雷米普利对心肌梗死后心衰大鼠非梗死区胶原的抑制作用

目的 研究心肌梗死后心衰大鼠非梗死区心肌血管紧张素Ⅱ(Ang Ⅱ)及其Ⅰ型受体(AT1-R)表达对心室重构的影响及雷米普利的干预作用.方法 结扎大鼠左冠状动脉前降支并饲养6 w的16只存活大鼠,随机分为模型组及雷米普利组,每组8只,另取8只大鼠为假手术组,连续灌胃给药4 w后测定大鼠血流动力学参数,ELISA方法检测血清及左心室非梗死区AngⅡ的含量,RT-PCR 法测定左心室非梗死区心肌组织AT1-R mRNA表达水平,Masson染色观察非梗死区心肌胶原的沉积.结果 雷米普利能明显升高左心室内压最大上升和最大下降速率(±dp/dt_(max)),降低左心室收缩压(LVSP)、左心室舒张末压(LVEDP)(P<0.05或P<0.01),但对心率(HR)、收缩压(SBP)、舒张压(DBP)无明显影响(P>0.05),同时明显降低血清及左心室非梗死区AngⅡ的含量及下调AT1-R mRNA 表达水平(P<0.01或P<0.001),Masson染色可见非梗死区心肌胶原沉积明显减轻.结论 雷米普利对梗死后心衰大鼠非梗死区心肌间质胶原重构有显著的抑制作用,其作用机制与下调AT1-R表达水平及减轻胶原沉积有关.     

中期因子对大鼠心肌梗死后心室重构及血管紧张素Ⅱ的影响

目的探讨外源性中期因子(MK)对心肌梗死后大鼠心室重构及血管紧张素Ⅱ(AngⅡ)的影响。方法建立急性心肌梗死(AMI)雄性Wistar大鼠模型45只,随机分为AMI对照组、MK治疗组,每组各15只。另设15只作假手术组。造模成功后1μg/200 g人重组MK在梗死周围分5点注射给药,4 w后检测血流动力学及心功能参数,心脏标本检测左室重量及左室重量指数(LVMI)、心肌梗死面积,并检测血浆和心肌AngⅡ水平。结果与假手术组比较,AMI组左室重量及左室重量指数、左室截面直径及心肌AngⅡ水平明显增高,而左室收缩压(LVSP)及左室内压最大上升和下降速率(±dp/dt)均明显降低(均P<0.01);与AMI组比较,MK治疗组左室重量及LVMI、左室截面直径明显降低(P<0.05或P<0.01),LVSP和±dp/dt均明显增高(P均<0.05),心肌梗死面积和心肌AngⅡ水平也明显低于AMI组。结论外源性的MK应用能减轻AMI后心室重构、保护心功能。     

低声压级水平次声对心肌梗死大鼠心肌纤维化的影响及机制研究

目的:观察次声对心肌梗死后大鼠心肌纤维化的影响及相关机制研究。方法:将30只SD大鼠随机分为3组,即假手术组、心肌梗死组及次声治疗组,每组10只。采用低声压级水平次声对心肌梗死大鼠治疗1周(2次/d,0.5 h/次),观察心肌胶原和血浆NO和血管紧张素-Ⅱ(AngⅡ)及大鼠心功能的变化。结果:与心肌梗死组大鼠比较(未治疗组),次声治疗组大鼠心肌胶原表达明显减少,血浆NO含量显著增加(P0.01),血浆AngⅡ含量显著降低(P0.01),心功能明显改善(P0.01)。结论:低声压级水平次声治疗能够明显减轻心肌梗死后大鼠心肌纤维化,其作用可能与血浆NO及AngⅡ含量变化有关。     

