食鱼对年轻人主动脉壁的影响和动脉粥样硬化早期病变的研究

用国家“七五”课题方法，对５１例渔区（舟山、宁波）意外死亡年轻人（１５～３９岁）尸检主动脉动脉粥样硬化（ＡＳ）早期病变进行了研究。数据经统计学处理，并与国家“七五”课题资料结果相比较。显示：渔区人主动脉内膜嗜苏丹病变（ＳＬ）面积百分比明显小于南宁，更小于北京；胸主动脉壁蛋白聚糖（ＰＧ）总量渔区低于南宁（Ｐ＜０．０１），硫酸乙酰肝素－蛋白聚糖（ＨＳ－ＰＧ）相对百分含量略高于南宁（Ｐ＞０．０５），亦高于北京（Ｐ＜０．０５）；主动脉内膜平滑肌细胞核数密度渔区大于南宁（Ｐ＜０．０５），面密度小于北京（Ｐ＜０．０５），中膜平滑肌细胞核面密度明显小于南宁及北京（Ｐ＜０．０１）；渔区主动脉ＡＳ病变检出率：Ⅰ、Ⅱ级病变与南宁、北京无差异，Ⅲ、Ⅳ、Ⅴ级病变均明显轻于南宁和北京（Ｐ＜０．０１）。结果提示：多食海鱼的生活习惯是导致鱼区人ＡＳ群的病变程度轻的重要因素之一。     

牛主动脉蛋白聚糖对培养的人主动脉平滑肌细胞生长的影响

为探讨蛋白聚糖在动脉粥样硬化发生发展中的作用,观察牛主动脉硫酸肝素蛋白聚糖、硫酸软骨素蛋白聚糖、硫酸皮肤－硫酸软骨素蛋白聚糖和三种蛋白聚糖的混合物对培养的人主动脉平滑肌细胞增殖的影响。用细胞计数计算硫酸肝素蛋白聚糖（１．５￣７．０ｍｇ／Ｌ）对培养的人主动脉平滑肌细胞增殖的抑制率分别为０．５５％和７６％;硫酸软骨素蛋白聚糖（１５．０￣６０．０ｍｇ／Ｌ）的抑制率分别为２３％、３４％和６５％;硫酸皮肤素     

动脉粥样硬化高低发区年轻人冠状动脉硫酸软骨素蛋白聚糖的比较研究

选取动脉粥样硬化高发区（北京）１９例、低发区（宁波）１３例年轻人冠状动脉，行硫酸软骨素蛋白聚糖免疫组织化学染色，应用图象分析系统对切片中硫酸软骨素蛋白聚糖行定量分析及比较。１例心脏标本的冠状动脉行硫酸软骨素蛋白聚糖免疫电镜染色。观察分析结果为：①硫酸软骨素蛋白聚糖阳性物质是丝网状分布于细胞外间质中，内膜中硫酸软骨素蛋白聚糖含量高于中膜；②胶体金颗粒多分布于细胞外间质的疏松区，少量贴附于胶原纤维上；③北京地区年轻人冠状动脉内硫酸软骨素蛋白聚糖含量高于宁波地区。提示硫酸软骨素蛋白聚糖在冠状动脉内含量差异可能与高、低发区冠状动脉粥样硬化发病率不同有关。     

动脉粥样硬化高低发区年轻人冠状动脉硫酸软骨素蛋白聚糖的比较研究

选取动脉粥样硬化高发区（北京）１９例、低发区（宁波）１３例年轻人冠状动脉，行硫酸软骨素蛋白聚糖免疫组织化学染色，应用图象分析系统对切片中硫酸软骨素蛋白聚糖行定量分析及比较。１例心脏标本的冠状动脉行硫酸骨素蛋白电镜染色。观察分析结果为：①硫酸骨素蛋白聚糖阳性物质呈丝网状分布于细胞外间质中，内膜中硫酸软骨素蛋白聚糖含量高于中膜；②胶体金颗粒多分布于细胞外间质的疏松区，少量贴附于胶原纤维上；③北京地区年     

