氨氯地平阿托伐他汀钙对高血压合并血脂异常患者血管功能的影响

目的研究复方氨氯地平阿托伐他汀钙对高血压合并高脂血症患者血管功能的影响。方法入选180例高血压合并血脂异常患者,按随机双盲法分为对照组90例(氨氯地平5 mg/d)和试验组90例(复方氨氯地平阿托伐他汀钙1片/d),治疗12个月。测定治疗前后患者的血压、血糖、血脂、颈动脉内中膜厚度(IMT)、肱动脉内径及血浆内皮素1(ET-1)及一氧化氮(NO)水平。结果与氨氯地平相比,复方氨氯地平阿托伐他汀钙可延缓颈动脉IMT的进展[(-0.17±0.07)mm比(-0.11±0.05)mm,P<0.05],并提高患者NO水平[(35.0±6.5)μmol/L比(19.5±6.4)μmol/L,P<0.05]和肱动脉扩张能力(10.1%±3.1%比8.8%±3.2%,P<0.05),降低ET-1水平[(-31.8±6.5)ng/L比(-21.8±7.1)ng/L,P<0.05];但二者的降压作用差异无统计学意义[(-29±7.5/-16.5±7.5)mm Hg比(-26±9.0/-13.5±9.0)mm Hg,P>0.05]。结论复方氨氯地平阿托伐他汀钙较氨氯地平血管保护功能更强。     

冠心病患者危险因子的社区干预研究

目的研究社区综合干预在改善冠心病患者血脂水平及提高患者生命质量中的作用. 方法对156例冠心病患者随机分为两组,其中社区综合干预组86例,对照组70例.在两组原药物干预不变且无显著差异的前提下,对综合干预组进行定点、定时监测,同时进行家庭随访、社区综合干预,并与对照组进行前瞻性的对照研究.结果入组前患者收缩压(154.5±8.6) mm Hg(1 mm Hg=0.133 kPa), 舒张压(93.3±5.8) mm Hg,总胆固醇(6.38±1.25) mmol/L,甘油三酯(1.86±0.86) mmol/L,高密度脂蛋白胆固醇(1.38±0.81) mmol/L,低密度脂蛋白胆固醇(4.02±1.39) mmol/L.综合干预2年后,患者收缩压(129.5±10.3) mm Hg,舒张压(76.6±6.9) mm Hg,总胆固醇(5.27±0.98) mmol/L,甘油三酯(1.40±0.19) mmol/L, 高密度脂蛋白胆固醇(2.01±0.65) mmol/L, 低密度脂蛋白胆固醇(1.61±0.95) mmol/L, 干预前后比较, 差异有显著性(P<0.05),与对照组比较,差异有显著性(P<0.05);2年后综合干预组的并发症、致残率和病死率分别为3.49%、0、1.16%,明显低于对照组的25.71%、7.14%、5.71%,二组比较差异有显著性(P<0.001);综合干预组2年后患者的生命质量、依从性及生活满意度明显提高,且与对照组比较,差异有显著性(P<0.01).结论社区综合干预有改善冠心病患者血脂及提高生命质量的作用,应成为冠心病防治的新的医学模式.     

二甲双胍对代谢综合征患者血压的影响

目的研究二甲双胍长期使用对代谢综合征(MS)患者血压的影响.方法87例轻度高血压与空腹血糖(FPG)6.1～8.0 mmol/L或2 h血糖(2 h PG)7.8～12.0 mmol/L的MS患者随机分作2组低脂饮食组43例,予低脂饮食;二甲双胍组44例,予低脂饮食并二甲双胍0.25,3次/d,连用24周;比较2组治疗前与治疗24周的血压与胰岛素抵抗、血脂等影响血压重要指标的变化.结果与治疗前比较,二甲双胍组治疗24周的收缩压(SBP)、舒张压(DBP)与脉压(PP)显著降低(P＜0.01).与低脂饮食组比较,治疗24周后二甲双胍组在改善胰岛素抵抗、调脂的同时,收缩压(137±5比142±6)mm Hg、舒张压(88±6比92±4)mm Hg与脉压(40±9比44±8)mm Hg也显著降低(P＜0.01,P＜0.05).结论二甲双胍治疗MS具有降低血压作用.     