复方芪丹液对急性心肌梗死后大鼠心室重构血管活性物质的影响

目的观察实验性急性心肌梗死(AMI)后大鼠心脏结构的变化和动物血浆、心肌组织的内皮素(ET)、血管紧张素Ⅱ(AngⅡ)的水平,探讨复方芪丹液防治AMI后心室重构(VR)的作用机制。方法结扎大鼠冠状动脉左前降支,造成动物实验性AMI模型,体表心电图Ⅱ导示ST-T弓背抬高,证实AMI形成后,将大鼠随机分为6组,于术后第2日开始灌胃给药,连续4周。麻醉处死大鼠,观察各组大鼠心脏指数、心室重量、心肌细胞大小等心脏结构和血浆及心肌组织中ET、AngⅡ的含量。结果服用复方芪丹液4周后,与模型组比较,中药大、中剂量和开博通皆可明显降低AMI大鼠心脏指数(P<0.01)和左室重量;对血浆和心肌组织中ET、AngⅡ含量亦较模型组明显降低(P<0.01和P<0.05),并可减少左室心肌细胞的面积、周长和直径。结论复方芪丹液可显著降低AMI大鼠左室重量、心脏指数,抑制大鼠左室心肌细胞的增大,降低大鼠血浆及心肌组织中ET和AngⅡ的含量。抑制大鼠血浆和心肌组织的血管活性物质可能是防治AMI后早期VR的作用机制之一。     

C1酯酶抑制剂对大鼠急性心肌缺血再灌注损伤的保护作用

目的探讨C1酯酶抑制剂对大鼠心肌缺血再灌注损伤的保护作用及其可能机制。方法将48只Wistar大鼠随机分为:假手术组、模型组、治疗组、预适应组,每组12只。建立急性心肌缺血再灌注损伤模型,模型组、治疗组、预适应组大鼠结扎左前冠状动脉30 min后再灌注2 h,假手术组不结扎。检测血清肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)活性;检测各组大鼠心肌梗死范围;免疫组织化学法检测组织细胞间黏附分子1(ICAM 1)的表达及RT-PCR检测ICAM-1 mRNA的表达。结果与假手术组比较,模型组大鼠左心室收缩压、左心室压力最大上升速率及最大下降速率(±dp/dt_(max))明显降低,左心室舒张末压、CK、CK-MB、ICAM-1、ICAM-1 mRNA明显升高(P<0.01);与模型组比较,治疗组和预适应组大鼠左心室收缩压、±dp/dt_(max)明显升高(P<0.01),左心室舒张末压、CK、CK-MB、ICAM-1、ICAM-1 mRNA明显降低(P<0.05,P<0.01),心肌梗死面积明显缩小(P<0.01)。结论 C1酯酶抑制剂可能通过阻断ICAM-1的表达,从而限制中性粒细胞聚集起到心肌保护作用。     

microRNA-497在麝香保心丸调控急性心肌梗死心室重构中作用机制的实验研究

目的探讨microRNA-497(miRNA-497)在麝香保心丸调控急性心肌梗死心室重构中的作用机制。方法将75只SD大鼠随机分为A组、B组、C组、D组、E组,每组15只。A组为空白对照组,B组、C组、D组、E组采用结扎左冠状动脉前降支法建立急性心肌梗死模型。C组给予miRNA-497激动剂和麝香保心丸干预,D组给予miRNA-497抑制剂和麝香保心丸干预,E组给予麝香保心丸干预,B组给予等量生理盐水。6周后,比较各组大鼠一般情况、心功能指标[左室收缩末压(LVESP)、左室内压最大上升速率(LV+dp/dt_(max))、左室舒张末压(LVEDP)、左室内压最大下降速率(LV-dp/dt_(max))]、急性心肌梗死面积、心肌细胞凋亡率、心肌组织形态学变化、miRNA-497表达量。结果与B组比较,C组大鼠一般情况及心肌组织病理学改变无明显改善,D组、E组大鼠一般情况及心肌组织病理学改变有改善,且D组较E组改善更明显。D组、E组大鼠LVEDP、急性心肌梗死面积、心肌细胞凋亡率明显低于B组、C组(P0.05),且D组大鼠LVEDP、急性心肌梗死面积、心肌细胞凋亡率明显低于E组(P0.05);D组、E组大鼠LV+dp/dt_(max)、LVESP、LV-dp/dt_(max)明显高于B组、C组(P0.05),且D组大鼠LV+dp/dt_(max)、LVESP、LV-dp/dt_(max)明显高于E组(P0.05);C组大鼠LVEDP、LV+dp/dt_(max)、LVESP、LV-dp/dt_(max)、急性心肌梗死面积、心肌细胞凋亡率与B组比较,差异均无统计学意义(P0.05)。B组、C组、D组、E组大鼠心肌组织中miRNA-497表达量明显高于A组(P0.05);C组大鼠心肌组织中miRNA-497表达量明显高于B组(P0.05);D组、E组大鼠心肌组织中miRNA-497表达量明显低于B组、C组(P0.05),D组大鼠心肌组织中miRNA-497表达量低于E组(P0.05)。结论 miRNA-497是麝香保心丸改善急性心肌梗死后心室重构中的关键分子,这为急性心肌梗死后心室重构提供了新的研究方向。     