牛主动脉蛋白聚糖对培养的人脐静脉内皮细胞生长的影响

为观察牛主动脉中蛋白聚糖对培养的人脐静脉内皮细胞生长的影响及其在动脉粥样硬化形成中的作用，用解聚提取，离子交换及凝胶过滤柱层析法从牛主动脉内，中膜分离出硫酸乙酰肝素蛋白聚糖、硫酸软骨素蛋白聚糖和硫酸皮肤素－硫酸软骨素蛋白聚糖。     

瓜蒌薤白半夏汤对兔动脉粥样硬化模型主动脉蛋白聚糖的作用

目的从调整动脉壁蛋白聚糖代谢角度观察化痰治法代表方剂——瓜蒌薤白半夏汤抗动脉粥样硬化的药理机制。方法3月龄新西兰兔30只,随机分为正常组、模型组、治疗组。模型组和治疗组均给予高脂饮食造成动脉粥样硬化模型,治疗组同时给予瓜蒌薤白半夏汤灌胃。6周后取材,检测血脂,观察主动脉粥样硬化病变程度,提取主动脉蛋白聚糖,酶解为糖胺多糖,再进行醋酸纤维素薄膜电泳分析,测定各种糖胺多糖组份含量。结果正常组血胆固醇和低密度脂蛋白含量分别为13.43±3.12mmol/L、8.53±1.37mmol/L,动脉壁蛋白聚糖组份硫酸软骨素、硫酸皮肤素含量分别为21.93±1.82mg/g、15.56±1.61mg/g;与正常组比较,模型组表现为典型的动脉粥样硬化病理变化,血总胆固醇和低密度脂蛋白含量明显升高,分别为23.63±4.31mmol/L、15.63±1.27mmol/L(P<0.01),动脉壁蛋白聚糖组份硫酸软骨素、硫酸皮肤素含量明显升高,分别为31.23±1.41mg/g、19.36±1.64mg/g(P<0.01或P<0.05);与模型组比较,治疗组动脉粥样硬化灶病变程度明显减轻,动脉壁蛋白聚糖组份硫酸软骨素、硫酸皮肤素含量明显降低,分别为22.33±1.58mg/g、14.36±1.71mg/g(P<0.01或P<0.05),但血胆固醇和低密度脂蛋白无明显的降低,分别为20.54±3.59mmol/L、14.53±1.32mmol/L。结论瓜蒌薤白半夏汤可降低粥样硬化病变动脉壁硫酸软骨素蛋白聚糖、硫酸皮肤素蛋白聚糖含量,从而减轻动脉粥样硬化病变,但降低血脂作用不明显。     

硫酸乙酰肝素蛋白聚糖及肝素对巨噬细胞脂质蓄积的抑制作用

用苏丹Ⅳ染色观察巨噬细胞内脂质聚积的变化；通过酶－荧光法检测巨噬细胞内胆固醇含量并检测125Ⅰ标记氧化型低密度脂蛋白降解量来反映巨噬细胞清道夫受体的活性，以探讨硫酸乙酸肝素蛋白聚糖及肝素对巨噬细胞脂质蓄积的影响及机制。结果发现，氧化型低密度脂蛋白（100mg／L）组巨噬细胞的胞浆内可见较多苏丹Ⅳ着色红染颗粒，氧化型低密度脂蛋白（100mg／L）十硫酸乙酰肝素蛋白聚糖（15．5mg／L）组0及氧化型低密度脂蛋白（100mg／L）十肝素（200mg／L）组巨噬细胞内红色颗粒明显少于氧化型低密度脂蛋白组；氧化型低密度脂蛋白十硫酸乙酰肝素蛋白聚糖组及氧化型低密度脂蛋白十肝素组巨噬细胞内总胆固醇和胆固醇酯的含量明显低于氧化型低密度脂蛋白组（P＜0．05，P＜0．01）；硫酸乙酰肝素蛋白聚糖组及肝素组125Ⅰ标记的氧化型低密度脂蛋白降解量均低于对照组。结果提示，硫酸乙酰肝素蛋白聚糖和肝素可能是通过下调清道夫受体活性减少了巨噬细胞对氧化型低密度脂蛋白的摄取而抑制脂质在巨噬细胞内的聚集和泡沫细胞的形成。     

