老年人收缩期高血压左室肥厚与心律失常关系的探讨

目的探讨老年人收缩期高血压（ＯＩＳＨ）左室肥厚（ＬＶＨ）与心律失常的发生及其关系。方法对９６例ＯＩＳＨ患者进行超声心动图和Ｈｏｌｔｅｒ检查,比较有ＬＶＨ及无ＬＶＨ两组各类心律失常的发生情况。结果９６例ＯＩＳＨ患者并发ＬＶＨ者６２例（６４．６％）;ＬＶＨ组复杂性房性与室性心律失常例数分别为５５例（８８．７％）与４８例（７７．４％）,其构成比显著高于无ＬＶＨ组的３５．３％（１２例）与３２．４％（１１例）（均为Ｐ＜０．０１）。结论ＯＩＳＨ患者ＬＶＨ与复杂性房性和室性心律失常密切相关。     

冠状动脉血流储备与高血压左室肥厚患者室性心律失常的关系

对２２例正常人（Ａ组）、３０例高血压无左室肥大（ＬＶＨ）的病人（Ｂ组）及４０例高血压伴ＬＶＨ的病人（Ｃ组）的冠状动脉血流储备（ＣＦＲ）用经食道多普勒超声的方法进行了检查，以研究室性心律失常的发生与高血压伴ＬＶＨ及ＣＦＲ的可能关系。研究发现，与Ｂ组病人相比，Ｃ组病人ＣＦＲ显著降低，室性心律失常及复杂室性心律失常的发生率显著增高（分别为９０％，６０％比３０％，１０％，Ｐ＜０．０１）；Ｃ组病人中有ＣＦＲ降低者室性心律失常及复杂室性心律失常的发生率最高（９６．８％及６７．７％）．Ｃ组病人中无ＣＦＲ降低者，其室性心律失常及复杂室性心律失常之发生率与高血压无ＬＶＨ但有ＣＦＲ降低者相似（分别为６６．７％，２２．２％及６０％，２０％）。研究结果提示，在高血压病人ＬＶＨ及ＣＦＲ降低是室性心律失常发生的两个相加作用的危险因素。     

血管紧张素转换酶基因多态性与高血压左室肥厚的关系

目的探讨血管紧张素转换酶（ＡＣＥ）基因多态性与高血压左室肥厚的关系。方法对１０４例高血压病患者，采用二维引导下的Ｍ型超声心动图检测有无左室肥厚（ＬＶＨ），同时作２４小时动态血压监测，采血检测ＡＣＥ基因多态性（ＰＣＲ方法）。１１３例正常人作基因频率检测。结果（１）高血压ＬＶＨ（＋）与ＬＶＨ（－）两组动态血压指标除夜间平均ＳＢＰ、平均动脉压（ＭＡＰ）差异有显著性外，２４小时及白天平均ＳＢＰ、ＤＢＰ、ＭＡＰ和夜间平均ＤＢＰ两组间差异均无显著性。（２）ＬＶＨ（＋）组Ｉ基因频率明显高于ＬＶＨ（－）组，ＬＶＨ（＋）组Ｉ基因型明显高于ＬＶＨ（－）组。（３）１１３例正常人基因型频率分布：Ｉ为０．５８，Ｄ为０．４２。结论本研究提示，ＡＣＥ基因多态性与左室肥厚明显相关，Ｉ基因型者似更易发生左室肥厚。ＡＣＥ基因型频率分布东方人与西方人不同。     

