Non-cardiac nucleic acid composition and protein synthesis rates in hypertension: studies on the spontaneously hypertensive rat (SHR) model

Various studies have shown the involvement of extracardiac tissues in hypertension, including the hepato-intestinal tract, musculo-skeletal system, skin, and the kidney. It was our hypothesis that these perturbations in non-cardiac tissues would also include alterations in protein metabolism. Thus, the reported differences in soleus contractile protein composition may be related to changes in muscle protein synthesis or reduced protein synthetic efficiencies. The aim of the present study was to characterise tissue composition of nucleic acids and rates of protein synthesis in non-cardiac tissues, such as liver, skeletal muscle (i.e., the Type I fibre-predominant soleus and Type II fibre-predominant plantaris), kidney, bone (tibia), skin and the gastrointestinal tract in a genetic model of hypertension (i.e., spontaneously hypertensive rats (SHRs), 15 weeks old) compared to their genetic aged-matched counterparts, i.e., normotensive Wistar-Kyoto (WKY) controls. Rates of protein synthesis were measured in vivo after injection with a flooding dose of L-[4-(3)H]phenylalanine. The results showed changed tissue wet weights (g per organ) for plantaris (+10%, P<0.05), liver (+25%, P<0.01), brain (-9%, P<0.01), jejunum (+39%, P<0.001) and tibia (+17%, P<0.001) in SHRs compared to WKY controls. Protein content (g or mg per organ) was increased in the liver (+32%, P<0. 01) and tibia (+37%, P<0.05). RNA contents (mg per organ) were increased in plantaris (+17%, P<0.01), liver (+22%, P<0.01) and jejunum (+11%, P<0.05). DNA (mg per organ) was increased in plantaris (+16%, P<0.025) and jejunum (+12%, P<0.025). The protein synthetic capacities (i.e., C(s), mg RNA/g protein) were higher in soleus (+41%, P<0.01) and plantaris (+6%, P<0.05) muscles of SHRs compared to WKYs, whereas values were lower in liver (-11%, P<0.01) and kidney (-6%, P<0.01) of SHRs compared to WKYs. The fractional rate of protein synthesis (i.e., k(s), the percentage of the protein pool renewed each day) was not significantly different for any of the tissues, though the rate of protein synthesis per unit RNA (i.e., k(RNA), mg protein/day per mg RNA) was reduced in the soleus (-24%, P<0.05) and the synthesis rate per unit DNA, i.e., k(DNA) (mg protein/day per mg DNA) was increased in the tibia (+31%, P<0.025). This is the first report of significant differences between indices of protein metabolism in extracardiac tissues in hypertension, which may reflect endocrine factors and/or the systemic influence of hypertension per se.     

丹参预防自发性高血压大鼠左室肥厚的实验研究

目的　观察丹参对自发性高血压大鼠左室肥厚 (LVH)的作用 ,并探讨其作用机制。方法　 18只 8周龄的自发性高血压大鼠随机分成 3组 :一组于 8周处死 ,另两组分别经腹腔注射丹参和蒸馏水 (1g·kg-1·d-1)共 10周。测量大鼠尾动脉收缩压 (SBP)及左心室重量指数 (LVMI)。应用HE、VG染色、免疫组织化学的方法 ,结合计算机图像分析技术 ,检测心肌细胞的直径和面积、心肌组织胶原体积比例 (CVF)、血管周围胶原面积和管腔面积比例 (PVCA)以及蛋白激酶C(PKC)的表达。结果　与 8周龄的自发性高血压大鼠相比 ,18周龄大鼠的SBP、LVMI、心肌细胞的直径和面积、CVF、PVCA显著增加 ,PKC表达上调 ,丹参治疗可抑制LVH的发展和心肌组织PKC的表达 ,但收缩压无明显改变。结论　长期应用丹参治疗可预防自发性高血压大鼠左室肥厚的形成 ,其机制可能与丹参降低了心脏蛋白激酶C的表达有关。     