年龄及地区因素对年轻人动脉壁的影响及其和动脉粥样硬化早期病变发生发展的关系

本研究在动脉粥样硬化（ＡＳ）和冠心病（ＣＨＤ）高发区（北京）、低发区（南宁），于１９８６年～１９８９年间，共收集了意外死亡年轻人（１５～３９岁）新鲜尸检标本３２４例。用形态测量和生化分析的方法研究了两地同龄年轻人主动脉内膜脂质浸润、内膜厚度、平滑肌细胞（ＳＭＣ）和基质中蛋白聚糖（ＰＧｓ）的变化以及地区差异，以探索其与ＡＳ发生发展的关系，为ＡＳ的防治提供依据。主要结果：主动脉内膜ＳＭＣ核的密度尤其面积密度均是北高于南（Ｐ＜０．０１）。ＳＭＣ核密度与同组切片阿新蓝染色阳性物质量呈负相关；同组标本的生化分析ＰＧｓ总量和有抑制ＳＭＣ增殖的ＨＳ－ＰＧ含量均北低于南（Ｐ＜０．０１）；主动脉内膜脂质浸润的嗜苏丹病变（ＳＬ），除男性腹主动脉ＳＬ面积百分比北高于南（Ｐ＜０．０１）外，两地接近。上述结果提示有抑制ＳＭＣ增殖的ＨＳ－ＰＧ含量降低可能为北京主动脉内膜ＳＭＣ增殖的原因之一，还提示随南宁地区近年来人群血情胆固醇水平上升，在主动脉内膜ＳＬ已有所反映，这一变化趋势从预防ＡＳ或ＣＨＤ角度应引起注意。     

人主动脉硫酸乙酰肝素蛋白聚糖对培养的胎儿主动脉平滑肌细胞c－fos基因mRNA表达的影响

人主动脉硫酸乙酰肝素蛋白聚糖对培养的胎儿主动脉平滑肌细胞ｃ－ｆｏｓ基因ｍＲＮＡ表达的影响刘俊明，丛祥凤，张春玲，张英珊（中国医学科学院心血管病研究所，阜外医院，北京１０００３７）人主动脉壁中的蛋白聚糖与动脉粥样硬化斑块的形成密切相关，而平滑肌细胞（Ｓ...     

蛋白聚糖与糖尿病微血管病变

蛋白聚糖在糖尿病微现变的发生发展过程中起重要的作用，大量研究表明其在糖尿病微血管病变时出现质和量的变化。糖尿病肾病和糖尿病视网膜病变时硫酸软骨素，透明质酸，硫酸皮肤等多种蛋白聚糖在纤维化细胞外基质组织局部表达明显升高，而硫酸类肝素蛋白聚糖无明显变化或表达下降，在糖尿病视网膜病变时表达明显下降。此外，由于硫酸软骨素蛋白聚糖中小分子核心蛋白聚糖decorin能结合并中和转化生长因子β1的活性，为糖尿病肾病的治疗提供一种可能的方法。     