2型糖尿病患者颈动脉粥样硬化与血糖血脂水平的关系

目的探讨2型糖尿病患者颈动脉粥样硬化程度与血糖、血脂等因素的相关性。方法对100例2型糖尿病初诊患者和40例我院血糖正常的健康体检者(对照组)行颈动脉超声检查,测定颈动脉内-中膜厚度(IMT)平均值及粥样硬化斑块情况,同时测定患者糖化血红蛋白(HbA1c)、血脂[总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)]等项目,分析糖尿病患者颈动脉硬化情况与血糖、血脂的关系。结果 100例糖尿病患者有不同程度颈动脉粥样硬化者占75%(75例),明显高于健康对照组(25%,P<0.01)。糖尿病有斑块组IMT平均为(1.42±0.21)mm,糖尿病无斑块组IMT平均为(1.00±0.18)mm,两组比较差异有统计学意义(P<0.01)。糖尿病有斑块组患者的HbA1c、LDL-C水平明显高于和HDL-C水平明显低于无斑块组患者[HbA1c:8.1%±1.6%比6.2%±1.8%;LDL-C:(4.8±0.9)mmol/L比(4.2±0.8)mmol/L;HDL-C:(0.8±0.3)mmol/L比(1.0±0.5)mmol/L,均为P<0.05]。结论糖尿病患者颈动脉硬化的程度与血糖、血脂水平存在显著的相关性。     

塞来昔布与小剂量阿司匹林合用对动脉粥样硬化的影响

目的　观察特异性环氧合酶2抑制剂塞来昔布与小剂量阿司匹林合用对小鼠动脉粥样硬化进展的影响。方法　8周龄雄性载脂蛋白E基因敲除的C5 7BL/ 6小鼠分为阿司匹林组(n =10 )、阿司匹林+塞来昔布组(n=11)及安慰剂对照组(n =8) ,均予西方饮食喂养,分别以阿司匹林、阿司匹林+塞来昔布及安慰剂灌胃;同龄同遗传背景野生型小鼠为正常对照组(n =6 ) ,常规饲料喂养。16周龄处死,酶法分析测定血脂,冰冻切片光镜下定位主动脉根部,油红O染色评估粥样硬化病变情况。结果　两用药组及安慰剂组血脂水平均显著高于正常对照组(P<0 .0 1) ,两用药组总胆固醇水平略低于安慰剂组(30 .2±5 .5mmol/L与2 8.6±6 .2mmol/L对37.8±8.1mmol/L ,P<0 .0 5 ) ,而甘油三酯水平高于安慰剂组(3.4±0 .5mmol/L与3.0±0 .6mmol/L对2 .3±0 .7mmol/L ,P <0 .0 5 ) ,两用药组之间血脂水平无差异。主动脉根部横切面油红O染色显示,各用药组及安慰剂组见明显粥样硬化斑块形成;用药组的斑块面积及管腔狭窄度均较安慰剂组显著降低(P <0 .0 1) ,而残余管腔显著扩大(P <0 .0 1) ,且阿司匹林+塞来昔布组的斑块面积较阿司匹林组进一步减小(0 .0 4 2±0 .0 2 6mm2 对0 .0 6 8±0 .0 2 2mm2 ,P <0 .0 5 )。结论　阿司匹林可一定程度上降低载脂蛋白E基因     

运动疗法联合饮食控制对高血压、高血脂患者血压、血脂的疗效

目的:探讨运动疗法联合饮食控制对高血压、高血脂患者血压、血脂的疗效。方法:选择我院64例原发性高血压、高血脂患者,按入院顺序随机均分为:联合治疗组(运动疗法联合饮食控制进行治疗),饮食调节组(仅使用饮食调节进行干预治疗)。八个月后比较两组患者血压、血脂水平变化。结果:与治疗前比较,联合治疗组患者治疗八个月后血压明显下降,低密度脂蛋白-胆固醇(LDL-C)、总胆固醇(TC)、甘油三酯(TG)水平明显下降,高密度脂蛋白(HDL-C)水平显著升高(P0.05);治疗后,与饮食调节组比较,联合治疗组血压[(139.7±13.2)/(89.1±8.7)mmHg比(123.2±10.4)/(71.6±8.5)mmHg]、LDL-C[(4.7±0.4)mmol/L比(3.8±0.5)mmol/L]、TC[(4.9±1.2)mmol/L比(4.2±1.1)mmol/L]、TG[(2.0±0.5)mmol/L比(1.2±0.5)mmol/L]水平均明显下降,HDL-C[(1.2±0.3)mmol/L比(1.5±0.4)mmol/L]水平明显上升(P均0.05)。结论:与饮食调节比较,运动疗法联合饮食控制可显著降低高血压高血脂患者血压、血脂水平,疗效更为明显,值得临床推广。     