丹参酮ⅡA预防自发性高血压大鼠左室肥厚的机制

目的观察丹参酮ⅡA对自发性高血压大鼠左室肥厚的作用，并研究其对心肌bcl-2蛋白表达的影响。方法18只8周龄的自发性高血压大鼠随机分成3组：对照组、丹参组和高血压组，每组6只。测量大鼠尾动脉收缩压（SBP）及左心室重量指数（LVMI）。应用HE染色、VG染色、免疫组织化学的方法，结合计算机图像分析技术，检测心肌细胞的直径和面积、心肌组织胶原体积比例（CVF）、血管周围胶原面积和管腔面积比例（PVCA）。用Western blot法检测心肌细胞bcl-2蛋白的表达。结果与对照组相比，高血压组大鼠的SBP、LVMI、心肌细胞的直径和面积、CVF、PVCA显著增加，bcl-2蛋白的表达降低（P〈0．05），丹参酮ⅡA治疗可抑制左心室肥厚（LVH）的发展和上调bcl-2蛋白的表达，但收缩压无明显改变。结论长期应用丹参酮ⅡA治疗可预防自发性高血压大鼠左室肥厚的形成，其机制可能与丹参酮ⅡA上调心肌细胞凋亡蛋白bcl-2的表达有关。     

丹参酮IIA对自发性高血压大鼠左室肥厚的影响及机制

目的 :观察丹参酮IIA对自发性高血压大鼠左室肥厚的作用 ,并探讨其作用机制。方法 :18只 8周龄的自发性高血压大鼠随机分成 3组 :一组于 8周处死 ,另两组分别经腹腔注射丹参酮IIA和蒸馏水 (1g·kg-1·d-1) ,共 10周。测量大鼠尾动脉收缩压 (SBP)及左心室重量指数 (LVMI)。应用HE染色、VG染色、免疫组织化学的方法 ,结合计算机图像分析技术 ,检测心肌细胞的直径和面积、心肌组织胶原体积比例 (CVF)、血管周围胶原面积和管腔面积比例 (PVCA)以及蛋白激酶C(PKC)的表达。结果 :与 8周龄的自发性高血压大鼠相比 ,18周龄大鼠的SBP、LVMI、心肌细胞的直径、面积、CVF、PVCA显著增加 ,PKC表达上调 ,丹参酮IIA治疗可抑制LVH的发展和心肌组织PKC的表达 ,但收缩压无明显改变。结论 :长期应用丹参酮IIA治疗可预防自发性高血压大鼠左室肥厚的形成 ,其机制可能与丹参酮IIA降低了心脏PKG的表达有关     

Regression of left ventricular hypertrophy with losartan potassium therapy in patients with hypertension

The aim of this study was to assess the effects of losartan potassium, an angiotensin II receptor antagonist, on systolic blood pressure; diastolic blood pressure; and left ventricular dimensions, functions, and mass index (LVMI) in patients with mild-to-moderate essential hypertension. Twenty patients aged 40 to 65 years with either uncontrolled or previously untreated hypertension and echocardio-graphically documented left ventricular hyptertrophy (LVH) defined by LVMI >130 g/m² for men and >110 g/m² for women were included in the study. Blood pressure measurements were taken at 2-week intervals. Blood samples were taken before treatment and after 3 months of treatment for determination of lipid concentrations and other laboratory variables used to monitor safety, and two-dimensional M-mode and Doppler echocardiographic measurements were obtained. Losartan was associated with a statistically significant reduction of mean systolic blood pressure from 173 ± 6 mm Hg to 135 ± 10 mm Hg and diastolic blood pressure from 100 ± 4 mm Hg to 82 ± 7 mm Hg without a change in heart rate. Significant decreases were identified in interventricular septal and left ventricular posterior wall thicknesses (from 12.5 ± 0.8 mm to 11.5 ± 0.8 mm and 12.1 ± 1.0 mm to 11.1 ± 0.8 mm, respectively). LVMI decreased from 138.8 ± 18.7 g/m² to 126.0 ± 21.8 g/m² after 3 months of treatment. Left ventricular dimensions and ejection fraction did not change significantly compared with baseline values. The Doppler echocardiographic assessment of mitral E/A ratio, which is a marker of diastolic function, increased significantly from baseline. Except for a significant increase in mean serum lactate dehydrogenase activity, laboratory findings (including serum lipid concentrations) remained constant. No clinical adverse effects attributable to losartan were observed. Results of this study suggest that losartan is an effective, well-tolerated drug that reduces LVH, improves left ventricular diastolic functions, and controls systolic and diastolic blood pressures in patients with mild-to-moderate essential hypertension.     