急性前壁心肌梗死伴不同下壁导联ST段改变的临床特点

目的探讨ST段抬高急性前壁心肌梗死(简称心梗)伴不同下壁导联ST段改变患者的梗死相关血管以及梗死面积及心功能情况。方法73例急性前壁心梗患者,根据入院时心电图下壁导联ST段改变情况将患者分为3组:A组为Ⅱ、Ⅲ、aVF中至少两个导联ST段抬高;B组为Ⅱ、Ⅲ、aVF中至少两个导联ST段压低,C组为Ⅱ、Ⅲ、aVF中少于两个导联ST段有改变。比较三组CK最大值,左室射血分数以及梗死相关血管(IRCA)。结果CK最大值3组比较A组最低(1280±531IU/Lvs2034±911,1677±630IU/L,P<0.01);左室射血分数A组最高(0.54±0.09vs0.48±0.07,0.47±0.08,P<0.01);三组IRCAA组中85.7%的患者位于“绕过心尖的左前降支(LAD)”的中远段,有14.3%的患者位于右冠状动脉(RCA)的近段;B组的患者中全部为非“绕过心尖的LAD”,其中有70.4%的患者位于非“绕过心尖的LAD”的近段;C组中有96.7%的患者为非“绕过心尖的LAD”,其中有73.3%的患者位于非“绕过心尖的LAD”的近中段,三组比较差异有显著性(P<0.01)。结论IRCA为LAD的急性前壁心梗时下壁ST段改变可能与LAD长度和病变部位有关;前壁合并下壁ST段同时抬高的患者若IRCA为“绕过心尖的LAD”,其梗死面积较小,心功能较好。     

Change in glycated haemoglobin levels after initiating second‐line therapy in type 2 diabetes: a primary care database study

The aim of the present study was to compare the absolute reduction in glycated haemoglobin (HbA1c) levels at 6 months after initiating second‐line glucose‐lowering therapy in patients with type 2 diabetes treated with metformin monotherapy in general practices. A total of 7009 patients were identified (Disease Analyser Germany: January 2004 to December 2014). The patients' mean ± standard deviation (s.d.) age was 63 ± 11 years, 55.5% were male and their mean ± s.d. HbA1c level was 8.0 ± 1.6%. The initiated second‐line therapies included: dipeptidyl peptidase‐4 (DPP‐4) inhibitors (38.7%); sulphonylureas (36.3%); insulin (13.3%); glucagon‐like peptide‐1 receptor agonists (GLP‐1RAs; 2.5%); thiazolidinediones (5%); and other agents (glinides, aldose‐reductase inhibitors; 4.1%). The mean absolute HbA1c change from baseline was ?0.9% (DPP‐4 inhibitors, ?0.9%; sulphonylureas, ?0.9%; insulin, ?1.1%; GLP‐1RAs, ?0.7%; thiazolidinediones, ?0.9%; and other, ?0.7%; all p < 0.001). Overall, 58% of patients reached the HbA1c target of <7% (DPP‐4 inhibitors, 61.7%; sulphonylureas, 56.7%; insulin, 45.6%; GLP‐1RAs, 62.2%; thiazolidinediones, 69.7%; and other, 57.5%). Compared with sulphonlyureas, DPP‐4 inhibitors, GLP‐1RAs and thiazolidinediones were associated with an increased odds of reaching HbA1c <7% [odds ratio (OR) 1.24, 95% confidence interval (CI) 1.09–1.40; OR 1.43, 95% CI 1.01–2.04; and OR 1.70, 95% CI 1.30–2.23, respectively], whereas insulin was related to a lower odds (0.66, 95% CI 0.55–0.78). In conclusion, in patients with type 2 diabetes very similar reductions in HbA1c after 6 months of second‐line therapy were achieved regardless of the type of therapy.     