氟伐他汀对颈动脉内膜增厚的治疗效果

目的:观察氟伐他汀预防颈动脉内膜中层厚度(CIMT)增厚的效果。方法:选择年龄45岁以上、低冠心病危险、CIMT增厚(1.2～3.5mm)、低密度脂蛋白胆固醇(LDL-C)浓度升高的540例患者,随机均分为安慰剂对照组和氟伐他汀组。观察两组治疗前后血脂水平变化以及最大CIMT变化率、CIMT进展情况等。结果:治疗两年后,与安慰剂对照组比较,氟伐他汀组总胆固醇[(6.18±0.13)mmol/L比(5.03±0.81)mmol/L]、甘油三酯[(2.45±0.72)mmol/L比(1.97±0.56)mmol/L]、LDL-C[(4.09±1.81)mmol/L比(2.95±1.10)mmol/L]水平均明显降低(P<0.05或<0.01),高密度脂蛋白胆固醇[(1.04±0.32)mmol/L比(1.25±0.30)mmol/L]水平明显升高,P<0.05;CIMT[(0.989±0.373)mm比(0.748±0.220)mm],CIMT进展率(0.0131mm/年比0.0014mm/年)明显减小(P<0.05,P<0.001)。结论:对于具有动脉硬化证据的中老年人,氟伐他汀能够显著降低低密度脂蛋白胆固醇水平,颈动脉内膜中层厚度及其进展率。     

血脂及载脂蛋白E基因多态性与结肠腺瘤的关系

目的探讨血脂及载脂蛋白E(ApoE)基因多态性与结肠腺瘤的相关性,方法对98例结肠腺瘤患者和40例正常对照者,酶法测定血浆脂质水平,聚合酶链反应-限制性片段长度多态性(PCR-RFLP)法测定 ApoE 基因型。差异性分析采用 X~2和 t 检验。结果结肠腺瘤组、远侧结肠腺瘤组和绒毛状腺瘤组血浆胆固醇水平分别为(5.32±0.85)、(5.58±0.63)和(5.49±0.69)mmol/L,高于对照组、近侧结肠腺瘤组和非绒毛状腺瘤组的(4.28±0.62)、(4.82±0.58)和(4.76±0.58)mmol/L(P<0.05);而结肠腺瘤组血浆高密度脂蛋白胆固醇水平为(1.39±0.25)mmol/L,低于对照组的(1.51±0.29)mmol/L(P<0.05);结肠腺瘤组各基因型血脂水平差异无统计学意义;结肠腺瘤组 ApoEε3/ε4基因型频率(7.1%)低于对照组(17.5%,P<0.05)。结论血浆胆固醇水平增高者结肠腺瘤发生的危险性增加,ApoEeε/ε4基因型携带者其结肠腺瘤发生的危险性减少。     