QT-interval variability and autonomic control in hypertensive subjects with left ventricular hypertrophy

Left ventricular hypertrophy is a risk factor for sudden death. Malignant ventricular arrhythmias originate from altered cardiac repolarization. Ample data have described spatial abnormalities in cardiac repolarization [QT interval (QT) dispersion] in subjects with hypertension; more data are needed on temporal changes. This study was designed to assess the QT variability index (QTVI), the slope between QT and the RR interval (QT-RR(slope)) and spectral QT variability in subjects with arterial hypertension. The results were compared with those from a population at high risk of sudden death, i.e. patients with hypertrophic cardiomyopathy (HCM) who had received an implantable cardioverter/defibrillator (ICD), and those from normotensive control subjects. A total of 44 hypertensive subjects, six patients with HCM and an ICD and 33 control subjects underwent simultaneous short-term recording (256 beats) of QT, RR and systolic blood pressure variability, in the supine position, during controlled breathing. QTVI and spectral components of QT variability in the hypertensive group were significantly higher than in normotensive control subjects (P<0.001), but significantly lower than in patients with HCM and an ICD (P<0.001). The severity of left ventricular hypertrophy correlated significantly with QTVI and the ratio of low-frequency (LF) to high-frequency (HF) power obtained from the RR variability spectra (RR(LF/HF), slope=0.24, P<0.05; QTVI, slope=4.06, P<0.0001; intercept, slope=2.40, P<0.05; chi(2)=38.8; P<0.0001). The QT--RR slope was significantly higher only in patients with HCM and an ICD (P<0.001). In conclusion, the increased QTVI and the correlation of this index with left ventricular hypertrophy indicates that hypertension increases temporal cardiac repolarization abnormalities. At the level of the cardiac sinus node, this alteration is associated with increased sympathetic and reduced vagal modulation. As already noted in patients with HCM, the increased QTVI could be a factor responsible for triggering malignant ventricular arrhythmias in subjects with hypertension.     

自发性高血压大鼠NHE-1基因表达与左心室肥厚的相关性

目的：探讨自发性高血压大鼠（SHR）NHE-1基因表达与左心室肥厚的相关性.方法：对SHR和同源血压正常大鼠（WKY）进行平均血压、左室重量（LVW）和体重（BW）的测定，同时采用实时定量荧光检测两组大鼠心肌组织中NHE-1 mRNA的拷贝数.结果：SHR组与WKY组相比，SHR组的LVW、LVW/BW明显高于WKY组（r左室重=0.700，r左室重/体重之比=0.617，P＜0.01），大鼠的平均血压与LVW量、LVW/BW呈正相关（P＜0.01）；SHR组的心肌组织NHE-1 mRNA的表达增高（P＜0.01）.结论：SHR的心肌组织NHE-1 mRNA的表达增高，提示NHE-1可能参与心肌肥厚的发生、发展过程.     