Hemodynamic Effects of the Nitric Oxide Donor DETA/NO in Mice

(Z)‐1‐[N‐(2‐aminoethyl)‐N‐(2‐ammonioethyl)amino]diazen‐1‐ium‐1,2‐diolate (DETA/NO) is a recently synthesized member of NO‐releasing, polyamine zwitterions, the so‐called NONOates, that spontaneously liberate NO in aqueous solutions. The aim of this study was to determine the hemodynamic effects of DETA/NO in normotensive and hypertensive mice. Male Swiss Outbred mice were implanted with TA11PA‐C20 blood pressure devices (Data Sciences International, USA). After recovery (7–10 days), blood pressure was monitored for 10 days while mice were receiving saline (0.1 ml/20 g/day, s.c.). Mice were then treated every four hours for 1 day with either DETA/NO 60 mg/kg i.p. or the inactive metabolite, diethylenetriamine 38 mg/kg (molar equivalent) i.p. After a 2 week wash‐out period, mice were treated with adrenocorticotrophic hormone (ACTH: 500 µg/kg/day, s.c.) for 10 days and re‐challenged with DETA/NO or diethylenetriamine. Results were expressed as mean ± SEM. After 10 days of saline treatment, baseline systolic and diastolic blood pressure (BP) were similar for animals subsequently receiving DETA/NO or the amine (123 ± 1/95 ± 3 and 124 ± 1/92 ± 0.2 mmHg) respectively. DETA/NO induced a profound fall in BP [Systolic: 74 ± 4 mmHg (? 40 ± 3%); Diastolic: 46 ± 4 mmHg (? 52 ± 4%)] and an increase in heart rate [729 ± 33 bpm (32 ± 2%)] within the first 80 minutes. Diethylenetriamine had no effect. ACTH treatment increased BP in both groups (137 ± 16/108 ± 12 and 161 ± 1/142 ± 1 mmHg) respectively. DETA/NO induced a profound fall in blood pressure [Systolic: 92 ± 11 mmHg (? 32 ± 7%); Diastolic: 68 ± 10 mmHg (? 35 ± 10%)] and an increase in heart rate [613 ± 36 bpm (18 ± 6%)] within the first 80 minutes. Again diethylenetriamine had no significant effect. There was no significant effect on body weight with any treatment. Thus DETA/NO has potent blood pressure lowering effects in both normotensive and hypertensive mice.     

Clinical Value of the Tissue Doppler S Wave to Characterize Left Ventricular Hypertrophy as Defined by Echocardiography

Left ventricular hypertrophy (LVH) may be a physiological finding and may also be associated with different disease entities and hence, with different outcomes. Regional myocardial function can be assessed with color Doppler tissue imaging, specifically by the waveform of the isovolumic contraction (IC) period and the regional systolic wave (“s”). Methods and Results: We studied five groups (G): healthy, sedentary young volunteers (G1, n:10); healthy sedentary adult volunteers (G2, n:8); and subjects with LVH (left ventricular mass index >125 g/m²) including: high performance athletes (G3, n:21), subjects with hypertension (G4, n:21), subjects with hypertrophic cardiomyopathy (HCM) (G5, n:18). We measured peak “s” wave velocity (cm/sec) at the basal and mid septum, the IC/s ratio, and basal to mid‐septal velocity difference (BMVD) of the “s” wave. Regional “s” wave values (cm/sec) were G1 = 5.6 ± 1; G2 = 5.4 ± 0.8; G3 = 5.7 ± 0.6; G4 = 5.3 ± 1.1; G5 = 4.2 ± 1.1 (P < 0.0001). The IC/s ratio was G1 = 0.28 ± 0.18; G2 = 0.39 ± 0.21; G3 = 0.23 ± 0.10; G4 = 0.42 ± 0.15; G5 = 0.64 ± 0.15 (P < 0.0001). The BMVD (cm/sec) was G1 = 2 ± 0.51; G2 = 1.71 ± 0.29; G3 = 1.78 ± 0.44; G4 = 1.26 ± 0.96; G5 = 0.45 ± 0.4 (P < 0.0001). IC/s < 0.38 discriminated physiological from pathological forms of hypertrophy (sensitivity 90%; specificity 88%). Peak “s” wave velocity discriminated HCM from other causes of hypertrophy, with a cutoff value of 4.46 cm/sec (sensitivity 72%; specificity 90%). BMVD <0.98 cm/sec detected HCM with 89% sensitivity and 86% specificity. Conclusions: Peak “s” wave velocity and two indices: IC/s and BMDV are novel parameters that may allow to discriminate physiological from pathological forms of hypertrophy as well as different subtypes of hypertrophy. (ECHOCARDIOGRAPHY 2010;27:370‐377)     