喹那普利对高血压病患者血压和糖代谢及脂代谢的作用

血管紧张素转换酶抑制剂(ACEI)对高血压病患者的良好降压效果研究较多并已得到公认,但对糖代谢及脂代谢的作用还研究的不够。喹那普利(Quinapuil)是1种疗效更好作用广泛的新型ACEI。本文报告作者关于喹那普利对高血压病患者血压和糖代谢及脂代谢的作用进行研究的结果。对象与方法共选择40例轻中度高血压病患者为研究对象并分为两组:1组:28例,伴发肥胖症;2组:12例,不伴发肥胖症。全部患者均在门诊采用喹那普利(10～20mg/d)治疗,疗程3个月。对全部患者均在治疗前和治疗后1个月及3个月检测血压及心率,测定血糖与血脂[总胆固醇、高密度脂蛋白(HDL)胆固醇、低密度脂蛋白(LDL)胆固醇和甘油三酯]水平并对结果进行统计学处理。结果治疗前1组的血压与心率分别为198.3±7.15/113.4±2.97mmHg(26.44±0.95/15.1±0.37kPa,1kPa=7.5mmHg)与75.1±1.50次/min,2组的血压与心率分别为187.7±7.30/112.5±4.25mmHg与73.2±2.09次/min。治疗后1组1个月时的血压与心率分别为142.6±2.97/89.3±1.57mmHg与73.7±2.05次/min,3个月时的血压与心率分别为135.0±5.85/85.6±3.91mmHg与75.7±2.06次/min;2组1个月时的血压与心率分别为145.0±6.61/89.5±3.02mmHg与74.1±1.37次/min,3个月时的血压与心率分别为136.7±7.74/86.7±3.85mmHg与77.3±1.42次/min。表明治疗后1个月时的血压两组患者均比治疗前显著下降(P<0.05),3个月时的血压均基本降至正常;而治疗后1个月与3个月时的心率两组均与治疗前基本相同。上述4项血脂指标水平1组治疗后1个月与治疗前比较均无显著差异;而治疗后3个月总胆固醇、LDL胆固醇和甘油三酯均比治疗前显著下降(P<0.05),HDL胆固醇比治疗前显著增高(P<0.05)。2组上述4项血脂指标水平治疗后1个月及3个月与治疗前比较均无显著差异。血糖水平1组治疗前为4.9±0.12mmol/L、治疗后1个月及3个月分别为4.7±0.12mmol/L与4.8±0.15mmol/L;2组治疗前为4.7±0.09mmol/L;治疗后1个月及3个月分别为4.6±0.12mmol/L与4.6±0.36mmol/L。表明两组患者的血糖水平治疗后1个月及3个月均比治疗前有所下降。讨论研究结果表明,喹那普利对高血压病患者不仅有肯定而显著的降压效果,而且能改善糖代谢并对伴发肥胖症的患者有显著地改善脂代谢的作用。另外,喹那普利无明显副作用,对心率无影响。所以对高血压病患者、尤其伴发肥胖症和/或糖代谢障碍时可以应用。     

女性高血压患者绝经前后及绝经年限与血脂水平关系探讨

目的探讨女性高血压患者绝经前后及绝经年限与血脂变化的关系。方法女性高血压患者131例,分绝经前组(34例)及绝经后组(97例),测晨起空腹静脉血中甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C),进行组间比较,并分析绝经年限与血脂水平的相关性。并与73例健康对照组比较。结果绝经前高血压组TC、LDL-C〔(5.27±0.47)mmol/L和(3.50±0.45)mmol/L〕显著高于对照组〔(4.33±0.70)mmol/L和(2.67±0.50)mmol/L,均为P<0.01〕。绝经后高血压组TG、TC、LDL-C〔(1.87±1.06)mmol/L、(6.41±0.78)mmol/L和(4.61±0.87)〕均显著高于对照组〔(1.26±0.79)mmol/L、(4.63±0.54)mmol/L和(2.79±0.47)mmol/L,均为P<0.01〕,HDL-C则低于对照组〔(1.36±0.32)和(1.57±0.33)mmol/L,P<0.01〕。高血压绝经后组TG、TC、LDL-C〔(1.87±1.06)mmol/L、(6.41±0.78)mmol/L和(4.61±0.87)mmol/L〕显著高于绝经前组〔(1.35±0.99)mmol/L,P<0.05;(5.27±0.47)mmol/L,P<0.01;(3.50±0.45)mmol/L,P<0.01〕,HDL-C低于绝经前组〔(1.36±0.32)和(1.51±0.26)mmol/L,P<0.05〕。TC、LDL-C与绝经年限呈显著正相关(r分别为0.88和0.81,P<0.01)。结论女性高血压患者绝经后血TG、TC、LDL-C增高,TC、LDL-C与绝经年限呈正相关,而HDL-C降低。     

Dietary soy has both beneficial and potentially adverse cardiovascular effects: a placebo-controlled study in men and postmenopausal women.