西洋参茎叶三醇组皂苷对大鼠压力超负荷性心室重构的保护作用

目的 观察西洋参叶20s-原人参三醇组皂苷(PQTS)对压力超负荷性大鼠心室重构的保护作用.方法 Wistar大鼠随机分为假手术组、模型组、阳性药卡托普利组及PQTS低、中、高剂量组.结扎大鼠腹主动脉建立压力超负荷性心室重构模型,PQTS按12.5、25.0、50.0mg·kg-1·d-1连续腹腔注射6周,检测心室脏器系数、心肌组织病理学及血流动力学参数,测定血清丙二醛( MDA)含量及超氧物歧化酶(SOD)活性,血浆前列环素(PGI2)、血栓素A2 (TXA2)、内皮素(ET)及血管紧张素Ⅱ(AngⅡ)含量.结果 与重构模型组比较,PQTS能明显抑制心室重构大鼠心肌组织的病理性改变,降低心室质量及心脏系数,明显升高收缩压、舒张压、平均动脉压、左室收缩压及左心室内压最大上升和下降速率(±dp/dtmax),降低心率及左室舒张末压,可明显降低血清MDA含量,升高SOD活性,亦能明显降低血浆ET、AngⅡ及TXA2含量,提高PGI2含量及PGI2/TXA2比值(P＜0.05或P＜0.01).结论 PQTS对大鼠心室重构具有明显保护作用,可能与其改善心室重构大鼠的左心收缩和舒张功能,增强抗氧化酶活性,减少自由基及缩血管活性物质对心肌的损伤,纠正PGI2/TXA2失衡等机制有关.     

卡维地洛增加心力衰竭大鼠心肌细胞血管紧张素转换酶2

目的探讨卡维地洛对心肌梗死后大鼠心肌组织血管紧张素转换酶2(ACE2)的影响。方法结扎大鼠左冠状动脉前降支复制心肌梗死后心力衰竭(CHF)模型,随机分为 CHF 组,卡维地洛组和假手术组。2月后检测血流动力学指标,计算左心室质量指数,放射免疫法测定心肌组织和血浆血管紧张素Ⅱ(AngⅡ)水平,RT-PCR 方法检测心肌组织 ACE2 mRNA 表达,Western-Blot 方法检测心肌组织 ACE2蛋白表达。结果 CHF 组与卡维地洛组8周死亡率都是20%,而假手术组为0%。卡维地洛明显改善 CHF 大鼠的血流动力学参数(LVEDP,LVSP,+dp/dt_(max)和-dp/dt_(min)),但仍然比假手术组差。CHF 组大鼠循环和心肌组织 Ang Ⅱ水平明显升高[循环AngⅡ:(194±19)比假手术组(132±15)ng/L,心肌 AngⅡ:(6.7±0.4)比假手术组(3.8±0.3)ng/g,P 均<0.01],心肌组织 ACE2 mRNA 和蛋白表达增强[ACE2 mRNA:(1.09±0.07)比假手术组(0.81±0.06),P<0.01;ACE2蛋白:(0.68±0.08)比假手术组(0....     

营养不良大鼠左心功能的改变与克山病病因关系的探讨

以左室收缩压峰值LVSP、左室内压最大上升速率dp/dt_(max)、E_(max)等指标测定了饲以克山病区(山东邹县)地瓜干煎饼三个月的营养不良大鼠的左心收缩功能及心脏容量负荷耐受性。结果:28只营养不良大鼠的心率HR、LVSP、dp/dt_(max)、E_(max)分别为295±59beats/min、12.4±3.8Kpa、279.3±104.9Kpa/sec、13.4±4.7Kpa/mm。皆明显低于正常对照 P<0.01。大剂量生理盐水快速静脉注射后上述指标明显低于注射前。P<0.01,而正常大鼠无明显改变 P>0.05。结果表明:营养不良大鼠左心收缩功能降低,容量负荷耐受性减弱。从而从心肌功能水平为营养不良因素在克山病发病中的作用提供了实验依据。     