丹参对自发性高血压大鼠左室肥厚及心脏局部醛固酮的作用

目的　探究长期应用丹参对自发性高血压大鼠 (SHR)左室肥厚的预防作用及其可能机制———抑制心脏局部醛固酮的作用。方法　实验动物采用WKY大鼠及SHR ,部分SHR给予丹参注射液腹腔注射 12周。测量收缩压、左心室重量指数 ;左心室组织切片用HE染色和VanGieson染色 ,全自动图象分析系统进行分析。用放免法测定心脏局部醛固酮含量。各组指标进行显著性检验。结果　与WKY大鼠相比较 ,SHR有较高的血压 ,左室胶原含量及心脏局部醛固酮含量升高 (P <0 .0 5 )。而应用丹参后 ,除收缩压外各指标均有显著性下降 (P<0 .0 5 )。结论　丹参能预防自发性高血压大鼠左室肥厚 ,抑制左室胶原合成 ,其机制可能于抑制心脏局部醛固酮作用有关     

丹参防治自发性高血压大鼠左室肥厚机制的研究

目的　观察丹参防治左室肥厚的作用机制。方法　用自发性高血压大鼠为心肌肥厚模型 ,18只 8周龄的自发性高血压大鼠随机分成三组 :一组于 8周时处死 ,另两组分别经腹腔注射丹参或蒸馏水[(1ml/ (kg·d) ]10周。测量大鼠尾动脉收缩压 (SBP)及左心室重量指数 (LVMI)。检测大鼠心肌组织中去甲肾上腺素 (NE)、多巴胺 (DA)、肾上腺素 (E)及超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶(GSH Px)、过氧化脂质 (LPO)、血管紧张素 Ⅱ (AngⅡ )的含量。结果　①丹参组大鼠SBP及LVMI指标与高血压组比较均明显降低 ;②丹参可抑制NE、DA含量的降低和E含量的增高 ;③丹参可增强心肌组织SOD和GSH Px 活性 ,减少LPO的生成 ;④丹参可降低左心室肥厚组织Ang Ⅱ含量的增高。结论　丹参能有效防治自发性高血压大鼠左室肥厚的发生。它作用机制与丹参调整和改善心脏局部儿茶酚胺、氧自由基代谢有关 ,而且还与丹参抑制体内肾素 -血管紧张素系统 (RAS)代谢相关。     

卡维地洛对自发性高血压大鼠左室心肌肥厚作用的细胞和分子水平研究

目的:观察基础和卡维地洛干预条件下,高血压大鼠和Wistar大鼠心脏成纤维细胞增殖细胞核抗原蛋白表达及脱氧核糖核酸合成变化对心肌纤维化的影响。方法:实验于2001-10/2002-12在解放军空军总医院临床试验中心及解放军第四军医大学唐都医院高血压实验室完成。实验选用12周龄血压176～190mmHg(1mmHg=0.133kPa)的高血压大鼠10只,培养心脏成纤维细胞,按随机数字法将其分为空白对照组和0.01,0.10,1.00,10.00μmol/L卡维地洛干预72h组;选择血压120～132mmHg的Wis-tar健康大鼠10只,培养心脏成纤维细胞为正常对照组。消化法培养大鼠心脏成纤维细胞,采用免疫组化法观察增殖细胞核抗原蛋白在心脏成纤维细胞细胞核表达的变化,3H-胸腺嘧啶核苷掺入法测定脱氧核糖核酸合成。结果:在基础条件下培养72h,高血压大鼠空白对照组的心脏成纤维细胞增殖细胞核抗原含量犤(131.2±11.0)A·mm2犦及3H-胸腺嘧啶核苷掺入量犤(606.0±54.7)min-1犦明显高于正常大鼠空白对照组犤(107.2±16.3)A·mm2,(495.2±49.8)min-1,t=2.725,3.3489;P<0.05犦。0.10,10.00μmol/L卡维地洛分别干预72h,高血压大鼠心脏成纤维细胞增殖细胞核抗原含量显著低于高血压大鼠空白对照组犤(96.6±9.78),(87.0±12.5),(69.2±11.3)A·mm2t=5.258,5.926,8.770,P<0.01犦;1.00,10.00μmol/L卡维地洛分别干预72h时,Wistar大鼠心脏成纤维细胞增殖细胞核抗原含量分别为(81.4±10.6),(72.2±10.8)A·mm2显著低于正常大鼠空白对照组犤t=2.956,P<0.05;t=3.994,P<0.01犦。0.10,1.00,10.00μmol/L卡维地洛分别干预72h时,高血压大鼠心脏成纤维细胞3H-胸腺嘧啶核苷掺入量分别为犤(452.0±35.9),(317.2±36.2)和(279.6±24.7)min-1犦均显著低于高血压大鼠空白对照组(t=5.261,9.838,12.153,P<0.01);Wistar大鼠组3H-胸腺嘧啶核苷均明显低于正常大鼠空白对照组犤(388.2±35.0),(322.6±32.7),(277.8±25.3)min-1,t=3.931,6.478,8.705,P<0.01犦。在不同浓度卡维地洛作用下,高血压大鼠心脏成纤维细胞的3H-胸腺嘧啶核苷掺入量随增殖细胞核抗原蛋白表达的增强而增高,两者呈显著正相关(r=0.856,P<0.01)。结论:卡维地洛不仅能抑制与脱氧核糖核酸合成密切相关的胸腺嘧啶核苷酸的活性,而且也能抑制增殖细胞核抗原的表达,直接影响了脱氧核糖核酸的复制,进而抑制心脏成纤维细胞增殖后的左室重构。     

