大肠息肉661例临床与病理分析

目的探讨大肠息肉的临床及病理特征。方法肠镜检查发现小息肉直接用活检钳分次钳除送病理,大息肉取活检病理检查,同时按性别、年龄、发生部位、病理学结果等因素进行分析。结果7804例检出息肉661例（8．47％）,共924个息肉,多发223例,单发438例;炎性息肉167例、增生性息肉144例、腺瘤性息肉例351例;26例癌变（3．93％）;息肉随体积增大癌变率逐渐增加（P〈0．05）;绒毛状腺瘤恶变最高,其为次绒毛状管状腺瘤,管状腺瘤最低（P〈0．05）。结论大肠息肉发生率较高,存在一定程度癌变,故发现息肉均应送病理检查,以明确息肉的性质。     

2018～2023年北京市某医院患者血清维生素D水平特征分析

目的 分析2018年4月至2023年3月北京清华长庚医院成年患者血清25-羟基维生素D[25(OH)D]水平的分布特征和变化趋势。方法 共纳入9 470例在2018年4月至2023年3月于北京清华长庚医院进行血清25(OH)D检测的患者,回顾性分析患者25(OH)D水平在不同性别、年龄、检测季节和年份之间的差异。结果 全体受试者的25(OH)D水平的中位数(四分位数)为16.52(11.58,23.26)ng/mL,其中有6 019(63.6%)例患者为维生素D缺乏(<20ng/mL),2 398(25.3%)例患者为维生素D不足(20～30ng/mL),仅有1 053(11.1%)例患者为维生素D充足状态(>30ng/mL)。患者的25(OH)D水平在不同年龄间和检测的不同季节间差异明显,主要表现为18～39岁年龄组人群较低,春季和秋季水平较低。从2018年到2023年5年间逐年分析显示患者的25(OH)D水平没有明显随年份的变化趋势。结论 目前医院患者的维生素D水平偏低,18～39岁年龄组人群和春季、冬季检测的患者中25(OH)D缺乏的比例较高,提示临床医护应关注就诊患...     

曲美他嗪联合阿托伐他汀治疗原发性高血压伴阵发性心房颤动的疗效观察

Objective To study the efficacy of trimctazidine combined with atorvastatin for primary hypertension with paroxysmal auricular fibrillation,and its effects on LAD and CRP. Methods 160 patients of pri-mary hypertension with paroxysmal auricular fibrillation were randomly divided into 4 groups. Forty patients were treated with amiodarone (control group),600 mg/d for the first week,400 mg/d for the second week and 200 mg/d later;40 patients were treated with atorvastatin (20 mg/d,3 times per day) in addition to amiodarone (the atorvasat-in group);40 patients were treated with trimetazidine (20 mg/d,3 times per day) in addition to armiodarone (the trimetazidine group);40 patients were treated with combination of trimetazidine and atorvastatin in addition to amiod-atone (the combination group),and the dose was the same as the above groups. The treatment was started within 24 hours of recovering from paroxysmal auricular fibrillation and lasted for 1 year. Results After 1 year there was 1 pa-the control group,and 62.5% (25/40) for the atorvasatin group,64.1% (25/39) for the trimetazidine group,and 84.6% (33/39) for the combination group. Compared to the control group,the effective rate of the 3 treatment groups were all significantly higher (X2=4.56、5.13、17.55,P<0.05). The effective rate of the combination group was significantly higher than that of the atorvasatin group and the trimetazidine group (X2=4.95、4.30,P<0.05),and there was no significant difference of effective rate between the atorvasatin group and the trimetazidine group(X2= >0.05). After treatment LAD was (40.96+1.81) mm in the control group,(38.65±1.90) mm in the atorvasatin group,(39.15±1.85)mm in the trimetazidine group,and (37.22±1.74) mm in the combination group. LAD of the 3 treatment groups were all significantly different from the control group(F=3.42,P<0.05). LAD of the combina-tion group was significantly smaller than that of the atorvasatin group and the trimetazidine group (P<0.05),and there was no significant difference of the LAD between the atorvasatin group and the trimetazidine group(P>0.05). There was no significant difference between the 4 groups on CRP before treatment (F=0.96,P>0.05). After treat-ment CRP was (8.85±1.45) mg/L in the control group,(5.96±1.26) mg/L in the atorvasatin group,(6.81± 1.37) mg/L in the trimetazidine group,and (3.75±1.15) mg/L in the combination group. CRP of the 3 treatment groups were all significantly different from the control group (F=3.63,P<0.05). CRP of the combination group was significantly lower than that of the atorvasatin group and the trimetazidine group (P<0.05),and there was no signif-icant difference of CRP between the atorvasatin group and the trimetazidine group (P>0.05). Conclusion The treatment with trmetazidine combined with atorvastatin could prevent recurrence of paroxysmal auricular fibrillation though anti-inflammatory and inhibiting the remodeling of left atrial.     