不同时间左心室注射地尔硫对大鼠顿抑心肌功能的影响

目的观测不同时间左心室注射地尔硫对大鼠顿抑心肌功能的影响。方法 Wistar雄性大鼠25只,随机分为5组,假手术组(A组)、顿抑心肌组(B组)、缺血期注射地尔硫组(C组)、再灌注早期注射地尔硫组(D组),再灌注晚期注射地尔硫组(E组),每组5只,观察心率(HR)、左心室收缩末期压(LVESP)、左心室舒张末期压(LVEDP)、左心室内压最大上升速率及最大下降速率(±dp/dt_(max))的变化。结果与A组大鼠比较,除C组再灌注30、60、90、120 min,D组再灌注60、90、120 min时,其他各组在缺血及再灌注后均出现HR增快,LVESP、LVEDP、±dp/dt_(max)降低(P<0.05);C组再灌注30 min、D组再灌注90 min时HR、LVESP、LVEDP、±dp/dt_(max)已恢复至术前水平。与B组大鼠比较,C组再灌注15、30、60、90、120 min,D组再灌注90、120 min HR下降,LVESP、LVEDP、±dp/dt_(max)明显改善(P<0.05)。结论在缺血和再灌注早期左心室注射地尔硫可促进顿抑心肌功能的恢复,而再灌注晚期应用则无明显作用。     

Effect of Cilazapril on Ventricular Remodeling Assessed by Doppler-Echocardiographic Assessment and Cardiac Gene Expression

The purpose of this study is to determine whether the administration of the ACE inhibitor cilazapril can lessen the adverse effects of ventricular remodeling, including systolic and diastolic dysfunction, modulation of fetal gene expression, increase of collagen genes, and depression of the sarcoplasmic reticulum (SR) Ca²⁺ ATPase gene in a myocardial infarcted (MI) rat model. At 1 day after MI, the animals were randomly assigned to cilazapril treatment or no treatment. We performed Doppler-echocardiographic examinations and measured cardiac mRNA in rats at 1 month and 3 months after MI (each group n = 8). The weights of the right (RV) and left ventricles (LV) in 1- and 3-month MI rats were significantly larger than those of the control rats. Cilazapril significantly prevented the increase. The MI rats showed systolic dysfunction, as evidenced by decreased fractional shortening (control, 34 ± 3% vs. MI, 17 ± 3%; P <0.01) and ejection fraction measured by the modified Simpsons method (control, 61 ± 2% vs. MI, 36 ± 3%; P < 0.01) in rats at 1 month after operation. MI rats showed diastolic dysfunction, defined as increased peak early filling velocity, increased deceleration rate of the early filling wave, decreased late filling velocity, and an increase in the ratio of early filling to late filling velocity. Cilazapril significantly prevented systolic and diastolic dysfunction in rats after MI. The increases in -MHC, -skeletal actin, ANP, and collagen I and III mRNAs in the nonischemic LV and RV were significantly suppressed by treatment with cilazapril. Depressed SR Ca²⁺-ATPase mRNA (nonischemic LV, 0.7-fold, P < 0.05 vs. control; RV, 0.5-fold, P < 0.05 vs. control) at 3 months after MI was significantly restored to normal levels by cilazapril. Cilazapril improved the adverse remodeling process by attenuating the progression of systolic and diastolic dysfunction, and prevented abnormal cardiac gene expression following MI.     

Cardiac Thyrotropin-releasing Hormone Inhibition Improves Ventricular Function and Reduces Hypertrophy and Fibrosis After Myocardial Infarction in Rats

BackgroundCardiac thyrotropin-releasing hormone (TRH) is a tripeptide with still unknown functions. We demonstrated that the left ventricle (LV) TRH system is hyperactivated in spontaneously hypertensive rats and its inhibition prevented cardiac hypertrophy and fibrosis. Therefore, we evaluated whether in vivo cardiac TRH inhibition could improve myocardial function and attenuate ventricular remodeling in a rat model of myocardial infarction (MI).Methods and ResultsIn Wistar rats, MI was induced by a permanent left anterior descending coronary artery ligation. A coronary injection of a specific small interfering RNA against TRH was applied simultaneously. The control group received a scrambled small interfering RNA. Cardiac remodeling variables were evaluated one week later. In MI rats, TRH inhibition decreased LV end-diastolic (1.049 ± 0.102 mL vs 1.339 ± 0.102 mL, P < .05), and end-systolic volumes (0.282 ± 0.043 mL vs 0.515 ± 0.037 mL, P < .001), and increased LV ejection fraction (71.89 ± 2.80% vs 65.69 ± 2.85%, P < .05). Although both MI groups presented similar infarct size, small interfering RNA against TRH treatment attenuated the cardiac hypertrophy index and myocardial interstitial collagen deposition in the peri-infarct myocardium. These effects were accompanied by attenuation in the rise of transforming growth factor-β, collagen I, and collagen III, as well as the fetal genes (atrial natriuretic peptide, B-type natriuretic peptide, and beta myosin heavy chain) expression in the peri-infarct region. In addition, the expression of Hif1α and vascular endothelial growth factor significantly increased compared with all groups.ConclusionsCardiac TRH inhibition improves LV systolic function and attenuates ventricular remodeling after MI. These novel findings support the idea that TRH inhibition may serve as a new therapeutic strategy against the progression of heart failure.     

