抑制泛素特异性蛋白酶7改善血管紧张素Ⅱ诱导的心肌细胞肥大

目的 探究泛素特异性蛋白酶7(USP7)抑制剂FT671在血管紧张素Ⅱ(AngⅡ)诱导的H9c2细胞肥大中的作用和潜在机制。方法 将H9c2细胞随机分为四组：对照组、FT671组、AngⅡ组、FT671+AngⅡ组。利用α-actinin细胞免疫荧光染色检测心肌细胞表面积;Western blot检测心房钠尿肽(ANP)、脑钠肽(BNP)、B细胞淋巴瘤-2(Bcl-2)、B细胞淋巴瘤-2相关X蛋白(Bax)、白细胞介素-6(IL-6)、单核细胞趋化蛋白-1(MCP-1)、肿瘤坏死因子-α(TNF-α)、NOD样受体热蛋白结构域相关蛋白3(NLRP3)以及NADPH氧化酶4(Nox4)的蛋白表达水平;RT-PCR检测ANP、BNP、β-肌球蛋白重链(β-MHC)、IL-6、MCP-1、TNF-α的mRNA表达;TUNEL染色检测细胞凋亡情况;细胞计数试剂8(CCK8)实验检测各组细胞活力;活性氧(ROS)染色检测细胞内氧化损伤水平。结果 与对照组相比,AngⅡ组USP7蛋白表达明显增加,而使用FT671后,USP7表达明显被抑制。与AngⅡ组相比,FT671+AngⅡ组心肌细胞面积减小;...     

心肌特异性Hsp27对ISO诱导小鼠心肌肥厚的保护作用

目的探讨人热休克蛋白(Hsp27)基因产物对异丙肾上腺素(ISO)诱导的小鼠心肌肥厚的影响。方法以本研究室建立的心肌特异性表达Hsp27转基因(TG)小鼠为模型,腹腔注射ISO[30mg/(kg·d)]共7d。实验在规定时间结束后,测定心脏质量与胫骨长度的比值(HW/TL)、心脏二维超声(echo),Masson三色染色观察心肌纤维化改变,各组均以野生型鼠(WT)为对照组。结果(1)ISO处理使TG鼠和WT鼠的HW/TL与生理盐水处理对照组比较分别增加了7·46%和17·65%,WT组增加比率有统计学差异(P<0·01);(2)echo显示ISO使TG心脏收缩期后壁厚度增加(P<0·05),而WT组心脏前、后壁在收缩、舒张末期均有显著的增加(P<0·05~0·01)。(3)每搏输出量、短轴缩短率、心脏射血分数没有统计学差异。WT鼠心肌纤维化明显多于TG鼠。结论Hsp27可显著抑制ISO诱导的小鼠早期心肌重构。其机制有待进一步探讨。     

泛素蛋白酶体系在扩张型心肌病发生发展中的作用研究进展

泛素蛋白酶系统为体内主要蛋白质降解途径之一,为大型ATP依赖的酶学级联系统,广泛存在于各类细胞,参与细胞周期调控、包膜蛋白运输、细胞凋亡、抗原呈递、炎症反应等多种生理或病理过程。本文就泛素蛋白酶体系在扩张型心肌病病理过程中的作用作一综述。     

蜂胶总黄酮对异丙肾上腺素致病理性心肌肥厚小鼠心功能的影响

目的探讨蜂胶总黄酮(TFP)对异丙肾上腺素(ISO)诱导的病理性心肌肥厚(PCH)小鼠心功能的影响。方法 8周龄雄性小鼠20只,适应性饲养1 w,随机分为对照组、ISO组、TFP组及ISO+TFP组。预先口服TFP(25 mg·kg-1·d-1)7 d之后持续给予ISO(25 mg·kg-1·d-1)7 d制备小鼠PCH模型。试验结束后24 h进行超声心动图检测,计算心脏重量/体重(HW/BW)比值,检测心房钠尿肽(ANP)的mRNA和蛋白表达水平。结果与对照组比较,ISO组小鼠收缩期左室内径(LVIDs)、舒张期左室内径(LVIDd)及左室收缩末期容积(LVVs)均明显升高,而射血分数(EF)、缩短分数(FS)明显降低,HW/BW及ANP蛋白、mRNA水平亦明显升高(P0.05);与ISO组比较,TFP+ISO组LVIDs、LVIDd及LVVs均明显降低,而EF、FS明显升高(P0.05),HW/BW及ANP蛋白、mRNA水平亦明显降低(P0.05)。结论 TFP可对抗ISO诱导的小鼠PCH,并对心功能损伤具有保护作用。     