吡格列酮联合厄贝沙坦对原发性高血压患者左心室肥厚及血清脑钠肽的影响

目的 探讨吡格列酮对原发性高血压患者左心室肥厚及脑钠肽的影响.方法 原发性高血压伴左心室肥厚患者80例完全随机分成2组,各40例.常规治疗组给予厄贝沙坦（150 mg/d）,吡格列酮组给予厄贝沙坦（150 mg/d）＋吡格列酮（15 mg/d）,均治疗6个月.比较2组治疗前后左心室质量指数（LV MI）、血清脑钠肽浓度的变化.结果 治疗后2组患者LVMI、血清脑钠肽浓度均下降（P＜0.05）,2组治疗后比较,吡格列酮组LVMI、血清脑钠肽浓度下降为[（126.2±10.4）g/m2、（113.6±42.9）ng/L,较常规治疗组[分别为（135.5±11.2）g/m2、（138.8±45.8）ng/L]明显（P＜0.05）.结论 吡格列酮能逆转高血压病患者的左心室肥厚,并降低血清脑钠肽浓度.     

曲美他嗪对高血压病伴阵发性房颤患者左房内径及血清CRP水平的影响

目的 探讨曲美他嗪治疗高血压病伴阵发性房颤的疗效及可能机制。方法 将同期收治的高血压病伴阵发性房颤患者80例随机分为观察组和对照组各40例,均予钙离子拮抗剂和（或）利尿剂降压,并于房颤复律后24h内开始口服胺碘酮,第1、2周分别为600、400mg／d,其后改为200mg／d;观察组在此基础上口服曲美他嗪20mg／次,每日3次。两组均服药18。观察两组治疗前后疗效及左房内径、血清CRP水平变化。结果 观察组有效率显著高于对照组（P〈0．05）;治疗后观察组左房内径显著小于对照组、血清CRP水平显著低于对照组（P〈0．05）。结论 曲美他嗪治疗高血压病伴阵发性房颤疗效确切,可能机制为抑制炎症反应及左房重构。     

曲美他嗪对不稳定型心绞痛患者内皮素、一氧化氮水平的影响

目的:研究曲美他嗪对不稳定型心绞痛内皮素(ET)、一氧化氮(NO)的影响。方法:不稳定型心绞痛患者80例随机分为曲美他嗪组(40例)与常规治疗组(40例),治疗前及治疗4周后测定血浆ET、NO水平。40例健康人作为正常对照组,在静息空腹状态下采血测定血浆ET、NO水平。结果:不稳定型心绞痛患者血浆NO水平明显下降,与正常对照组比较有显著性差异(P<0.01);血浆ET水平明显升高,与正常对照组比较有显著性差异(P<0.01);曲美他嗪组与常规治疗组治疗前血浆ET、NO水平比较无显著性差异(P>0.05)。曲美他嗪组治疗后血浆NO水平明显升高,血浆ET水平明显降低,与治疗前比较有显著性差异(P<0.01),与常规治疗组治疗后比较也有显著性差异(P<0.01)。结论:曲美他嗪对不稳定型心绞痛患者具有保护内皮功能的作用。     