高血压病左室结构功能变化及血浆内皮素的相关性

目的：探讨高血压病患者左室结构,功能变化与血浆内皮素（ＥＴ）的关系。方法：原发性高血压不伴左室肥厚（ＬＶＨ）组（ＥＨ）３５例,伴ＬＶＨ组（ＥＨ＋ＬＶＨ）２８例,正常对照组３０例,放射免疫法测定血浆ＥＴ水平,超声心动图检测心脏结构与功能,计算机左室重量指数（ＬＶＭＩ）,平均室壁厚度（ＭＷＴ）,相对室壁厚度（ＲＷＴ）。结果：ＥＨ组及ＥＨ＋ＬＶＨ组血浆ＥＴ高于正常对照组（Ｐ〈０．０１）,ＥＨ＋ＬＶＨ组ＥＴ高于ＥＨ组（Ｐ〈０．０１）。ＥＴ与ＬＶＭＩ,ＭＷＴ室间隔厚度,左室后壁厚度呈正相关（ｒ分别为０．４２４,０．３１６,０．２６８和０．３１７,均Ｐ〈０．０１）,ＥＴ与Ｅ／Ａ呈负相关（ｒ＝－０．３０４,Ｐ〈０．０１）。结论：ＥＴ与高血压和ＬＶＨ相关。     

老年人收缩期高血压左肥厚与心律失常关系的探讨

目的 探讨老年人收缩期高血压（ＯＩＳＨ）左室肥厚（ＩＶＨ）与心律失常的发生及其关系。方法 对９６例ＯＩＳＨ患者进行超声心动图和Ｈｏｌｔｅ检查,比较有ＬＶＨ及无ＬＶＨ两组各类心律失常的发生情况。结果 ９６例ＯＩＳＨ患者并发ＬＶＨ者６２例（６４．６％）;：ＶＨ组复杂性房性与室性心律失常便例数分别为５５例（８８．７％）与４８例（７７．４％）,其构成比高于无ＬＶＨ组的３５．３％（１２例）与３２．４％（１１     

老年高血压患者房性心律失常与左心结构和功能改变的关系

作者应用超声心动图及多普勒超声检测不伴左室肥厚的５１例老年高血压病患者左心结构和功能参数。以２４ｈ动态心电图房性早搏总数大于１００次和（或）出现短阵房性心动过速（Ａ组）与房性早搏总数小于１００次（Ｂ组）为标准，将老年高血压患者分为Ａ组（２６例）和Ｂ组（２５例）。结果：左房内径、左室舒张末期内径、室间隔厚度、左室后壁厚度、室间隔／左室后壁之比两组无明显差异；收缩功能指标ＥＦ和ＦＳ两组无明显差异。舒张功能参数ＰＶＡ、ＰＶＥ和ＰＶＡ／ＰＶＥ两组也无明显差异。但Ａ组总室性心律失常发生率高于Ｂ组（７７％对４８％，Ｐ＜０．０５）。结果提示：老年高血压非左室肥厚患者房性早搏或短阵房速的发生与左房内径等心脏结构和左心功能无明显关联     

老年陈旧性心肌梗死患者心性猝死危险性预测指标的探讨

目的探讨４项非创伤性检查指标对老年人陈旧性心肌梗死后心性猝死危险性的预测价值。方法老年人陈旧性心肌梗死７９例，分为猝死组（２２例）和非猝死组（５７例），对比分析两组间４项指标的差异。结果（１）猝死组的左室射血分数（ＬＶＥＦ）和心率变异性指数（ＨＲＶＩ）明显低于非猝死组（Ｐ＜０．０１），而ＱＴ离散度和２４小时动态心电图室性期前收缩（ＶＰＢｓ）＞３０个／小时的发生率在两组间差异无显著性。（２）Ｌｏｇｉｓｔｉｃ多因素回归分析显示ＬＶＥＦ是预测心性猝死危险性的独立指标。如以ＬＶＥＦ４５％为界分组，ＬＶＥＦ＜４５％组的ＶＰＢｓ＞３０个／小时的发生率明显高于ＬＶＥＦ＞４５％组（Ｐ＜０．０１），ＨＲＶＩ明显低于ＬＶＥＦ＞４５％组（Ｐ＜０．０５）。结论老年人心肌梗死伴左心功能不全者易发生心脏自主神经功能失调，诱发严重室性心律失常，导致心性猝死。     