丹参酮ⅡA对自发性高血压大鼠左室肥厚的影响及机制

目的观察丹参酮ⅡA对自发性高血压大鼠左室肥厚的作用,并探讨其作用机制.方法18只8周龄的自发性高血压大鼠随机分成3组一组于8周处死,另两组分别经腹腔注射丹参酮IIA和蒸馏水(1 g·kg-1·d-1),共10周.测量大鼠尾动脉收缩压(SBP)及左心室重量指数(LVMI).应用HE染色、VG染色、免疫组织化学的方法,结合计算机图像分析技术,检测心肌细胞的直径和面积、心肌组织胶原体积比例(CVF)、血管周围胶原面积和管腔面积比例(PVCA)以及蛋白激酶C(PKC)的表达.结果与8周龄的自发性高血压大鼠相比,18周龄大鼠的SBP、LVMI、心肌细胞的直径、面积、CVF、PVCA显著增加,PKC表达上调,丹参酮IIA治疗可抑制LVH的发展和心肌组织PKC的表达,但收缩压无明显改变.结论长期应用丹参酮ⅡA治疗可预防自发性高血压大鼠左室肥厚的形成,其机制可能与丹参酮ⅡA降低了心脏PKG的表达有关.     

Effect of carvedilol on pulse pressure and left ventricular hypertrophy in spontaneously hypertensive rats with adriamycin nephropathy

Recent studies indicated pulse pressure as a risk factor for left ventricular hypertrophy, myocardial infarction, congestive heart failure and stroke as well as chronic renal failure progression.The present study examined the effects of carvedilol and its combination with captopril on blood pressure, left ventricular hypertrophy, kidney vascular changes and kidney function in spontaneously hypertensive rats with adriamycin nephropathy.Four groups of 20 SHR each were involved: (1) control group: SHR; (2) ADR group: SHR treated with ADR (2 mg/kg i.v. twice in 20 days); (3) ADR-C group: SHR treated with ADR and carvedilol (30 mg/kg/day) and (4) ADR-CC group: SHR treated with ADR and carvedilol (30 mg/kg/day) and captopril (60 mg/kg/day). Systolic-, diastolic- and mean-pressures and pulse pressure were determined at weeks 6 and 12 after the second ADR injection; and body weight, creatinine clearance and proteinuria at weeks −3, 6 and 12. The rats were sacrificed at week 6 or 12, the weights of the left and right ventricles and kidneys measured and the kidney vascular index was calculated as described by Bader and Mayer.Both carvedilol alone and combined with captopril significantly reduced systemic blood pressure but the effect of the latter was more pronounced and registered from week 4 till the end of the study. Carvedilol and its combination with captopril significantly decreased SBP, DBP and MAP. They also decreased PP, prevented the development of LVH, and renal vascular changes and slowed the progression of chronic renal failure and these effects were stronger in the ADR-CC group than in the ADR-C group. The antihypertensive drugs failed to prevent proteinuria in ADR SHR. Significant positive correlations were found between PP (but not SBP, DBP and MAP) and both proteinuria and Ccr in all groups of rats.In conclusion, carvedilol alone, but more strongly in combination with captopril, significantly reduced blood pressure, PP, LVH, renal blood vessel changes and chronic renal failure progression.     

