复方鹿角合剂对不能耐受ACEI的心肾阳虚心衰患者的心肾保护作用及初步机制研究

目的 观察复方鹿角合剂对不能耐受血管紧张素转化酶抑制剂(ACEI)心肾阳虚型慢性心衰(CHF)患者的心肾保护作用及可能机制.方法 150例在我院确诊为CHF且不能耐受ACEI的心肾阳虚患者,随机分为对照组(标准化治疗,n=78))和治疗组(复方鹿角合剂+标准化治疗,n=72),随访治疗3个月.观察治疗前后患者中医症候疗效、心功能分级、左室射血分数(LVEF)、血脑利钠肽(BNP)、血肌酐(SCr)、内生肌酐清除率(CCr)、血浆肾素、血管紧张素Ⅱ和醛固酮水平等.结果 经过3个月的治疗,治疗组在改善中医症候方面优于对照组(83.33％对76.92％,P＜0.05).相对于对照组,治疗组不仅心功能分级有效改善(83.33％对70.51％,P＜0.05),且BNP[ (423.12±431.09)对(501.13±558.77)pg/mL,P＜0.05]、Scr[(102.40±101.12)对(128.17±108.23) μmol/L,P＜0.05]和血浆血管紧张素Ⅱ [(98.88±144.12)对(129.54±176.15) pg/mL,P＜0.05]降低;LVEF[ (46.45±3.20)对(44.56±2.87),P＜0.05]和Ccr[(62.04±42.12)对(52.65±31.28) mL/(min·1.73m2),P＜0.05]升高.结论 复方鹿角合剂能有效改善不能耐受ACEI的心肾阳虚心衰患者的心肾功能,机制可能与其降低血管紧张素 Ⅱ水平的作用有关.     

舒张性心力衰竭临床诊治分析

目的探讨舒张性心力衰竭（DHF）的临床特点及诊治情况。方法回顾性分析我院2006年5月至2009年12月住院治疗的66例DHF患者的临床资料。在积极治疗原发病的基础上,以缓解心力衰竭症状为主,同时针对心力衰竭演变过程中的潜在机制采取治疗措施。结果本组66例DHF患者经积极治疗后,症状完全消失、心功能I级以上56例（84.84%）;心功能I或Ⅱ级8例（12.12%）;有效64例（96.97%）。2例（3.03%）临床症状改善不明显自动出院,无死亡病例。结论本组存在心力衰竭的症状和体征,心脏超声示DHF;DHF的治疗在针对基础疾病采取对症治疗措施基础上,以β受体阻滞剂、血管紧张素转换酶抑制（ACEI）、血管紧张素Ⅱ受体阻滞剂（ARB）以及为主。     

顽固性高血压的降压药物治疗分析

目的观察不同配伍组合的降压药物在治疗顽固性高血压方面的疗效。方法选取常德第一中医院200例顽固性高血压患者随机分为A、B、C3组,分别予以不同的治疗方案治疗。治疗8周后采取自身对照比较治疗前后血压指标,评估其临床疗效。结果 3组患者血压均得到较好控制。结论小剂量联合使用降压药物可有效降压,临床治疗高血压患者效果满意。     

来氟米特、ACEI联合治疗IgAN的临床前瞻性对照研究

目的探讨来氟米特、ACEI联合治疗IgAN的疗效和安全性。方法选择肾活检确诊为IgAN的病例40例,根据随机配对法,分设治疗组、对照组,每组各20例。观察来氟米特、ACEI联合疗法降低蛋白尿的临床疗效、副反应,并与激素联合ACEI疗法进行比较;观察来氟米特、ACEI联合疗法对肾功能的影响,并比较本疗法与激素联合ACEI疗法两组间肾功能的差异;治疗1年后重复肾活检,观察本疗法对改善病理病变的程度或阻止肾小球硬化及小管间质病变的疗效。结果治疗组和对照组均能降低蛋白尿、减少尿红细胞、升高血浆白蛋白及改善肾功能,两组治疗前后的差异具有统计学意义（P〈0.05）,同时治疗组较对照组在改善尿蛋白及升高血浆白蛋白疗效有显著性差异（P〈0.05）,尤其治疗组较对照组在改善远期肾功能方面的疗效有非常显著性差异（P〈0.01）。两组治疗前后病理病变程度均有所减轻,差异有统计学意义（P〈0.05）。治疗组较对照组治疗后病理病变的减轻程度的差异有统计学意义（P〈0.05）。结论来氟米特、ACEI联合治疗IgAN能够降低蛋白尿和减少尿红细胞,抑制肾小球系膜增生、细胞外基质产生,同时能够防止肾小球硬化的发生或发展,能够改善IgAN的远期肾功能。     

肾素血管紧张素系统与造血调控研究进展

肾素-血管紧张素系统(RAS)的主要生物学作用体现在对血压和水、电解质的调 控上。近年来的研究表明,RAS参与造血调控,其主要活性物质血管紧张素Ⅱ(AngⅡ)促进红系造 血,而其受体拮抗剂(ARB)和血管紧张素转换酶抑制剂(ACEI)抑制红系造血。     

强肾固精方联合ACEI类药物治疗肾性高血压和肾性贫血的临床研究

目的:验证强肾固精方联合ACEI类药物降低慢性肾炎患者的血压和提高血红蛋白含量总的临床效果。方法:选取2014年2月至2014年6月在唐山市中医医院住院及门诊的慢性肾小球肾炎患者160例,随机分为观察组(强肾固精方联合贝那普利组)和对照组(贝那普利组),每组80例。观察2组患者治疗前和治疗后血压和血红蛋白的数值,分析改善情况。结果:观察组在降低血压和提高血红蛋白的方面明显优于对照组,差异有统计学意义(P0.05)。结论:强肾固精方联合ACEI类药物可明显降低血压和提高血红蛋白含量,对慢性肾炎有良好的疗效。     

Sleep duration on workdays or nonworkdays and cardiac–cerebral vascular diseases in Southern China

ObjectivesThis study aimed to assess the relationship between sleep duration on work or nonworkdays and myocardial infarction (MI) and stroke in Southern China.MethodsA cross-sectional survey was conducted among 15,364 participants of age ≥15 years in Southern China from November 2013 to August 2014. Data on self-reported duration of sleep on workdays or nonworkdays as well as history of MI and stroke were collected in the questionnaire. The subjects were examined for weight, height, waist circumference, and blood pressure. Multivariate logistic regression analyses were performed to evaluate the association of sleep duration with MI and stroke.ResultOverall, compared with a sleep duration of 6–8 h, individuals who slept <6 h on workdays and nonworkdays were associated with increased risk for MI (odds ratio [OR] = 3.17, 2.04). Furthermore, individuals who slept >8 h on workdays and nonworkdays were associated with an increased risk for stroke (OR = 1.86, 1.54). Although this association persisted in men and subjects aged <65 years, we also observed that long sleep duration on workdays was associated with MI, especially among women, and short sleep duration on nonworkdays was associated with stroke among those aged 65 years or older. Participants with abnormal sleep duration and hypertension had higher risk of MI and stroke. Sleep debt was independently associated with MI risk, but not stroke (OR = 1.40; 95% confidence interval [CI]: 1.06–1.86), specifically among men aged <65 years.ConclusionsCompared with a sleep duration of 6–8 h, both short and long sleep duration were associated with the prevalence of MI and stroke and these associations were more pronounced among hypertensive persons, and tended to vary by age and sex. Moreover, sleep debt was linked to greater MI risk among men aged <65 years. These findings suggest that we should develop a healthy biological clock.