高血压患者左室肥厚及主动脉根内径与动态血压的关系

目的探讨ＡＢＰ与左室后壁厚度（ＬＶＰＷＴ），室间膈厚度（ＩＶＳＴ）及主动脉内径（ＡＯＤ）之间的联系。方法对８８例原发性高血压患者应用超声心动图及动态血压计同时测定其ＬＶＰＷＴ、ＩＶＳＴ、ＡＯＤ及动态血压各参数值。结果左室肥厚（ＬＶＰＷＴ或／和ＩＶＳ）者５０例，主动脉根扩张者６０例。相关分析显示ＬＶＰＷＴ、ＬＶＳＴ及ＡＯＤ、动态血压各参数平均值呈显著正相关（Ｐ＜０．０５），其中与２４ｈ平均收缩压、最高收缩压及夜间平均收缩压相关最密切（Ｐ＜０．０１），此外ＬＶＰＷＴ，ＩＶＳＴ及ＡＯＤ与２４ｈ最高收缩压与最低收缩压之差（ΔＡＢＰｓ）及２４ｈ最高舒张压与最低舒张压之差（ΔＡＢＰｓ）亦呈正相关（Ｐ＜０．０５），其中与ΔＡＢＰｓ相比更密切（Ｐ＜０．０１）。结论血压波动性是左室肥厚及主动脉根内径的影响因素。     

老年高血压患者房性心律失常与左心结构和功能改变的关系

作者应用超声心动图及多普勒超声检测不伴左室肥厚的５１例老年高血压病患者左心结构和功能参数。以２４ｈ动态心电图房性早搏总数大于１００次和（或）出现短阵房性心动过速（Ａ组）与房性早搏总数小于１００次（Ｂ组）为标准，将老年高血压患者分为Ａ组（２６例）和Ｂ组（２５例）。结果:左房内径、左室舒张末期内径、室间隔厚度、左室后壁厚度、室间隔／左室后壁之比两组无明显差异；收缩功能指标ＥＦ和ＦＳ两组无明显差异。舒张功能参数ＰＶＡ、ＰＶＥ和ＰＶＡ／ＰＶＥ两组也无明显差异。但Ａ组总室性心律失常发生率高于Ｂ组（７７％对４８％，Ｐ＜０．０５）。结果提示:老年高血压非左室肥厚患者房性早搏或短阵房速的发生与左房内径等心脏结构和左心功能无明显关联     

培哚普利,卡托普利和硝苯地平对高血压左心室肥厚及心功能影响

目的观察培哚普利、卡托普利和硝苯地平对老年高血压心室肥厚（ＬＶＨ）及心功能的影响。方法将９４例老年轻、中度高血压ＬＶＨ病人随机分为培哚普利、卡托普利和硝苯地平３组。服用安慰剂２周后分别用药３个月，剂量递增，于实验前、用药前、用药后每月分别测定动脉血压，超声心动图左室舒张末内径、舒张期室间隔厚度、左室后壁厚度，并由此计算左室质量指数（ＬＶＭＩ），同时测定左室缩短分数，Ｅ／Ａ比值和射血分数。结果３组病人用药前一般情况无明显差别，用药后血压均有显著下降（Ｐ＜０．００１），组间无差异。ＬＶＭＩ培哚普利组（Ｐ＜０．０１）和卡托普利组（Ｐ＜０．００１）用药后有显著减低，Ｅ／Ａ比值明显升高（均Ｐ＜０．００１）。而硝苯地平组仅有Ｅ／Ａ比值升高（Ｐ＜０．０５）。左室缩短分数和射血分数３组均未见明显变化。结论对老年轻中度高血压ＬＶＨ病人，三药均可有效降低血压，卡托普利和培哚普利明显减轻ＬＶＨ，并改善左室舒张功能，硝苯地平亦可改善左室舒张功能     

Incidence of the coexistence of left ventricular false tendons and premature ventricular contractions in apparently healthy subjects