己酮可可碱对心肌肥厚大鼠基质金属蛋白酶2和9表达的影响

目的观察基质金属蛋白酶2和9在心肌肥厚大鼠模型中的变化,并采用己酮可可碱进行干预,以确定己酮可可碱对基质金属蛋白酶的影响及其在心肌肥厚过程中的作用。方法24只雄性SD大鼠随机分为对照组、去甲肾上腺素造模组(模型组)和去甲肾上腺素 己酮可可碱组(治疗组)。采用VG染色评价组织胶原表达,并测定心肌组织胶原含量,免疫组织化学法检测心肌组织基质金属蛋白酶2和9的蛋白表达。结果模型组大鼠发生左心室肥厚,胶原含量显著高于对照组(1.929±0.514mg/g比1.009±0.442mg/g,P<0.01);基质金属蛋白酶2和9表达(分别为131.1±9.8、125.3±4.1)显著低于对照组(P<0.01)。己酮可可碱治疗组心肌总胶原含量较模型组显著降低(1.151±0.215mg/g,P<0.01);基质中基质金属蛋白酶2和9的表达(分别为153.5±6.9、149.5±5.3)较模型组显著增高(P<0.01)。结论己酮可可碱能有效防治心肌肥厚的发生及细胞外基质重塑,这一效应可能与其降低心肌组织中基质金属蛋白酶2和9的高表达有关。     

压力超负荷性心肌肥厚大鼠心肌细胞内钙激活蛋白酶活性分布的研究

目的研究大鼠心肌肥厚时,钙激活蛋白酶(Calpain)在心肌细胞胞浆和细胞核的活性分布,并探讨细胞核钙摄取的改变,以进一步阐明心肌肥厚的发生机制.方法将100只健康雄性Wistar大鼠(150～200g)随机分为对照组(n＝50)和腹主动脉缩窄组(n＝50),制备腹主动脉缩窄大鼠心肌肥厚模型、差速离心和密度梯度离心提纯心肌细胞核,荧光法测酶活性,以45Ca2+测定细胞核摄取能力.结果与对照组相比,腹主动脉缩窄组大鼠左心室重量指数增加,伴有明显的血流动力学异常,有非常显著性差异(P＜0.01);其心肌细胞核Calpain活性亦增加40.78%,有显著性意义(P＜0.05);细胞浆Calpain活性下降21.71%,有非常显著性意义(P＜0.05).对照组心肌Calpain在细胞浆的活性显著高于在细胞核的活性,有非常显著性意义(P＜0.01),而腹主动脉缩窄组心肌Calpain在细胞核的活性与在细胞浆的活性无显著差异;细胞核45Ca2+摄入量也显著增加(较对照组高28%～97%,P＜0.01).结论肥厚心肌Calpain由细胞浆向细胞核转位、细胞核内Calpain活性增加,细胞核钙摄取能力增强,提示压力超负荷时Ca2+与Calpain调节的细胞核反应水平加强,可能在介导心肌肥厚的细胞核功能调控中起重要作用.     

PCBP2在压力负荷诱导的小鼠心肌肥厚发生中的作用

目的 探讨PCBP2在压力负荷诱导的小鼠心肌肥厚发生过程中的作用。方法 选取8～10周龄的雄性C57BL/6小鼠20只,体重23～28 g;随机分为2组,每组各10只,分别施以主动脉缩窄术（TAC组）和假手术（Sham组）。术后4周应用超声心动图评价小鼠的心脏功能,应用心脏重量与体重之比（HW/BW）定量评价心肌肥厚程度。Real-time PCR检测心肌肥厚标志物Nppa、β-MHC（Myh7）的mRNA水平,同时检测PCBP2 mRNA水平。Western blot方法检测Nppa、β-MHC及PCBP2的蛋白水平。比较分析两组之间的差异。结果 与Sham组相比,TAC组小鼠的心肌肥厚程度明显增加（TAC组 vs Sham组=8.23±1.88 mg/g vs 4.89±0.68 mg/g）,左心室射血分数（TAC组 vs Sham组=59.15±3.58% vs 41.38±2.22%）及短轴收缩率（TAC组 vs Sham组=43.87±1.37% vs 33.61±0.92%）明显降低（P<0.05）。TAC组的心肌肥厚标志物Nppa、β-MHC 的mRNA水平及蛋白水平均明显高于Sham组（P<0.05）。然而,TAC组PCBP2 mRNA水平及蛋白水平却明显低于Sham组（P<0.05）,与心肌标志物Nppa、β-MHC的变化趋势相反。结论 PCBP2在压力负荷诱导的小鼠心肌肥厚发生过程中起着负性调节作用,上调PCBP2表达可能会抑制心肌肥厚的发展。     