缬沙坦、苯那普利及合用时对心肌梗死后心室重构影响的比较

目的　对比血管紧张素转化酶抑制剂 ( ACEI)、选择性 型血管紧张素 受体拮抗剂 ( ARB)以及合用时对心肌梗死 ( MI)后心室重构的影响 ,并初步探讨其作用机制。方法　冠状动脉左前降支结扎后 2 4小时的 SD大鼠被随机分至 B组 (苯那普利 2 m g/ kg/ d)、V组 (缬沙坦 15 mg/ kg/ d)、B+ V组 (苯那普利 1mg/ kg/ d+缬沙坦 7.5 mg/ kg/d)和 C组 (空白对照组 ) ,假手术组 ( S组 )作为正常对照。治疗 6周后测量体重、心脏重量、非梗死心肌胶原含量 ,以及血管紧张素转化酶 ( ACE)、血管紧张素 ( Ang )、醛固酮 ( Ald)的活性或含量。结果　 MI后 6周左心室 ( L V)、右心室 ( RV)重量以及右心室与左心室重量比、心肌胶原含量显著增加 ( C组比 S组 ,P<0 .0 5 ) ,苯那普利、缬沙坦及合用均显著降低以上指标 (与 C组比较 ,均 P<0 .0 5 )。 C组心脏局部 Ang 、ACE和 Ald较 S组明显升高 ( P<0 .0 1) ,三种治疗组均使其显著降低并恢复至正常 (与 C组比较 ,均 P<0 .0 1;与 S组比较 ,均 P>0 .0 5 )。结论　 l.心脏局部肾素 -血管紧张素系统 ( RAS)在左心室重构中发挥重要的作用。2 .ACEI、ARB均有减轻 MI后左心室重构方面的作用。 3 .合用 ACEI与 ARB具有良好的叠加作用     

福辛普利、依贝沙坦及二者合用对心肌梗死后心室重塑影响的实验研究

目的：对比福辛普利、依贝沙坦及二合用对大鼠心肌梗死后心室重塑的影响。方法：通过结扎冠状动脉左前降支诱导大鼠心肌梗死，心肌梗死后24h将大鼠随机分为：（1）安慰剂组；（2）福辛普利组；（3）依贝沙坦组；（4）福辛普利＋依贝沙坦组；另设假手术组。2周后检查以下指标：（1）平均动脉压，左室舒张末压；（2）心室重量／体重；（3）非梗死区胶原含量；（4）非梗死区非心肌细胞增生数量。结果：安慰剂组与假手术组相比左室舒张末压增加（P＜0．05），且心室重量／体重、非梗死区胶原含量及非心肌细胞增生数量增加显（P＜0．01）。福辛普利组和依贝沙坦组与安慰剂组相比平均动脉压下降、心室重量／体重及非心肌细胞增生数量下降，二合用与安慰剂组比较以上指标下降显（P＜0．01）；两药单用和合用与安慰剂组相比左室舒张末压下降（P＜0．05）。两药单独和联合应用均阻止了非梗死区胶原沉积（P＜0．01，与安慰剂组相比），两个单独用药组高于假手术组（P＜0．05），而联合治疗组与假手组间无统计学差异。福辛普利组、依贝沙坦组及二合用组三间各指标差异均无统计学意义。结论：福辛普利和依贝沙坦均可限制心肌梗死后心肌肥大、抑制左室非梗死区胶原沉积和非心肌细胞增生；二合用2周未见上述作用更显。     