The incidence of the coexistence of left ventricular false tendons and premature ventricular contractions (PVCs) was evaluated prospectively. Over 14 months, left ventricular false tendons were found in 71 (6.4%) of 1117 consecutive patients examined echocardiographically. Two types of false tendons were observed: longitudinal, from the ventricular septum to the posteroapical wall (n = 62), and transverse, between the septum and the lateral wall (n = 9). Among 62 patients with PVCs and no underlying heart disease, false tendons were detected in 35 (56%); 28 had unifocal and seven had bifocal PVCs. Episodes of ventricular tachycardia were documented in one of the 28 patients with unifocal PVCs and in one of the seven patients with bifocal PVCs. These PVCs were poorly controlled by antiarrhythmic drugs but easily suppressed by exercise. Left ventricular false tendons were detected in 36 patients on routine echocardiographic examinations performed in the other 1055 subjects, and 10 of these patients were judged to have no underlying heart disease. PVCs were detected in two (20%) of these 10 patients. Although a definite conclusion that left ventricular false tendons are arrhythmogenic cannot be derived from these results, the unexpectedly high incidence of the coexistence suggests that left ventricular false tendons may be an etiologic factor in the development of PVCs, especially the rate-dependent and medically uncontrollable PVCs seen in apparently healthy individuals.     

Expression of atrial natriuretic polypeptide in ventricles of heart with hypertrophic cardiomyopathy: an immunohistochemical study of endomyocardial specimens]

To investigate the ventricular expression of atrial natriuretic polypeptide (ANP) in human hypertrophic heart, we conducted an immunohistochemical study using endomyocardial biopsy specimens obtained from the right side of the interventricular septum (RVB), left ventricular free wall (LVB), or both of 39 patients with hypertrophic cardiomyopathy (HCM), and 9 control subjects without hypertrophy. No HCM patients had apparent congestive heart failure. ANP was not present in control subjects' RVB or LVB specimens, but was found in HCM patients', showing its characteristic distribution patterns (RVB > LVB, p < 0.05); it was present in 15 of 36 RVB (42%) and 2 of 25 LVB (8%). No clinical data, including echocardiographic, hemodynamic and angiographic data, were directly related to ventricular ANP expression in HCM. According to histological data, however, ANP-present RVB specimens of HCM had larger myocytes, severer fibrosis and myofiber disarray than the specimens without ANP. This indicates that a failing state may not be a prerequisite for ANP expression in human hypertrophic ventricles, but that ventricular ANP expression may occur concomitantly with myocyte hypertrophy as an adaptive response to focal stress due to "histological overloads" such as disarray and fibrosis in HCM, which may be reflected in the characteristic distribution patterns of intraventricular ANP.     

频发室性期前收缩的频次及负荷对患者心脏结构及功能的影响

目的探讨频发室性期前收缩(PVC)患者的期前收缩频次及负荷与心脏结构及心功能的关系。方法选择PVC患者67例,根据期前收缩频次及负荷,采用四分位数间距法分为频次A组和负荷A组17例,频次B组和负荷B组17例,频次C组和负荷C组17例,频次D组和负荷D组16例;另选择无PVC患者20例为对照组。分析期前收缩频次及负荷与心功能的关系。结果与对照组比较,期前收缩频次C组、频次D组左心房内径、左心室心肌重量、左心室舒张末内径(LVIDD)、期前收缩负荷C组LVIDD、负荷D组LVIDD、左心室舒张末容积和收缩末客积、每搏心输出量明显升高(P<0.05,P<0.01),LVEF明显降低(P<0.05)。期前收缩负荷与左心室心肌重量、LVIDD、左心房内径呈正相关(r=0.41 5、r=0.426、r=0.269,P<0.05,P<0.01);期前收缩频次与LVEF呈负相关(r=-0.432,P<0.01),与LVIDD呈正相关(r=0.390,P<0.01)。结论期前收缩频次与PVC心脏结构及左心室收缩功能显著相关,提示随着期前收缩频次增加其功能下降、左心室扩大;随着期前收缩负荷增大,左心室肥厚程度增加。     