To address the cardiovascular effects of dietary soy containing phytoestrogens, we measured blood pressure (BP), lipids, vascular function (systemic arterial compliance and pulse wave velocity), and endothelial function (flow-mediated vasodilation) in a randomized, double-blind trial. Two hundred thirteen healthy subjects (108 men and 105 postmenopausal women), 50-75 yr old, received either soy protein isolate (40 g soy protein, 118 mg isoflavones) or casein placebo for 3 months. There were 34 withdrawals (16%), with 179 subjects (96 men and 83 women) completing the protocol. After intervention in the soy group, compared with casein placebo, urinary phytoestrogens increased, accompanied by a significant fall in BP reflected by the BP model (P < 0.01) encompassing mean change (+/-SEM) in systolic (-7.5 +/- 1.2 vs. -3.6 +/- 1.1 mm Hg, P < 0.05), diastolic (-4.3 +/- 0.8 vs. -1.9 +/- 0.7 mm Hg, P < 0.05), and mean BP (-5.5 +/- 1 vs. -0.9 +/- 1 mm Hg, P < 0.008). In the lipid model, soy induced greater changes, compared with placebo (P < 0.001). On individual analysis, significant contributors included a reduction in the low- to high-density lipoprotein ratio (-0.33 +/- 0.1 vs. 0.04 +/- 0.1 mmol/L, P < 0.05) and triglycerides (-0.2 +/- 0.05 vs. -0.01 +/- 0.05 mol/L, P < 0.05) and an increase in Lp(a) lipoprotein (+/- 95% confidence interval) [42 (range, 17-67) vs. 4 (range, -22-31) mg/L, P < 0.05], whereas total, low-density lipoprotein, and high-density lipoprotein cholesterol improved in both groups; but no treatment effect was demonstrated. The arterial functional model demonstrated no difference between groups; although again, overall function improved in both groups. On individual analysis, peripheral PWV (reflecting peripheral vascular resistance) improved with soy (P < 0.01), whereas flow-mediated vasodilation (reflecting endothelial function) declined (in males only), compared with casein placebo (P < 0.02). No effect of treatment on the hypothalamic-pituitary-gonadal axis was noted in males or females. In normotensive men and postmenopausal women, soy improved BP and lipids but, overall, did not improve vascular function. Potential adverse effects were noted, with a decline in endothelial function (in males only) and an increase in Lp(a). Further research in hypertensive and hyperlipidemic populations is needed.     

国产比索洛尔对高血压2型糖尿病患者糖代谢的影响

目的观察国产比索洛尔对高血压合并2型糖尿病患者糖代谢及血压的影响情况。方法将符合纳入标准的高血压合并2型糖尿病患者随机分组。观察治疗前后患者糖化血红蛋白(HbA1c)、空腹血糖、糖耐量和血压等的变化。结果共有92例患者完成研究,其中比索洛尔组47例,卡托普利组45例。治疗前和经12周治疗后两组HbA1c、空腹血糖、餐后2h血糖、收缩压和舒张压差异均无统计学意义(P=0.05)。结论本研究表明比索洛尔作为高选择性β1受体阻滞剂,对于原发性高血压合并2型糖尿病患者糖代谢无明显不良影响,同时具有良好的降压效果。     

高血压病患者动态血压参数与左室肥厚及颈动脉内-中膜厚度的关系

目的探讨高血压病患者动态血压参数对左室肥厚及颈动脉内-中膜厚度检测的意义.方法将初诊的高血压病患者147例经超声心动图和颈动脉超声检查分为左室肥厚组(n=45例)和非左室肥厚组(n=102例),颈动脉内-中膜增厚组(n=52例)和非内-中膜增厚组(n=95例),经询问病史、体检、测定动态血压参数,血脂、血糖等生化指标进行比较.结果 (1)左室肥厚组与非左室肥厚组的临床指标比较差异无统计学意义(P>0.05).(2)左室肥厚组与非左室肥厚组的动态血压参数比较分别为24 h平均收缩压(140.7±14.1)比(128.3±12.3)mm Hg(1 mm Hg=0.133 kPa),24 h平均舒张压(86.4±8.9)比(81.6±9.3)mm Hg,白昼平均收缩压(142.8±13.9)比(130.9±11.1)mm Hg,白昼平均舒张压(86.9±8.8)比(83.4±9.0)mm Hg,夜间平均收缩压(129.0±13.2)比(114.6±11.4)mm Hg,夜间平均舒张压(77.2±9.4)比(67.5±8.1)mm Hg,24 h脉压(54.2±10.2)比(46.9±9.6) mm Hg,白昼脉压(55.9±10.5)比(47.5±9.1)mm Hg,夜间脉压(51.8±10.7)比(47.1±8.7)mm Hg,24 h收缩压变异系数(8.4±2.0)比(7.2±1.9),24 h舒张压变异系数(9.5±2.2)比(8.0±2.1),动态血压非勺型昼夜节律55.6%比25.5%,其差异有统计学意义(P<0.05).(3)颈动脉内-中膜增厚组与非内-中膜增厚组的上述临床指标比较,差异无统计学意义(P>0.05),与动态血压参数比较差异有统计学意义(P<0.05).结论高血压病动态血压参数异常者左室肥厚及颈动脉内-中膜增厚的发生率增多.     