曲美他嗪对异丙肾上腺素所致大鼠心肌肥厚的影响

目的探讨曲美他嗪（TMZ）对异丙肾上腺素（ISO）致大鼠心肌肥厚的影响及可能的作用机制。方法30只Sprague-Ddwley（SD）大鼠,随机分为3组。正常对照组、ISO组、TMZ组,每组10只。通过大剂量注射ISO制成心肌肥厚模型,以TMZ干预,观察心肌组织病理学变化和心肌细胞超微结构改变,计算心脏质量/体质量（HW/BW）,测定心肌三磷酸腺苷（ATP）、丙二醛（MDA）、超氧化物歧化酶（SOD）和血清乳酸脱氢酶（LDH）、肌酸激酶（CK）含量。结果TMZ组与ISO组比较,HW/BW、LDH、CK、SOD和ATP有显著差异（P<0.05）,而与正常对照组比较无显著差异。TMZ组心肌组织病理损伤程度及细胞超微结构改变程度,较ISO组明显减轻,而接近正常对照组。结论TMZ可拮抗ISO所致的大鼠心肌肥厚,其机制可能与改善心肌能量代谢、提高组织对缺氧的耐受力、消除氧自由基等有关。     

Rho激酶抑制剂对异丙肾上腺素诱导大鼠心肌肥厚的影响

目的 研究Rho激酶抑制剂对异丙肾上腺素(isoproterenol,Iso)诱导大鼠心肌肥厚的影响及其机制.方法 40只雄性Wistar大鼠随机分为5组:空白对照组、Iso模型组、法舒地尔(fasudil,Fas)低剂量组、高剂量组及卡托普利(captopril,Cap)组,每组8只.除空白对照组外,各组皮下注射Iso建立大鼠心肌肥厚模型.给药结束后分别测定各组大鼠体重(BW)、心脏重量(HW),计算心脏重量指数(HW/BW);测定左室收缩压(LVSP)、左室舒张末压(LVEDP)、左心室压力上升及下降最大速率(±dp/dtmax)等指标;取心肌组织作病理学检测;RT-PCR测定心肌组织RhoA、Rho激酶mRNA表达.结果 Iso模型组大鼠HW/BW增大;LVEDP增加,而LVSP、±dp/dtmax下降;心肌细胞直径增大、胶原纤维增生;左心室组织RhoA、Rho激酶mRNA表达上调.使用Fas和Cap干预,上述指标均出现不同程度的改善.结论 肾上腺素β受体兴奋所诱导的心肌肥厚伴有Rho激酶信号通路的激活,Rho激酶抑制剂可改善Iso所致心肌肥厚动物模型的心功能和病理学变化.     

腺苷A1受体激动剂2-氯化腺苷抑制异丙肾上腺素诱导大鼠心肌肥厚的作用及机制

目的通过观察腺苷A1受体激动剂2-氯化腺苷(2-CADO)对异丙肾上腺素所致大鼠心肌肥厚的抑制作用及能量代谢的改变,探讨腺苷A1受体激动剂对肥厚心肌能量代谢的调节作用及其可能的作用机制。方法大剂量异丙肾上腺素皮下注射建立大鼠心肌肥厚模型。SD大鼠40只,雌雄不限,分为空白对照组、肥厚模型组、2-CADO组[2-氯化腺苷0.6 mg/(kg.d)腹腔注射]、普萘洛尔组[28 mg/(kg.d)普萘洛尔灌胃],每组10只。造模完毕第2天给药,连续8周。检测大鼠全心质量指数(HMI)、左心质量指数(LVMI);取左心室组织进行Masson染色,观察细胞横径(TDM)改变;碱水解法进行羟脯氨酸(Hyp)含量测定;紫外分光光度法检测心肌组织乳酸(LA)和游离脂肪酸(FFA)含量;激光共聚焦显微镜定量检测线粒体膜电位(MMP)。结果与空白对照组相比,肥厚模型组HMI、LVMI显著上升,心肌组织形态发生肥厚样改变;Hyp、LA和FFA含量显著升高,MMP下降了44%。与肥厚模型组相比,2-CADO组HMI、LVMI下降,TDM明显降低,Hyp、LA和FFA含量显著降低,MMP上升了50%。结论 2-CADO可以抑制异丙肾上腺素导致的心肌肥厚,其机制可能与改善肥厚心肌的能量代谢有关。     