原发性高血压患者左心室肥厚与室性心律失常及心率变异性的关系

为探讨原发性高血压患者左心室肥厚与室性心律失常及心率变异性的关系。将原发性高血压患者分为无左心室肥厚组和左心室肥厚组，通过心脏B超观察原发性高血压患者心脏的结构与功能，通过动态心电图观察其24h室性期前收缩情况及心率变异性各时域指标。结果发现，左心室肥厚组患者的24h室性期前收缩发生率及室性期前收缩级别明显高于无左心室肥厚组（P＜0．01）；两组患者心率变异性各指标差异无显著性（P＞0．05）；与室性期前收缩级别相关的独立危险因素依次为室间隔厚度、左心室舒张末期内径和患者的年龄（P＜0．05，P＜0．001，P＜0．05）。以上提示原发性高血压合并左心室肥厚患者严重室性心律失常的发生率明显增高，而左心室肥厚与心率变异性无相关性。室间隔厚度、左心室舒张末期内径与年龄是原发性高血压患者发生室性心律失常的独立危险因素。     

参松养心胶囊联合美托洛尔治疗冠心病合并室性心律失常的效果观察

目的分析参松养心胶囊联合美托洛尔治疗冠心病伴室性心律失常的效果。 方法将100例冠心病伴室性心律失常患者根据随机数表法分为对照组与观察组,各50例。全部患者均接受基础治疗,在此基础上给予对照组患者美托洛尔胶囊口服,观察组在对照组用药基础上联合使用参松养心胶囊,全部患者均连续用药8周。分别于治疗前、治疗4周、治疗8周时为患者实施常规12导联心电图检查与24 h动态心电图检查,检测并比较两组患者治疗各时点的QTc离散度(QTcd)、短阵室速次数、室性期前收缩次数;记录患者治疗期间不良反应发生情况。 结果观察组治疗总有效率高于对照组,差异有统计学意义(P<0.05);治疗4周、治疗8周,两组患者QTcd值、短阵室速次数、室性期前收缩次数均较治疗前降低,且观察组降低幅度高于对照组,差异有统计学意义(P<0.05);两组患者药物治疗期间不良反应发生率比较,差异无统计学意义(P>0.05)。 结论采用美托洛尔联合参松养心胶囊治疗冠心病伴室性心律失常,患者心脏电生理特性显著改善,动作电位延长,治疗效果优于单用美托洛尔,且安全性好。     

Expression and distribution of atrial natriuretic peptide in human hypertrophic ventricle of hypertensive hearts and hearts with hypertrophic cardiomyopathy.

To investigate the ventricular expression of atrial natriuretic peptide (ANP) in human hypertrophic hearts, we conducted an immunohistochemical study of 130 endomyocardial biopsy specimens obtained from the right side of the ventricular septum (RVB), left ventricular free wall (LVB), or both from a total of 80 patients: 44 patients with hypertrophic cardiomyopathy (HCM), 14 with apical hypertrophic cardiomyopathy (APH), 13 with hypertensive hearts (HHD), and nine without hypertrophy (controls). No patients had apparent congestive heart failure. ANP was not seen in ventricular myocytes in controls but was identified in biopsy specimens of hypertrophic hearts, and its distribution was characteristic in each hypertrophic group: 15 RVB (37%) and two LVB (7%) of the HCM group, one RVB (7%) and two LVB (18%) of the APH group, and zero RVB (0%) and five LVB (46%) of the HHD group. Clinical data (including echocardiographic, hemodynamic, and angiographic data) were not directly related to ventricular ANP expression in HCM, APH, or HHD with one exception. In HHD patients, LVB specimens with ANP showed greater ventricular wall thickness than LVB specimens without ANP. According to histological data, however, the ANP-present RVB specimens of HCM or ANP-present LVB specimens of HHD had greater myocyte size than did the ANP-absent specimens. In addition, in HCM patients, the ANP-present RVB specimens showed more severe fibrosis and myofiber disarray than did the ANP-absent specimens. We conclude that a failing state and hemodynamic overload are not likely to be indispensable for ANP expression in human hypertrophic ventricles and that ventricular ANP expression occurs as a response to disease-specific changes: hemodynamic overload in HHD and histological changes such as myocardial fiber disarray, hypertrophy of myocytes, and fibrosis in HCM, which may reflect the characteristic distribution of intraventricular ANP.     