Effects of testosterone and progressive resistance training in eugonadal men with AIDS wasting. A randomized, controlled trial

BACKGROUND: Substantial loss of muscle mass occurs among men with AIDS wasting. OBJECTIVE: To investigate the independent effects of testosterone therapy and progressive resistance training in eugonadal men with AIDS wasting. DESIGN: Randomized, controlled trial. SETTING: University hospital. PATIENTS: 54 eugonadal men with AIDS wasting (weight < 90% ideal body weight or weight loss > 10%). INTERVENTION: In a 2 x 2 factorial design, patients were assigned to receive testosterone enanthate (200 mg/wk) or placebo injections and progressive resistance training (three times weekly) or no training for 12 weeks. MEASUREMENTS: Cross-sectional muscle area and other indices of muscle mass. RESULTS: Cross-sectional muscle area increased in response to training compared with nontraining (change in arm muscle mass, 499 +/- 349 mm2 vs. 206 +/- 264 mm2 [P = 0.004]; change in leg muscle mass, 1106 +/- 854 mm2 vs. 523 +/- 872 mm2 [P = 0.045]) and in response to testosterone therapy compared with placebo (change in arm muscle mass, 512 +/- 371 mm2 vs. 194 +/- 215 mm2 [P< 0.001]; change in leg muscle mass, 1,236 +/- 881 mm2 vs. 399 +/- 729 mm2 [P = 0.002]). Levels of high-density lipoprotein cholesterol decreased in response to testosterone therapy compared with placebo (-0.03 +/- 0.13 mmol/L vs. 0.05 +/- 0.13 mmol/L [-1 +/- 5 mg/dL vs. 2 +/- 5 mg/dL]; P= 0.011) and increased in response to training compared with nontraining (0.05 +/- 0.13 mmol/L vs. 0.00 +/- 0.16 mmol/L [2 +/- 5 mg/dL vs. 0 +/- 6 mg/dL]; P = 0.052). CONCLUSIONS: In contrast to anabolic therapies that may have adverse effects on metabolic variables, supervised exercise effectively increases muscle mass and is associated with significant positive health benefits in eugonadal men with AIDS wasting.     

Augmentation of central arterial pressure in mild primary hyperparathyroidism

Primary hyperparathyroidism (PHPT) is associated with increased cardiovascular risk, although the mechanisms involved remain unclear. Recent evidence has shown increased pulse pressure to be a powerful predictor of cardiovascular events. As increases in pulse pressure are due largely to arterial stiffening, we measured arterial stiffness in 21 subjects with PHPT (18 women and 3 men; 46-71 yr old) and 21 age- and sex-matched healthy controls using pulse wave analysis, a technique that measures peripheral arterial pressure waveforms and generates corresponding central aortic waveforms. This allows determination of the augmentation of central pressure resulting from wave reflection and augmentation index, a measure of vessel stiffness. Metabolic parameters were also measured. The serum calcium level among PHPT subjects was (mean +/- SD) 2.74+/-0.14 mmol/L. pulse wave analysis showed that both augmentation and the augmentation index were significantly higher in the PHPT group vs. controls [16+/-5 vs. 10+/-4 mm Hg (P < 0.001) and 36+/-9% vs. 25+/-6% (P < 0.001)] despite comparable brachial systolic pressures between groups (136+/-13 vs. 134+/-18 mm Hg). Patients with PHPT had higher fasting serum insulin levels [median (range), 15.8 (7.4-39.4) vs. 11.6 (5.1-23) mU/L; P < 0.05] and triglyceride (1.6+/-0.6 vs. 1.2+/-0.4 mmol/L; P < 0.05), but lower high density lipoprotein cholesterol (1.4+/-0.4 vs. 1.6+/-0.3 mmol/L; P < 0.05). These data indicate that subjects with mild PHPT (calcium, <3.0 mmol/L) have increased arterial stiffness, as evidenced by higher augmentation of central aortic pressures. Enhanced vessel stiffness may arise from a combination of structural and functional vascular changes due to hypercalcemia and/or metabolic abnormalities. Increased vascular stiffness in subjects with PHPT may account in part for the increased cardiovascular risk in this group.     