Comparison between a basal-bolus and a premixed insulin regimen in individuals with type 2 diabetes–results of the GINGER study

Aim: To compare the efficacy and safety of an intensified insulin regimen, using insulin glargine (glargine) once daily and pre‐meal insulin glulisine (glulisine) (basal‐bolus), with a conventional therapy, using premixed insulin (premix) twice daily. Methods: This 52‐week, open‐label, randomized, multinational, multicentre trial included 310 subjects with type 2 diabetes (T2D) on premix, with or without metformin, who were randomized to a basal‐bolus regimen with glargine and glulisine (n = 153; mean ± s.d. age 60.2 ± 7.5 years; HbA1c 8.6 ± 0.8%; weight 87.0 ± 15.1 kg; T2D duration 12.8 ± 5.8 years) or twice‐daily premix (n = 157; age 60.9 ± 7.8 years; HbA1c 8.5 ± 0.9%; weight 84.3 ± 15.0 kg; T2D duration 12.5 ± 6.8 years). The primary endpoint was change in HbA1c from baseline to endpoint. Results: Mean decrease in baseline‐to‐endpoint HbA1c for basal‐bolus vs. premix was ?1.31 vs. ?0.80% (difference: ?0.476%; 95% Cl: ?0.714, ?0.238; p = 0.0001, ancova ). More subjects reached HbA1c ≤ 7.0% in the basal‐bolus group than in the premix group [68 (46.6%) vs. 43 (27.9%); p = 0.0004], while they also experienced significantly lower mean ± s.d. daytime (?2.7 ± 2.3 vs. ?2.3 ± 2.5 mmol/l; p = 0.0033) and postprandial (?3.1 ± 2.6 vs. ?2.5 ± 2.8 mmol/l; p < 0.0001) blood glucose. Endpoint daily insulin doses were 98.0 ± 48.7 vs. 91.3 ± 44.3 IU (p = 0.2104); mean weight gain was +3.6 ± 4.0 vs. +2.2 ± 4.5 kg (p = 0.0073). Mean number of overall hypoglycaemic events with basal‐bolus and premix was 13.99 and 18.54 events/patient year, respectively (difference: ?3.90; 95% CI: ?10.40, 2.60; p = 0.2385). Conclusions: An intensified basal‐bolus regimen using glargine/glulisine results in a significantly superior glycaemic control vs. premix therapy in a population with long‐standing insulin‐treated T2D, with no increase in the rates of hypoglycaemia.     

Hemodynamic effects of creatine phosphate in patients with congestive heart failure: A double-blind comparison trial versus placebo