急性心肌梗塞患者同时检测窦性心率震荡与心率变异性的临床意义

目的:探讨急性心肌梗塞(AMI)患者同时检测窦性心率震荡(HRT)和心率变异性(HRV)的临床意义.方法:选择78例AMI患者,根据室性早搏Lown分级AMI患者被分为高危组(41例)和低危组(37例);另选择无心血管疾病者61例为正常对照组.所有入选者均行24h动态心电图检查,测定HRT参数震荡初始(TO)、震荡斜率...     

Course of left-ventricular contraction in left bundle-branch block and its hemodynamic effects

The aim of the study was to analyse the left ventricular contraction pattern in left bundle branch block (LBBB), to create experimentally a comparable pattern in animals and to relate this to haemodynamic measurements. In 20 normal subjects and 16 patients with LBBB without coronary heart disease we performed computer-assisted segmental left ventricular wall motion analysis during various systolic periods using two-dimensional echocardiography. The normal subjects showed on average a uniform shortening of all segments in systole; in patients with LBBB, however, asynchronous contractions of various types and intensities were found. Examination of the contraction pattern of each LBBB patient within the confidence range of the normal subjects showed that in 94% there was an abnormally small shortening of one of the sectors at one time in the second part of systole, and in 74% in the region of the interventricular septum. A "septum index" showed significant differences (p less than 0.0025) between LBBB patients and normal subjects. By right ventricular stimulation of the apex (RVA) and the outflow tract (RVOT) we simulated these contraction patterns in 6 dogs. With RVA stimulation the left ventricular contraction pattern was nearly physiological, while with RVOT stimulation the septum movement was paradoxical. With RVA stimulation cardiac output measured by thermodilution was higher (3.45 vs. 3.11 l/min, p less than 0.002) and the left ventricular end-diastolic pressure lower (7.0 vs. 8.0 mm Hg, p less than 0.002) than on RVOT stimulation; aortic pressure and the first derivative of left ventricular pressure did not differ significantly.(ABSTRACT TRUNCATED AT 250 WORDS)     

比索洛尔联合苯那普利对脑出血后室性心律失常的疗效观察

目的分析比索洛尔联合苯那普利对脑出血后室性心律失常的治疗效果。 方法选取2016年5月至2017年6月荣成市人民医院收治的60例脑出血后室性心律失常患者,按随机数表法分为对照组与研究组。对照组患者接受比索洛尔治疗,研究组患者接受比索洛尔联合苯那普利治疗。采用24 h动态心电图对患者用药治疗前后心率、室性期前收缩次数进行监测,于治疗前后进行NIHSS评分。 结果治疗后,两组患者心率均较治疗前降低(P<0.05),研究组患者心率低于对照组(P<0.05)。研究组患者治疗后室性期前收缩的发生次数低于对照组,差异有统计学意义(P<0.05)。治疗后,两组患者NIHSS评分均较治疗前降低(P<0.05);观察组治疗后NIHSS评分低于对照组(P<0.05)。 结论比索洛尔联合苯那普利可以减少脑出血后室性心律失常患者室性期前收缩发生次数,有效治疗脑出血后室性心律失常,有利于神经功能的改善,可以进一步推广应用。     

室性心律失常患者心率变异性研究

目的探讨冠心病与非冠心病室性心律失常患者心率变异性的差异。方法选自2011年1月至2013年10月于我院行24h动态心电图检查的患者560例。按照患者24h动态心电图室性心律失常的类型、数目、形态及有无冠心病分为5组：健康对照组143例;简单室早非冠心病组100例;简单室早冠心病组102例;复杂室早非冠心病组106例;复杂室早冠心病组109例;各组年龄构成比、男女比例无显著差异。所有患者均进行24h心率变异性检测,并对检测结果进行分析。结果比较这五组患者的24h心率变异性时域分析指标,非冠心病室早组心率变异性时域分析指标增高;冠心病室早组心率变异性时域分析指标降低。室早冠心病组与非冠心病组24h心率变异性时域分析指标有显著差异。结论 24h心率变异性时域分析对于室早的危险分层、科学处理、合理治疗有重要意义,心率变异性时域分析是一项在室早诊疗过程中有价值的辅助检查。