Wnt信号通路在心肌肥厚中作用的研究进展

Wnt信号通路在细胞分化、胚胎发育、肿瘤发生及血管的形成等方面均发挥重要作用。近年来研究发现,在不同水平干预Wnt信号通路可影响心肌肥厚的发生,本文主要阐述Wnt信号通路与心肌肥厚之间相互关系的研究进展,探讨可能抑制心肌肥厚的新靶点。     

Left ventricular hypertrophy on long-term cardiovascular outcomes in patients with ST-elevation myocardial infarction

Abstract

Background: Left ventricular hypertrophy (LVH) had been associated with increased adverse cardiovascular events in hypertensive patients. Prognostic significance of LVH in patients with ST-elevation myocardial infarction (STEMI) is not established. This study aimed to investigate prognostic impact of LVH on the patients with STEMI. Methods: We analyzed the data and clinical outcomes of 30-day survivors with STEMI who underwent successful coronary intervention from 2003 to 2009. Definition of LVH was LV mass index (LVMI) >115?g/m² in male and >95?g/m² in female. Patients were classified into a LVH group and a non-LVH group. Occurrence of major adverse cardiovascular events (MACE; death, recurrent MI, target vessel revascularization (TVR)) within 5 years was evaluated. Results: We enrolled 418 patients and mean follow-up duration was 43?±?17 months. Two hundred and fourteen patients (51%) had LVH. The survival of the patients with LVH was significantly worse than the patients without LVH (log-rank p?=?0.024). In a multivariate regression model, the presence of LVH was independently associated with increased risk for all-cause mortality (OR, 2.37; 95% CI, 1.096–5.123, p?=?0.028). When the end points were analyzed based on LVH severity, all-cause mortality was significantly correlated with LVH severity (p?=?0.011). The severe LVH was independently associated with increased risk for all-cause mortality (OR, 5.110; 95% CI, 1.454–17.9, p?=?0.001). Conclusion: LVH was associated with increased rate of adverse clinical outcomes in 30-day survivors after STEMI, who underwent successful coronary intervention.     

Electrocardiographic and echocardiographic detection of myocardial infarction in patients with left-ventricular hypertrophy. The LIFE Study

BACKGROUND: Left-ventricular hypertrophy (LVH) is a recognized risk factor for myocardial infarction (MI). However, detection of MI by standard electrocardiographic (ECG) criteria may be hampered in patients with LVH. In this setting of hypertensive LVH, the accuracy of two-dimensional (2D) echocardiography in detecting incident MI is unknown. Thus, we compared the accuracy of 2D echocardiography with Minnesota-code ECG criteria in detecting incident MI, adjudicated during serial evaluation in patients with hypertension and LVH. METHODS: In the ECG substudy of the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) Study, complete baseline wall-motion (WM) evaluation was obtained in 904 hypertensive patients with ECG LVH who did not have a left-bundle branch block. Electrocardiography and echocardiograms obtained at annual follow-up visits were evaluated for ECG Q-waves by Minnesota codes and WM abnormalities, respectively (mean follow-up, 4.8+/-0.9 SD years). Occurrence of incident clinical MI during follow-up was adjudicated by an expert end-point committee. RESULTS: In two logistic models adjusting for confounders, incident MI was independently associated with either incident Q-waves by the Minnesota code (odds ratio [OR], 6.1; 95% confidence interval [CI], 2.4-15.3) or incident and worsened WM abnormalities (OR, 11.9; 95% CI, 4.5-32.0), and the association was stronger for WM abnormalities than for Q-waves (P < .0001). Detection of incident MI by ECG or 2D echocardiography was obtained with sensitivities of 29% and 68% and specificities of 95% and 84%, respectively. CONCLUSIONS: Wall-motion abnormalities on serial 2D ECGs recognize incident MI better than do Minnesota-code ECG criteria during follow-up of patients with hypertension and LVH.     