QT间期离散度与心肌梗死患者左心功能及心律失常的关系

应用超声声学定量技术和动态心电图观察QT间期离散度（QTd）对冠心病亚急性及陈旧性（伴再发心绞痛）心肌梗死患者左心功能和心律失常的影响。结果发现，心肌梗死组的QTd较正常组明显延长（P＜0．01）；其左室收缩功能与舒张功能与正常对照组相比亦受损。心肌梗死合并室性心律失常组与合并窦性心律组相比，前者QTd明显延长（P＜0．01）；心肌梗死合并室性心律失常组的左室收缩功能与舒张功能与心肌梗死合并窦性心律组相比亦受损。由此可见，冠心病亚急性及陈旧性（伴再发心绞痛）心肌梗死患者QTd延长，QTd的延长可能与左室收缩功能与舒张功能的受损及心律失常的发生有关。     

PCI对恢复期心肌梗死患者左室重构的作用

目的评价经皮冠状动脉介入治疗(PCI)急性心肌梗死恢复期对患者左室重构的临床作用。方法对50例首次心肌梗死患者,平均于发病(3.8±2.1)周行冠状动脉造影,并进行前瞻性研究。按梗死相关冠状动脉是否进行PCI及PCI成功与否分为PCI组(28例PCI成功患者)和对照组(22例未行PCI患者)。对PCI组患者,于术前[平均(4.5±3.3)d]及术后随访期[平均(6.9±1.3)个月]及对照组患者于相当于PCI组术前和随访期时间进行心脏超声检查,以评价左室容量和收缩及舒张功能的改变。结果PCI组术后随访期左室容量较术前减小、左室收缩功能明显改善,而左室舒张功能无明显变化。与对照组相比,PCI组随访期左室容量较小,而收缩及舒张功能明显好于对照组。结论在心肌梗死恢复期,PCI尚能阻止患者的左室重构,改善患者的远期左室功能,具明显临床有益作用。     

高血压病患者左室肥厚及构型改变与胰岛素抵抗的关系

目的:探讨高血压病(EH)患者胰岛素抵抗(IR)对左心室肥厚(LVH)和几何构型的影响。方法:检测124 例EH病人的左室重量指数(LVMI),相对室壁厚度(RWT),空腹血清葡萄糖(FSG)、空腹血胰岛素(FSI)浓度, 并计算胰岛素敏感性指数(ISI)。依照LVMI及RWT的数值124例EH病人被分为左室正常构型(51例),向心性构型(30例),向心性肥厚型(22例),离心性肥厚型(21例)。结果:RWT与年龄、体重指数(BMI)、收缩压(SBP)、舒张压(DBP)、平均心率呈正相关(r=0.16-0.22,P<0.05),与ISI呈负相关(r=-0.24),LVMI与SBP、DBP呈正相关(r=0.16-0.20,P<0.05),与ISI不相关。向心性重构组和向心性肥厚组年龄、RWT、HR、BMI大于正常构型组(P<0.05-<0.01),而ISI小于正常构型组(P<0.01)。结论:胰岛素敏感性降低与EH患者左心室肥厚无关,与RWT增加密切相关;ISI可能是EH患者发生左室向心性构型的重要影响因素之一。     

The Effects of Simvastatin on Left Ventricular Hypertrophy and Left Ventricular Function in Patients with Essential Hypertension

