药物涂层球囊治疗膝下动脉硬化性狭窄或闭塞致严重下肢缺血

目的 观察药物涂层球囊(DCB)治疗膝下动脉硬化性狭窄或闭塞致严重下肢缺血(CLI)的效果。方法 回顾性分析96例膝下动脉硬化性狭窄或闭塞致CLI患者,其中50例接受DCB治疗(DCB组)、46例接受普通球囊治疗(对照组),比较2组治疗效果、安全性及预后。结果 96例球囊均到达病变部位并成功完成扩张,未植入补救性支架。组间术前及术后即刻踝肱指数(ABI)、Rutherford分级及Wagner分级差异均无统计学意义(P均＞0.05);术后6、12个月DCB组ABI高于、Rutherford分级及Wagner分级均低于对照组(P均＜0.05)。术后6、12个月,DCB组一期通畅率均高于、管腔丢失均少于对照组(P均＜0.05),组间截肢率差异均无统计学意义(P均＞0.05)。Kaplan-Meier分析结果显示,术后12个月,DCB组免于临床驱动的靶病变血运重建率(CD-TLR)为89.81%,高于对照组的67.39%(P=0.008 8)。结论 DCB治疗膝下动脉硬化性狭窄或闭塞致CLI效果较好。     

Integration of vascular biology and magnetic resonance imaging in the understanding of atherothrombosis and acute coronary syndromes

Summary.  The interaction between the vulnerable atherosclerotic plaque prone to disruption and thrombus formation is the cornerstone of acute coronary syndrome (ACS). Although distinct from one another, the atherosclerotic and thrombotic processes appear to be interdependent, hence the term atherothrombosis. Inflammation is a crucial common pathophysiological mechanism. Overall, the association of plaque vulnerability and ACS has been well documented. Given the multifactorial origin of atherothrombosis the best preventive approach should be aggressive management of all the risk factors. New interventions should be directed toward decreasing vulnerability of the lesions thereby decreasing the risk of ACS.     

活血化瘀法治疗肢体闭塞性动脉硬化症136例效果探讨

目的探讨活血化瘀法治疗肢体闭塞性动脉硬化症临床应用效果。方法对照组接受临床常规西医治疗,研究组在西医常规治疗基础上加用中医活血化瘀法,记录两组肢体闭塞性动脉硬化症患者临床疗效。结果两组肢体闭塞性动脉硬化症患者均顺利完成相应治疗,研究组临床治疗总有效率(86.03%)显著高于对照组(61.76%),数据对比P0.05。结论肢体闭塞性动脉硬化症患者在常规西医治疗基础上加用中医活血化瘀法可显著提高其临床疗效,有利于保障患者生活质量及身心健康。     

长期危险饮酒与脂代谢糖耐量变化及动脉硬化的关系

目的探讨长期危险饮酒与脂代谢、糖耐量变化及动脉粥样硬化的关系，为长期危险饮酒人群动脉粥样硬化的早期预防及治疗提供依据。方法按世界卫生组织饮酒分类标准和1999年的糖耐量低减标准，从体检中心健康体检者中选出符合以上条件男性96例（A组）；根据体检者自愿的原则将A组分为禁酒组（A1组）48例，危险饮酒组（A2组）48例；非饮酒符合糖耐量正常者56例（B组）。先量体检者的收缩压，然后抽取A、B两组体检者的空腹和进食75g葡萄糖的2h血样，空腹血样分别测定空腹胰岛素（Fins）、空腹血糖（FBG）、三酰甘油（TG）、胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）和载脂蛋白A1（ApoA1）的浓度；餐后2h血样分别测定2h血糖（BG）和2h胰岛素（Ins）的浓度；6个月和2年后，以同样的方法测定A1组和A2组血样的相关项目。结果A组体检者血清中的FBG、2hBG、Fins、2h Ins、TG、TC、LDL-C的浓度均较B组明显升高，而HDL-C和ApoA1明显下降；6个月后，A1组与A2组及B组相比，脂代谢紊乱和胰岛素抵抗有了明显的改善，糖耐量低减状态明显好转；2年后A1组的所有检测指标基本接近B组水平，而A2组主要表现为高TG和TC及低HDL-C血症、代偿性高Ins血症、胰岛素抵抗，糖耐量状态显著恶化。结论禁酒或控制饮酒量，改变不良生活习惯，并对脂代谢紊乱进行积极的治疗，改善糖耐量状态，可有效控制和延缓动脉粥样硬化的发生和发展。     