Background: The use of metabolic drugs effective in addition to conventional therapy represents a significant challenge in patients with left ventricular dysfunction. Hypothesis: The aim of this double-blind, placebo-controlled study was to investigate the hemodynamic effects of acute intravenous (IV) administration of creatine phosphate (CP) and of short-term treatment in patients with congestive heart failure (CHF) from ischemic heart disease (IHD) or dilated cardiomyopathy in addition to conventional therapy. Methods: We compared the hemodynamic effects of exogenous creatine phosphate (CP) and placebo in a double-blind, crossover design study in 13 hospitalized patients (12 men, 1 woman, mean age 52 ± 8 years) with CHF. All patients were in New York Heart Association (NYHA) class II-III and received conventional pharmacologic therapy for CHF this was not changed during the study period. The study design consisted of two treatment periods (CP or placebo and placebo or CP, respectively) of 4 days each, separated by a 2-day washout interval. The intravenous infusion consisted of 6 g CP or placebo (acute treatment) or 6 g CP or placebo daily for 4 days (short-term treatment) diluted in 50 ml of NaCl 0.9%;infusion duration was about 10 min. Mono-bidimensional echocardiographic examination (Hewlett Packard So-nos 1000, with a 2.5 MHz transducer) was performed at baseline, after acute infusion, and 12 h after the end of short-term treatment. Data were analyzed by ANOVA and Student's t-test for paired data the results obtained after acute and short-term therapy were compared with the baseline values. Results: After placebo therapy, no significant change was observed. The results after treatment with CP showed a significant reduction of end-systolic diameter [baseline: 4.5 ± 0.6;acute: 4.2 ± 0.5, (p<0.001);short-term 4.3 ± 0.6 cm, (p<0.05)] and systemic vascular resistance (baseline: 1064.9 ± 483.7;acute: 947.5 ± 390.2 (p<0.05);short-term: 950.7 ± 394.3 dynescm^-5 (p<0.05);moreover, a significant increase of percent ejection fraction [baseline:48 ± 12%;acute 53 ± 12% (p<0.01);short-term 52 ± 11 % (p<0.01)], and of percent fractional shortening [baseline: 25 ± 7;acute 28 ± 8 (p<0.05);short-term 28 ± 7% (p<0.05)] was observed. Conclusion: CP was shown to improve cardiac function, even in the presence of a conventional CHF pharmacologic therapy.     

Localization of atherosclerotic lesions in the human basilar artery

The topography of atherosclerotic lesions in the human basilar arteries has been studied quantitatively by digitizing images of the excised vessels and producing contour probability maps. Fifteen basilar arteries were obtained at autopsy (age--61 +/- 2; males--6, females--9; black--6, white--9), fixed in formalin, opened along the ventral aspect and stained grossly with Sudan IV to delineate fat-containing lesions. Photographs of the flattened arteries were analyzed and the presence or absence of sudanophilic lesions was determined at approximately 1000 identical sites on all vessels. The probability of finding a lesion at each site was determined and a contour probability map was constructed. Fifty-two percent of the area of the mean contour map was involved with lesions. The extent of the sudanophilic lesions decreased as one proceeded distally from the origin of the basilar artery at the confluence of the vertebral branches (i.e. proximal 1/3--56%; middle 1/3--49%; distal 1/3--43%; P less than 0.04). Significantly more sudanophilic material was observed on the ventral (outer curvature) as opposed to the dorsal (inner curvature) surfaces (55%, 43% respectively; P less than 0.03). These data suggest that hemodynamic forces associated with confluent flow and curvature may be important in the localization of sudanophilic lesions in the proximal and ventral aspects of the human basilar artery.     

Detection of diastolic left ventricular function abnormalities in patients with coronary artery disease and normal systolic function

We angiographically calculated left ventricular (LV) filling in 50 patients, all of whom had normal systolic LV function and 21 (42%) of whom had coronary artery disease. Five volume determinations were made: at end systole (ESV), first third (DV 1/3, half (DV 1/2), and second third of diastole (DV 2/3), and at the end of diastole (EDV). To assess different modalities of filling, we calculated filling fractions in the first third (FF 1/3) as the ratio of volume filled in the first third diastole (DV 1/3-ESV) over total diastolic filling (EDV-ESV). Similar filling fractions (FF) were calculated at half (FF 1 /2), second third (FF 2/3), and last third (FF 3/3) of diastole. We found significant differences between normal and coronary artery disease patients as follows: FF 1/3: 37.4± 14.9 versus 23.8±11.9%, respectively (p<0.002); FF 1/2: 58.6±14.7 versus 45.3±15.1% (p<0.005); FF 2/3: 33.8±15.2 versus 39.0±10.4% (NS), and differences in the opposite direction in the FF 3/3: 28.8± 15.2 versus 37.2±11.9% (p<0.02), respectively. We conclude that LV filling is accomplished differently in patients with coronary artery disease even if they have normal systolic function.     

