGF—B）和弹性蛋白酶ⅢB阳性细胞率。结果：ACEI显著降低大鼠损伤动脉中膜PDGF—B和弹性蛋白酶ⅢB阳性细胞率（P〈0．01）。结论：ACEI通过抑制PDGF和弹性蛋白酶减轻内膜肥厚。     

莪术组分涂层支架预防猪冠状动脉再狭窄的研究

目的通过中华实验用小型猪冠状动脉再狭窄模型,观察中药莪术组分涂层支架抑制内膜增殖的有效性。方法将18只小型猪随机分为莪术组分涂层支架组(ZES组)、雷帕霉素涂层支架组(SES组)及金属裸支架组(BMS组),每组6只,分别在左前降支、左回旋支及右冠状动脉置入同一种支架各1枚。术后30 d冠状动脉造影后将猪处死,观察支架血管段的病理形态及影像学变化。结果 30 d时,与BMS组比较,ZES组和SES组平均管腔直径和平均管腔面积均明显增大(P<0.05),直径狭窄率和面积狭窄率明显减小(P<0.05);与SES组比较,ZES组和BMS组炎症积分明显降低,内皮化积分明显升高(P<0.05);3组损伤积分比较,差异无统计学意义(P>0.05);光学相干断层扫描及扫描电镜观察,SES支架组30 d时可见部分支架节段内皮化不全及炎性细胞浸润。结论 ZES支架可有效地抑制血管内膜增殖,具有良好的生物相容性。     

Retrograde access via the popliteal artery to facilitate the re‐entry technique for recalcitrant superficial femoral artery Chronic total occlusions

Subintimal recanalization is beneficial in selected patients with peripheral chronic total occlusions (CTO). However, in complex cases, re‐entry into the true arterial lumen may prove to be unsuccessful with a conventional guidewire or a re‐entry catheter when using standard femoral artery access. Our case series describes these technical dilemmas along with strategies that can be utilized to overcome these challenges. © 2011 Wiley‐Liss, Inc.     

Cardiac arrest caused by accidental severe hypothermia and myocardial infarction during general anesthesia

Therapeutic hypothermia is often used for traumatic brain injury because of its neuroprotective effect and decreased secondary brain injury. However, this procedure lacks clinical evidence supporting its efficacy, and adverse outcomes have been reported during general anesthesia. A 61-year-old man with a history of percutaneous coronary intervention (PCI) was admitted with traumatic brain injury. Immediately after admission, he underwent mild therapeutic hypothermia with a target temperature of 33.0°C for neuroprotection. During general anesthesia for emergency surgery because he developed a mass effect, hypothermic cardiac arrest occurred following an additional decrease in the core body temperature. Moreover, myocardial infarction caused by restenosis of the previous PCI lesion also contributed to the cardiac arrest. Although the patient recovered spontaneous circulation after an hour-long cardiopulmonary resuscitation with rewarming, he eventually died of subsequent repetitive cardiac arrests. When anesthetizing patients undergoing therapeutic hypothermia, caution is required to prevent adverse outcomes that can be caused by unintentional severe hypothermia and exacerbation of underlying heart disease.