丹参酮ⅡA对自发性高血压大鼠左室肥厚的作用及其机制

目的:观察丹参酮IIA对自发性高血压大鼠左室肥厚的作用,并研究其对心肌原癌基因c-fosmRNA表达的影响。方法:18只8周龄的自发性高血压大鼠随机分成3组:对照组于8周处死,另两组分别经腹腔注射丹参酮IIA1mL/(kg·d)(丹参组)(和蒸馏水1mL/(kg·d)(高血压组),共10周。测量大鼠尾动脉收缩压(SBP)及左心室重量指数(LVMl)。应用HE染色、VG染色、免疫组织化学的方法,结合计算机图像分析技术,检测心肌细胞的直径和面积、心肌组织胶原体积比例(CVF)、血管周围胶原面积和管腔面积比例(PVCA)。用逆转录聚合酶链反应(RT-PCR)检测心肌细胞原癌基因c-fosmRNA的表达。结果:与对照组的自发性高血压大鼠相比,高血压组大鼠的SBP、LVMI、心肌细胞的直径、面积、CVF、PVCA显著增加,c-fos表达明显,丹参酮IIA治疗可抑制左室肥厚(LVH)的发展和心肌细胞c-fosmRNA的表达,但收缩压无明显改变。结论:长期应用丹参酮IIA治疗可预防自发性高血压大鼠LVH的形成,其机制可能与丹参酮IIA抑制了心肌细胞c-fosmRNA的表达有关。     

Regression of left ventricular hypertrophy with moexipril, an angiotensin-converting enzyme inhibitor, in hypertensive patients

Left ventricular hypertrophy (LVH) is a common complication of essential hypertension and an independent risk factor for the development of cardiovascular disease. Therefore, antihypertensive treatment should decrease blood pressure (BP) and reverse LVH. However, antihypertensive drugs have been shown to have different effects on LVH despite similar effects on BP reduction. Although lowering BP produces a beneficial effect on LVH per se, meta-analyses of clinical trials have indicated that angiotensin-converting enzyme (ACE) inhibitors decrease left ventricular mass (LVM) to a greater extent than do some other antihypertensives. The aim of this study was to evaluate the effect of a 24-week treatment with the ACE inhibitor moexipril (15 mg once daily) on the regression of LVH in hypertensive patients. This was a multicenter, international, single-blind, single-group, nonrandomized study. After a wash-out placebo period of 2 weeks, 15 mg moexipril once daily was administered for 24 weeks followed by a 2-week follow-up placebo period. Subjects with mild to moderate essential hypertension were screened; those with LVH [defined as an LVM indexed for body surface area (LVMIs) >111 g/m in men and LVMIs >106 g/m in women] were eligible to participate in this study. Echocardiograms were recorded on videotape and sent to a centralized laboratory for reading by 2 independent experts blinded for treatment, center, and visit; the mean values of these readings were calculated and used for analysis. Valid echocardiographic data were obtained from 72 patients (50 males, 22 females) with a mean age of 49 +/- 11 years. Analysis showed significant decrease of LVMIs (121 +/- 20 versus 103 +/- 17 g/m; P < 0.001) and BP (152 +/- 12/96 +/- 9 versus 140 +/- 13/86 +/- 9 mm Hg; P < 0.001) with moexipril. For patients who met LVMI inclusion criteria after centralized, blinded readings, the decrease from baseline in LVMIs was 23.4 g/m. The decrease in LVMIs was independent from the regression to the mean phenomenon as observed from the follow-up placebo period. Moexipril 15 mg once daily administered for 24 weeks resulted in a significant reversal of LVH in patients with essential hypertension. The result compares favorably with results previously obtained in trials of similar duration with other ACE inhibitors.     