Pathophysiologic significance of left ventricular hypertrophy in dilated cardiomyopathy

Background and hypothesis: Patients with dilated cardiomyopathy (DCM) with left ventricular hypertrophy (LVH) have been found to have a better prognosis than patients without LVH. However, the pathophysiologic mechanism for that has not been investigated. We sought to clarify the pathophysiologic significance of LVH in DCM. Methods: We performed isoproterenol infusion echocar-diography (0.02 m?g/kg/min) in 17 patients with DCM, and measured plasma epinephrine and norepinephrine levels at rest and at the end of ergometer exercise in 14 of the 17 patients. Patients were classified into groups according to the presence (9 patients) (LVH+) or absence (8 patients) (LVH-) of LVH. Left ventricular hypertrophy was defined as an inter-ventricular thickness or posterior wall thickness ≥13 mm. Results: Although there was no significant difference between groups in fractional shortening at rest during isoproterenol infusion, fractional shortening was significantly higher in the LVH (+) group than in the LVH (-) group (29 ± 9 vs. 17 ± 8%;p<0.025). Although there was no significant difference in plasma norepinephrine level, it was significantly lower in the LVH (+) group than in the LVH (-) group (233 ± 169 vs. 519 ± 258 pg/ml;p<0.05) at the end point of the exercise. Conclusion: Systolic reserve, represented by the response to isoproterenol, is greater in patients with DCM with LVH than in those without LVH, and a lower plasma level of norepinephrine is needed to activate the myocardium during ex ercise in patients with DCM with LVH. This pathophysiologic characteristic could be one of the mechanisms which explain a better prognosis in patients with DCM with LVH.     

血脂康胶囊对自发性高血压大鼠心肌肥厚的早期干预研究

目的研究血脂康胶囊对幼年自发性高血压大鼠（spontaneous hypertensive rat, SHR）心肌肥厚的影响。方法24只6周龄雄性SHR分为低剂量血脂康胶囊组（A组,n=8）、高剂量血脂康胶囊组（B组,n=8）和安慰剂组（C组,n=8）,另设WKY（Wistar—kyoto rats）组（W组,n=8）。A组和B组分别以血脂康胶囊20mg·kg^-1·d^-1和200mg·kg^-1·d^-1 0．9％氯化钠溶液溶解后灌胃;C组和W组以等容积0．9％氯化钠溶液灌胃,连续8周。腹主动脉采血,用酶联免疫吸附测定方法测定血浆一氧化氮（NO）和氧化低密度脂蛋白（oxidized low-density lipoprotein, ox-LDL）浓度;超声心动图测定室间隔舒张期厚度（interventricular septal thickness, IVSd）和左心室后壁舒张期厚度（left ventricular posterior wall thickness, LVPWd）;取心肌标本,称取左心室质量,计算左心室质量指数（left ventricular mass index, LVMI）,制备心肌组织石蜡切片,苏木精一伊红染色,观察心肌细胞直径和心肌细胞面积。结果与W组比较,C组血浆一氧化氮浓度降低,ox-LDL浓度升高,LVMI、IVSd、LYPWd、心肌细胞直径和心肌细胞面积均增加,差异有统计学意义（P〈0．05）;与C组比较,B组上述指标明显改善,差异有统计学意义（P〈0．05）;而A组仅血浆一氧化氮和ox—LDL浓度改善。结论自发性高血压大鼠发生心肌肥厚,血脂康胶囊早期干预可改善SHR心肌肥厚。     

Role of E3 ubiquitin ligases in insulin resistance

E3 ubiquitin ligases are a large family of proteins that catalyse the ubiquitination of many proteins for degradation by the 26S proteasome. E3 ubiquitin ligases play pivotal roles in the process of insulin resistance and diabetes. In this review, we summarize the currently available studies to analyse the potential role of E3 ubiquitin ligases in the development of insulin resistance. We propose two mechanisms by which E3 ubiquitin ligases can affect the process of insulin resistance. First, E3 ubiquitin ligases directly degrade the insulin receptor, insulin receptor substrate and other key insulin signalling molecules via the UPS. Second, E3 ubiquitin ligases indirectly regulate insulin signalling by regulating pro‐inflammatory mediators that are involved in the regulation of insulin signalling molecules, such as tumour necrosis factor‐α, interleukin (IL)‐6, IL‐4, IL‐13, IL‐1β, monocyte chemoattractant protein‐1 and hypoxia‐inducible factor 1α. Determining the mechanism by which E3 ubiquitin ligases affect the development of insulin resistance can identify a novel strategy to protect against insulin resistance and diabetes.     