The effects of soy protein containing isoflavones on lipids and indices of bone resorption in postmenopausal women

OBJECTIVE: To assess the effect of a dietary soy protein supplement containing isoflavones on lipids and indices of bone resorption in postmenopausal women. DESIGN: Placebo-controlled, double-blind, randomized study. PATIENTS: One hundred and six postmenopausal women were randomized to dietary soy supplementation (n = 51) or placebo (n = 55) for 3 months, of which 78 were included in the final analysis. MEASUREMENTS: Lipid profiles including total, low-density lipoprotein (LDL) and HDL cholesterol as well as triacylglycerol were measured. Pyridinoline and deoxypyridinoline were used as markers of bone resorption. Urinary isoflavone excretion was measured to assess compliance. RESULTS: There was a significantly greater increase in urinary isoflavone excretion detected in the soy group compared to placebo. Lipid profiles improved with significant decreases in LDL cholesterol (-0.60 +/- 0.10 vs.-0.29 +/- 0.09 mmol/l, P < 0.05), triacylglycerol (-0.22 +/- 0.07 vs. +0.01 +/- 0.05 mmol/l, P < 0.005) and the LDL : HDL ratio (-0.32 +/- 0.10 vs. +0.20 +/- 0.10, P < 0.005) in the soy group compared to placebo. There were no significant differences between the soy and placebo groups for urinary excretion of pyridinoline (-3.8 +/- 3.1 vs.-0.8 +/- 3.1 nmol/mmolCr, P = 0.4) or deoxypyridinoline (-0.8 +/- 0.9 vs.-0.3 +/- 0.7 nmol/mmolCr, P = 0.4). CONCLUSIONS: In postmenopausal women, dietary supplementation with soy protein containing isoflavones does not appear to have oestrogenic effects on markers of bone resorption. Soy protein favourably affected lipids; however, these effects (fall in triacylglycerol and no change in HDL) differ from those observed with oral oestrogen. These findings suggest that soy may not have biologically significant oestrogenic effects on bone resorption and we hypothesize that the lipid effects may be mediated, at least in part, through nonoestrogenic mechanisms.     

Intensive cholesterol reduction lowers blood pressure and large artery stiffness in isolated systolic hypertension

OBJECTIVES: We sought to investigate the effects of intensive cholesterol reduction on large artery stiffness and blood pressure in normolipidemic patients with isolated systolic hypertension (ISH). BACKGROUND: Isolated systolic hypertension is associated with elevated cardiovascular morbidity and mortality and is primarily due to large artery stiffening, which has been independently related to cardiovascular mortality. Cholesterol-lowering therapy has been efficacious in reducing arterial stiffness in patients with hypercholesterolemia, and thus may be beneficial in ISH. METHODS: In a randomized, double-blinded, cross-over study design, 22 patients with stage I ISH received three months of atorvastatin therapy (80 mg/day) and three months of placebo treatment. Systemic arterial compliance was measured noninvasively using carotid applanation tonometry and Doppler velocimetry of the ascending aorta. RESULTS: Atorvastatin treatment reduced total and low-density lipoprotein cholesterol and triglyceride levels by 36 +/- 2% (p < 0.001), 48 +/- 3% (p < 0.001) and 23 +/- 5% (p = 0.003), respectively, and increased high density lipoprotein cholesterol by 7 +/- 3% (p = 0.03). Systemic arterial compliance was higher after treatment (placebo vs. atorvastatin: 0.36 +/- 0.03 vs. 0.43 +/- 0.05 ml/mm Hg, p = 0.03). Brachial systolic blood pressure was lower after atorvastatin treatment (154 +/- 3 vs. 148 +/- 2 mm Hg, p = 0.03), as were mean (111 +/- 2 vs. 107 +/- 2 mm Hg, p = 0.04) and diastolic blood pressures (83 +/- 1 vs. 81 +/- 2 mm Hg, p = 0.04). There was a trend toward a reduction in pulse pressure (71 +/- 3 vs. 67 +/- 2 mm Hg, p = 0.08). CONCLUSIONS: Intensive cholesterol reduction may be beneficial in the treatment of patients with ISH and normal lipid levels, through a reduction in large artery stiffness.     