缬沙坦对高血压伴左室肥厚患者心功能的影响

目的　研究缬沙坦对高血压左室肥厚患者心功能影响。方法　采用缬沙坦与咪哒普利 2组治疗 ,观察 2组高血压左室肥厚患者心功能的变化。结果　 2组舒张功能 (VtiE/VtiT)治疗前后比较有显著差异 ( P <0 0 5 ) ,VtiE/VtiT明显上升 ,收缩功能 (EF、FS)治疗前后比较无显著变化 (P >0 0 5 ) 2组间比较无显著差异 (P >0 0 5 )。结论　缬沙坦明显改善心脏舒张功能。     

多普勒超声心动图评价拉西地平对高血压患者左室肥厚的逆转作用

目的探讨拉西地平对高血压患者左室肥厚（LVH）的逆转作用。方法对53例高血压患者,在服用拉西地平治疗前,持续服药3个月后及持续服药6个月后,观察其对左室肥厚的逆转作用。结果服用拉西地平治疗3个月及6个月后,患者血压显著下降,左室肥厚逆转。结论服用拉西地平不仅能降低血压,长期服用还能逆转高血压引起的左室肥厚。     

厄贝沙坦、硝苯地平及美托洛尔逆转高血压病左心室肥厚的效果观察

目的比较厄贝沙坦、硝苯地平及美托洛尔治疗原发性高血压逆转左心室肥厚的作用。方法选择150例原发性高血压伴左心室肥厚患者,随机分为厄贝沙坦组(A组)、硝苯地平控释片(B组)及美托洛尔组(C组)各50例。全组患者未曾接受降压治疗(或仅用过利尿剂)或已停用降压药物3周以上。A组服用厄贝沙坦150~300 mg,1次/d,B组服用硝苯地平控释片30~60 mg,1次/d,C组服用美托洛尔25~50 mg,2次/d;疗程均为24周。观察治疗前后血压及超声心动图变化。结果各组患者治疗后血压均显著降低(P<0.01),组间降压幅度无明显统计学差异(P>0.05)。各组患者治疗后舒张期左室后壁厚度、舒张期室间隔厚度、左室舒张末期内径及左室重量指数均有显著改善(P<0.05,0.01)。而且A组左室重量指数下降优于B、C组(P<0.05)。结论三种药物在有效降压的同时均可逆转左心室肥厚,厄贝沙坦对左心室肥厚的逆转作用相对更强。     

Epidemiology of left ventricular hypertrophy in hypertension: implications for the clinic

Introduction: Left ventricular hypertrophy (LVH) is a common complication to hypertension, indicating the presence of hypertensive heart disease, which puts the patient at a very high risk for subsequent clinical cardiovascular events like sudden cardiac death, stroke, myocardial infarction and heart failure.

Areas covered: The epidemiology of LVH has changed in recent years as a consequence of the development of new diagnostic tools and demographic changes in hypertensive populations.

Expert commentary: In individual hypertensive patients, the presence and type of LVH and associated systolic and diastolic myocardial dysfunction is modified by the co-presence of other cardiovascular risk factors and comorbidities and as well as activation of the reninangiotensin-aldosterone system and other molecular mechanisms involved in LVH pathophysiology. The purpose of this review is to give a clinical update on LVH in hypertension.     

Relevance of echocardiographic left ventricular hypertrophy in mild hypertension

The current diagnostic criteria for uncomplicated mild hypertension inadequately distinguish the subgroup actually at increased risk for cardiovascular sequelae, from the large group not at increased risk, and therefore unlikely to benefit from current pharmacological intervention. Although finding of electrocardiographic left ventricular hypertrophy indicates increased risk, the ECG lacks sufficient sensitivity to be diagnostically useful in mild hypertension. It can be argued that echocardiographic screening for LV hypertrophy may better detect the subpopulation of mildly hypertensive patients at increased risk. The known relationships between ambulatory BP, LV hypertrophy and prognosis support this hypothesis. Further study is required, however, before echocardiography can be advocated for routine application to the diagnosis and management of mild hypertension.