This study is to evaluate the effects of Simvastatin on left ventricular hypertrophy and left ventricular function in patients with essential hypertension. Untreated or noncompliance with drug treatment patients with simple essential hypertension were treated with a therapy on the basis of using Telmisartan to decrease blood pressure (BP). There were 237 patients who had essential hypertension combined with left ventricular hypertrophy as diagnosed by echocardiography, taken after their BPs were decreased to meet the values of the standard normal. Among them, there were only 41 out of the original 237 patients, 17.3%, who had simple essential hypertension combined with left ventricular hypertrophy without any other co-existing disease. They were the patients selected for this study. All patients were randomly, indiscriminately divided into two groups: one was the control group (Group T), treated with the Telmisartan-based monotherapy; the other was the target group (Group TS), treated with the Telmisartan-based plus simvastatin therapy. The changes of left ventricular hypertrophy and left ventricular function were rediagnosed by echocardiography after 1 year. The results we obtained from this study were as follows: (i) The average BPs at the beginning of the study, of simple essential hypertension combined with left ventricular hypertrophy, were high levels (systolic blood pressure (SBP) 189.21 ± 19.91 mm Hg, diastolic blood pressure 101.40 ± 16.92 mm Hg). (ii) The Telmisartan-based plus simvastatin therapy was significantly effective in lowering the SBP (128.26 ± 9.33 mm Hg vs. 139.22 ± 16.34 mm Hg). (iii) After the 1-year treatment, the parameters of left ventricular hypertrophy in both groups were improved. Compared to group T, there were no differences in the characteristics of the subjects, including interventricular septum, left ventricular mass, left ventricular mass index, ejection fraction, left atrium inner diameter at baseline. The patients’ interventricular septum (Group TS 10.30 ± 1.80 mm vs. Group T 10.99 ± 1.68 mm, P < .05), LVM (Group TS 177.43 ± 65.40 g vs. Group T 181.28 ± 65.09 g, P < .05), and LVMI (Group TS 100.97 ± 37.33 g/m² vs. Group T 106.54 ± 27.95 g/m², P < .05), all dropped more prominently (P < .05) in group TS; the ejection fraction rose more remarkably in group TS (Group TS: 57.50 ± 16.41% to 65.43 ± 11.60%, P < .01 while showing no change in Group T); the left ventricular hypertrophy reversed more significantly and the left ventricular systolic function improved more. (iv) The left atrium inner diameter of Group TS decreased (P < .01), the ratio of E/A, which indicates the left ventricular diastolic function, continued to drop further, showing no change to the trend of left ventricular diastolic function declination. Patients who have hypertension with left ventricular hypertrophy usually suffer other accompanying diseases at the same time. Telmisartan-based plus Simvastatin treatment can significantly reduce SBP, reverse left ventricular hypertrophy, improve the left ventricular systolic function, but it has no effect on reversing the left ventricular diastolic function. This experiment indicated that Simvastatin can reverse left ventricular hypertrophy and improve left systolic function.     

高血压患者血压节律与靶器官损害的相关性研究

目的 探讨高血压患者血压节律变化与心、脑、肾等靶器官损害的相关性。方法 应用无创性血压监测仪对84例高血压患者进行24小时动态血压监测,对比血压节律正常(勺型组)和异常(非勺型组)患者心、脑、肾靶器官损害程度。结果 非勺型组24小时平均收缩压和舒张压、白昼平均舒张压、夜间平均收缩压和舒张压、收缩压及舒张压负荷值较勺型组升高(P<0.01);左心室重量和重量指数显著增加(P<0.05,0.01),24小时平均动脉压与左心室重量指数呈显著相关性r=0.55,P<0.01;尿微量白蛋白阳性率明显增高(P<0.05);脑梗死发生率明显增加(P<0.05);组间在偶测平均收缩压和舒张压、白昼平均收缩压均无显著性差异(P>0.05)。结论 血压昼夜节律异常较节律正常的高血压患者有更显著的靶器官损害。     

The Relationship Between Aortic Stiffness and Left Ventricular Dyssynchrony in Hypertensive Patients with Preserved Left Ventricular Systolic Function

Left ventricular (LV) dyssynchrony is often seen in patients with hypertension, even without heart failure. Arterial stiffness is well accepted as an important factor of increasing blood pressure and influencing ventricular function. The purpose of this study was to determine the relationship between aortic stiffness and LV dyssynchrony in hypertensive patients with preserved LV systolic function. Eighty hypertensive patients with preserved LV systolic function (LV ejection fraction > 50%) and 30 controls were studied. The LV systolic and diastolic dyssynchrony indices were determined as the standard deviation of the time interval from onset of the QRS complex to peak myocardial systolic velocity (Ts-SD) and to early diastolic velocity (Te-SD) and the maximal differences in Ts (Ts-Max) and Te (Te-Max) in 12 LV segments. Aortic stiffness index was calculated from aortic diameters in the systolic and diastolic phases, as measured by echocardiography and blood pressure. No relationship was observed between LV systolic and diastolic dyssynchrony indices (r = 0.057, P = .61). In simple regression, aortic stiffness parameter was related to left ventricular mass index (LVMI), E/A ratio, and LV diastolic dyssynchrony index. But using multiple linear regression, Te-Max remained as a single variable related to aortic strain and aortic stiffness index (r = ?0.271, P = .008 and r = 0.269, P = .008). LVMI was related to aortic distensibility using multiple linear regression (r = ?0.239, P = .02). Aortic stiffness index was related to LV diastolic dyssynchrony index and LVMI. These findings suggest that LV diastolic dyssynchronous changes may be caused by increased LV mass and arterial stiffness.