Decreased adrenergic response in hypertensive patients without left ventricular hypertrophy

To analyze the adrenergic responses and to compare them between hypertensive patients with and without left ventricular hypertrophy (LVH), left ventricular (LV) fractional shortening (FS) and end-systolic wall stress (ESS) were measured by echocardiography and the inotropic response to the infusion of isoproterenol (0.02 μg/kg/min for 5 min) was studied in 25 hypertensive patients without LVH [H(-)] and 30 hypertensive patients with LVH [H(+)]. LVH was determined by echocardiography. Age, gender, heart rate, systolic and diastolic blood pressures, LV end-systolic and end-diastolic diameters, and FS were matched between the groups. The tests were performed before introduction of antihypertensi ve treatment or 4 weeks after its discontinuation. ESS showed a significant inverse linear relation with FS in all the subjects before isoproterenol infusion. The inotropic response to isoproterenol was measured as the increase of FS corrected for the decrease of ESS (ΔFS/-ΔESS), that is, the slope of the change of the relation between FS and ESS. The change in ΔFS/-ΔESS was significantly smaller (0.49 ± 0.15 cm²/g, mean ± SD) in H(?) than in H(+) patients (1.01 ± 0.57 cm²/g) (p < 0.001). It is concluded that, compared with the H(+) group, adrenergic response is depressed in H (?) patients. This depression might be etioloically related to the phenomenon that LVH did not develop in the H(?) group in spite of the same level of pressure load as in the H(+) group.     

老年高血压左室肥厚患者的室性心律失常与心肌缺血

目的　了解老年原发性高血压左室肥厚患者的室性心律失常、心肌缺血的特点及两者的关系。方法　 90例老年 (≥ 6 0岁 )高血压患者经超声心动图测定左室质量指数 (LVMI) ,分为左室肥厚 (A组 )和非左室肥厚 (B组 )。经2 4h动态心电图测定 2 4h室性早搏总数 (VPCs)、Lown’s分级、ST段压低程度、持续时间及 2 4h发作次数。结果　A组室性心律失常的发生率明显增加 (P <0 .0 5 ) ,室性早搏 :75 %比 5 4% ,Lown’s 3～ 4级 :2 6 %比 4%。A组发作性ST段压低的发生率高 ,缺血持续时间长 (5 0 %比 15 % ,P <0 .0 5 )。所有缺血发作均为无症状性。室性心律失常与心肌缺血的昼夜节律变化基本相同。结论　无冠心病临床证据的老年原发性高血压左室肥厚患者的室性心律失常及心肌缺血的发生率增加 ,两者的昼夜节律变化基本相同     

Selection of optimal recording sites for limited lead body surface potential mapping in myocardial infarction and left ventricular hypertrophy

A lead selection algorithm was applied to find optimal recording sites for limited lead body surface potential maps. The studied population consisted of a set of 117 lead body surface potential maps recorded from 744 subjects (229, normal; 278, with myocardial infraction [MI]; and 237, with left ventricular hypertrophy [LVH]). One generic lead set derived from all disease groups was found. Also found were 3 disease-specific lead sets (normal, MI, and LVH) and one specific to abnormal subjects (MI and LVH combined). The performance of each lead set in estimating data from other disease groups was largely similar. This was with the exception of leads specific to LVH in the estimation of normal data and normal leads in the estimation of LVH data. Here, the difference was found to be significant (P < .001). The top 6 recording sites in each lead set did not occupy the same positions as the 6 precordial leads.Although disease-specific lead sets are of limited practical use, this study has illustrated that, largely, there is little difference between the performance of different lead sets. The suboptimality of the 6 precordial leads has also been illustrated.     

Treadmill exercise test in children with cardiomyopathy and postmyocarditic myocardial hypertrophy

Summary The treadmill exercise test with the Bruce protocol was performed in three patients with postmyocarditic myocardial hypertrophy (PMH) and ten patients with cardiomyopathy, including three with dilated cardiomyopathy (DCM), five with hypertrophic obstructive cardiomyopathy (HOCM), and two with hypertrophic and nonobstructive cardiomyopathy (HCM). The endurance time was below the normal level in all but one case and was normal or near normal in the three cases with PMH. ST depression was observed in five cases, none of which were of HCM. A marked increase in amplitude of the negative phase of the P wave in V₁ was observed in one patient with DCM. The response of blood pressure during the exercise was abnormal in patients with DCM and HCM but was normal in PMH.