Intravascular Stents in Congenital Heart Disease: Short- and Long-Term Results From a Large Single-Center Experience

Objectives. This report describes the results of the Food and Drug Administration’s phase 1 and 2 clinical trials of intravascular stents at Texas Children’s Hospital.Background. Since the late 1980s, intravascular stent implantation for the treatment of arterial and venous stenoses in congenital heart disease has been highly successful.Methods. Stents were placed in postoperative pulmonary artery (PA) stenoses, congenital PA stenoses or stenoses of systemic veins/venous anastomoses. Prospective collection of data according to protocol was done before intervention, after stent implantation and at follow-up catheterization.Results. At stent implantation, pressure gradients decreased significantly in all three groups (mean ± SD): from 46 ± 25 to 10 ± 13 mm Hg in postoperative PA stenoses (p < 0.001); from 71 ± 45 to 15 ± 21 mm Hg in congenital PA stenoses (p < 0.001); and from 7 ± 6 to 1 ± 2 mm Hg in stenoses of systemic veins/venous anastomoses stenoses (p < 0.001). Vessel diameters markedly increased: from 6 ± 3 to 12 ± 3 mm in postoperative PA stenoses (p < 0.001); from 3 ± 1 to 9 ± 1 mm in congenital PA stenoses (p < 0.001); and from 3 ± 4 to 12 ± 4 mm in stenoses of systemic veins/venous anastomoses (p < 0.001). In the postoperative and congenital PA stenoses groups, right ventricular pressure decreased (right ventricular pressure indexed to femoral artery pressure ratio): from 0.63 ± 0.2 to 0.41 ± 0.02 (p < 0.001) and from 0.71 ± 0.3 to 0.55 ± 0.35 (p = 0.04), respectively. Perfusion to a single affected lung increased from 31 ± 17% to 46 ± 14% (p < 0.001). On recatheterization (mean 14 months), results varied minimally. Repeat angioplasty of residual stent stenoses was safe and effective. Complications included four early patients with stent migration, three with stent thrombosis and two deaths. There were no late complications. Significant restenosis occurred in only three patients.Conclusions. Intravascular stents for the treatment of vascular stenoses in congenital heart disease provide excellent immediate and long-term results.     

Renal Protective Effects of Efonidipine in Partially Nephrectomized Spontaneously Hypertensive Rats

We investigated the effects of a calcium antagonist, efonidipine, which was reported to dilate not only afferent arterioles but also efferent arterioles, on progression of renal failure in salt-loaded partially nephrectomized spontaneously hypertensive rats (SHR). Forty-four SHR's with 5 of 6 nephrectomy were divided into four groups: group 1 as control (n=20); group 2, efonidipine-treated (n=8); group 3, enalapril-treated (n=8); and group 4, nifedipine-treated (n=8). The rats were given these drugs and a high-salt diet (5% NaCl) for 8 weeks. During the experiment, systolic blood pressure (SBP) and daily urinary protein excretion were measured eveiy 2 weeks. At the end of the study. seniin creatinine was deteimined, and renal tissues were obtained for light microscopic examination. SBI was markedly reduced by 8-week antihypertensive treatment. (control, 267±7 mmHg: efonidipine, 181 ± 7 mmHg; enalapril, 200±12 mmHg; nifedipine, 184±6 mmHg). Glomerular sclerosis developed markedly in the control group, but was partially prevented in all treated groups. Similarly, urinary protein excretion (UPE) was suppressed by efonidipine (180±16 mg/day) and enalapril (180±16 mg/day vs. 301±28 mg/day for control). In contrast, nifedipine failed to prevent the increase in urinaiy protein excretion (258±22 mg/day). In conclusion, efonidipine attenuates SBP increase and ameliorates glomerular injuty as well as nifedipine and enalapril. Furthermore, beneficial effects of efonidipine, but not nifedipine, on proteinuria suggest that different mechanisms mediate the improvement of proteinuria; one possible mechanism could be efferent arteriolar dilation, not reported in nifedipine.