Effects of omega-3 fish oils on lipid metabolism, glycemic control, and blood pressure in type II diabetic patients

We investigated the effects of omega-3 fish oil (FO) supplementation on lipid metabolism, glycemic control, and blood pressure (BP) in patients with type II diabetes mellitus. In 22 diabetic patients without overt hyperlipidemia, serum triglyceride, total cholesterol, high density lipoprotein (HDL)-cholesterol, HDL2-cholesterol, HDL3-cholesterol, and apolipoprotein A-I (apo A-I) levels did not change during omega-3 FO supplementation for 8 weeks. The mean serum apo B concentration increased significantly [baseline, 2.56 +/- 0.11 (+/- SEM) mmol/L; 4 weeks, 2.82 +/- 0.13 mmol/L; 8 weeks, 2.80 +/- 0.13 mmol/L; P less than 0.01]. The mean plasma postheparin lipoprotein lipase activity increased transiently during the fourth week (baseline, 168 +/- 17 U/mL; 4 weeks, 182 +/- 18 U/mL; P less than 0.05), whereas postheparin hepatic triglyceride lipase activity did not change. Glycemic control worsened transiently during the fourth week, (baseline, 7.7 +/- 0.4%; 4 weeks, 8.4 +/- 0.3%; P less than 0.05). Both systolic and diastolic BP decreased significantly throughout the study (systolic BP: baseline, 142 +/- 5 mm Hg; 8 weeks, 128 +/- 5 mm Hg; diastolic BP: baseline, 88 +/- 4 mm Hg; 8 weeks, 80 +/- 3 mm Hg; P less than 0.01). These findings suggest that in type II diabetics without overt hyperlipidemia, omega-3 FO supplementation does not improve either the glycemic control or serum lipids, and it is associated with a potentially detrimental rise in serum apo B concentrations. Until more information is available, use of such supplementation should be discouraged.     

极化液对缺血/再灌大鼠心肌细胞死亡及心脏功能的影响:胰岛素的关键作用

目的　探讨葡萄糖 胰岛素 钾极化液 (GIK)对心肌缺血 /再灌 (MI/R)后心肌细胞死亡(坏死和凋亡 )及心脏功能的影响 ,并比较和分析GIK各组分在其中的作用。方法　制备大鼠MI/R模型 ,分别用生理盐水、GIK、葡萄糖 钾液 (GK)或胰岛素干预分组。观察动脉血压、血糖、左室压等的变化 ,再灌注结束后检测心肌梗死或提取DNA检测心肌细胞凋亡。结果　MI/R造成明显的心脏功能障碍、心肌梗死和缺血区细胞凋亡。GIK与胰岛素 (而非GK)具有相似的减轻再灌注心肌损伤作用 ,包括减少心肌梗死范围 [(41 3± 8 3) %和 (39 6± 8 6) %比对照组 (54 4± 1 0 4) % ,q =4 34和q=4 90 ,P值均 <0 0 5]、减弱DNA梯带形成及促进再灌后心脏收缩 /舒张功能恢复。结论　GIK可减少心肌梗死、促进缺血心脏功能恢复 ,胰岛素可能通过抑制缺血心肌细胞凋亡在GIK心肌保护中发挥关键作用。     

Role of erythropoietin in cortisol-induced hypertension

The mechanism of cortisol-induced hypertension remains unknown. We investigated a possible role of erythropoietin (EPO) as a mediator of hypertension in healthy male subjects treated with cortisol. In Study 1, blood pressure (BP) and serum EPO concentrations were measured on alternate days in nine subjects treated with 80 mg of cortisol per day for 5 days. In Study 2 the same parameters were measured in eight subjects randomised to cortisol (80 mg/day) or placebo and 10 subjects randomised to cortisol (200 mg/day) or placebo for 5 days. In Study 1, cortisol caused a significant increase in systolic BP (SBP) (115 +/- 2 vs 126 +/- 2 mm Hg, control vs day 5, P < 0.001) and serum EPO concentrations (14.5 +/- 2.7 vs 24.3 +/- 2.7 mU/mL, P < 0.001). In Study 2 both doses of cortisol increased SBP (118 +/- 2 vs 113 +/- 2 mm Hg, 80 mg cortisol vs placebo, P < 0.05 and 129 +/- 3 vs 113 +/- 2 mm Hg, 200 mg cortisol vs placebo, P < 0.001). Serum EPO concentrations were significantly increased at 200 mg cortisol (25.2 +/- 11.9 vs 15.9 +/- 3.5 mU/mL, P < 0.01) but not 80 mg cortisol (21.3 +/- 2.9 vs 14.9 +/- 3.1 mU/mL). In the 200 mg group there was a positive correlation between the change in SBP and the change in serum EPO concentration (r2 = 0.43, P < 0.05). These results point to a possible role for EPO as the mediator of cortisol-induced hypertension. Journal of Human Hypertension (2000) 14, 195-198.