琥珀酸美托洛尔缓释片对冠心病无症状心肌缺血心率震荡和心率变异性的影响

目的 观察冠心病无症状心肌缺血心率震荡和心率变异性的改变及琥珀酸美托洛尔缓释片对心率震荡和心率变异性的影响.方法 对比观察美托洛尔治疗后的冠心病无症状心肌缺血患者心率震荡和心率变异性的改变,并与健康体检者对照.结果 治疗前,治疗组震荡斜率值、震荡初始值、SDNN、SDANN及SDNNindex明显低于对照组(P<0.05),rMSSD和PNN50与对照组比较差异无统计学意义(P>0.05);治疗后,震荡斜率值、震荡初始值、SDNN、SDANN及SDNNindex明显高于治疗前(P<0.05).结论 无症状心肌缺血患者存在心率震荡和心率变异性异常,美托洛尔可改善无症状心肌缺血患者心脏自主神经的调节功能.     

阿托伐他汀治疗肺动脉高压患者的疗效观察

目的观察阿托伐他汀对原发性和继发性肺动脉高压患者的临床、血流动力学、心功能、血浆血管紧张素Ⅱ、内皮素、一氧化氮、C-反应蛋白（CRP）、前列环素及血栓素A2的影响，探讨其疗效的作用机制。方法肺动脉高压患者70例随机分成2组，治疗组48例，对照组22例，2组均按基础疾病进行治疗，治疗组在此基础上加用阿托伐他汀，记录患者治疗前后的超声指标，心功能分级及运动耐量等，并分别于治疗前后测定血浆血管紧张素Ⅱ、内皮素、一氧化氮、C-反应蛋白、前列环素及血栓素A2的水平。结果治疗组在用阿托伐他汀及常规药物治疗后，肺动脉收缩压（PASP），肺血管阻力（PVR），右心房（RA），右心室（RV）内径下降明显；而左心室射血分数（LVEF）、左心排量（CO）显著升高；患者的纽约心脏协会（NYHA）心功能分级显著下降，运动耐量显著提高；血氧饱和度（SO2）无统计学意义。治疗组与对照组的疗效相比，PASP、PVR下降及NYHA心功能改善有统计学意义。治疗组血浆CRP、内皮素、血浆血管紧张素Ⅱ、血栓素山水平明显下降，血浆一氧化氮、前列环素水平明显上升，与对照组比较有统计学意义。结论阿托伐他汀可显著降低原发性或继发性肺动脉高压患者的肺动脉收缩压，肺血管阻力，并可提高患者的心功能状况及运动耐量。阿托伐他汀在肺动脉高压的治疗可能有较好的应用前景。     

血塞通软胶囊对心绞痛患者血浆内皮素和血小板α-颗粒膜蛋白的影响

血塞通软胶囊是从中药三七中提取的有效成分——三七总皂苷，具有扩张微小血管、抑制血小板聚集等功能，已证明对缺血性心脑血管患者有较好疗效。本次研究的目的是在西药治疗的同时应用血塞通软胶囊对心绞痛患者的临床疗效及血浆内皮素（ET）和血小板α-颗粒膜蛋白（GMP-140）水平的影响。     

低分子肝素在急性冠脉综合征的应用

急性冠脉综合征(ACS)是心血管疾病的急危重症,包括不稳定型心绞痛(UAP)、非Q波性心肌梗死(NQMI)和Q波性心肌梗死(QMI)。动脉粥样硬化斑块破裂是急性冠脉综合征的主要病理生理机制,斑块破裂后内皮组织暴露于血液,持续性刺激、诱发血小板聚集,凝血酶活化,纤维蛋白原转化为纤维蛋白,活化