老年2型糖尿病脑动脉狭窄相关性危险因素分析

目的分析老年2型糖尿病脑动脉狭窄相关性危险因素。方法对本院行全脑DSA检查有动脉狭窄的100例老年缺血性脑血管病患者分为两组：2型糖尿病组和非糖尿病组，检测空腹血糖（FPG）、胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白-胆固醇（LDL-C）、空腹胰岛素（FINS）、高密度脂蛋白-胆固醇（HDL-C）、血纤维蛋白原（FIB）、胰岛素抵抗指数（HOMA-IR），并进行分析对比。结果（1）糖尿病患者脑动脉狭窄的病变与NDM比不论其血管累及支数及弥漫性方面均存在明显差异。（2）糖尿病组患者FPG、TC、TG、LDL-C、FINS、FIB、HOMA-IR明显高于非糖尿病组，差异有统计学意义（P〈0．05），HDL-C低于非糖尿病组，差异有统计学意义（P〈0．05）。结论老年2型糖尿病患者脑动脉狭窄比非糖尿病患者更广泛，这与糖尿病患者血脂代谢紊乱、胰岛素抵抗指数、高血糖、血纤维蛋白原升高有关。     

紫杉醇药涂球囊扩张治疗ASO患者疗效及SIRT7水平对术后血管再狭窄的预测

目的分析自身免疫性早发性卵巢功能不全(POI)患者血清免疫指标水平,筛选出较为特异的免疫性指标。 方法选取46例自身免疫性POI患者(POI组)和46例健康女性(正常组),比较两组体液免疫指标、自身免疫指标、抗心磷脂综合征指标、甲状腺功能指标水平。 结果与正常组比较,POI组孕产次、经期及月经周期减少,卵泡刺激素、黄体生成素升高,雌二醇、抗苗勒氏管激素降低;体液免疫指标κ轻链、λ轻链、免疫球蛋白G、免疫球蛋白M、免疫球蛋白E升高,补体4降低;抗心磷脂综合征指标抗心磷脂IgA抗体(ACA-IgA)、ACA-IgG、抗β2糖蛋白1 IgM抗体升高;甲状腺功能指标游离三碘甲状腺原氨酸、游离甲状腺素、促甲状腺素受体抗体、甲状腺过氧化物酶抗体升高(P＜0.05),上述指标阳性率两组间比较差异有显著性(P＜0.05)。POI组内与自身免疫指标阳性率比较,体液免疫指标阳性率和甲状腺功能指标阳性率差异均有显著性。 结论自身免疫性POI患者血清体液免疫指标和甲状腺功能指标更容易发生异常。     

Mediation Analysis of Aortic Stiffness and Renal Microvascular Function

Aortic stiffening, assessed by carotid-femoral pulse wave velocity, is associated with CKD. Transmission of excessive flow pulsatility into the low-impedance renal microvasculature may mediate this association. However, direct analyses of macrovascular–microvascular relations in the kidney are limited. Using arterial tonometry, iohexol clearance, and magnetic resonance imaging, we related arterial stiffness, GFR, urinary albumin excretion, and potential mediators, including renal artery pulsatility index, renal vascular resistance, and arterial volume in the cortex, in 367 older adults (ages 72–92 years) participating in the Age, Gene/Environment Susceptibility-Reykjavik Study. In a model adjusted for age, sex, heart rate, and body size, aortic stiffness was related to GFR (Slope of regression B=−2.28±0.85 ml/min per SD, P=0.008) but not urine albumin (P=0.09). After accounting for pulsatility index, the relation between aortic stiffness and GFR was no longer significant (P=0.10). Mediation analysis showed that 34% of the relation between aortic stiffness and GFR was mediated by pulsatility index (95% confidence interval of indirect effect, −1.35 to −0.29). An additional 20% or 36% of the relation was mediated by lower arterial volume in the cortex or higher renal vascular resistance, respectively, when offered as mediators downstream from higher pulsatility index (95% confidence interval of indirect effect including arterial volume in the cortex, −2.22 to −0.40; 95% confidence interval of indirect effect including renal vascular resistance, −2.51 to −0.76). These analyses provide the first evidence that aortic stiffness may contribute to lower GFR by transferring excessive flow pulsatility into the susceptible renal microvasculature, leading to dynamic constriction or vessel loss.