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     

高血压左心室肥厚患者的心肌缺血和室性心律失常

为探讨高血压左心室肥厚（ＨＬＶＨ）患者心肌缺血情况以及心肌缺血与室性心律失常的关系。对９３例超声确定的ＨＬＶＨ病人行动静态９９ｍＴｃ－ＭＩＢＩ心肌断层显像，２４小时动态心电图检查，其中６９例行运动心电图（ＥＥＣＧ）检查，８例行冠状动脉造影。年龄，性别相配的４９例单纯性高血压病（ＳＨＴ）病人作对照。结果：（１）ＨＬＶＨ患者有４１．９％病人伴心肌缺血，其中６４．１％为无症状性心肌缺血。（２）左室重量指数（ＬＶＭＩ）和年龄在单纯ＨＬＶＨ组（ＳＬＶＨ）与ＨＬＶＨ伴缺血组（ＬＶＨＩ）之间没有统计学上的差异，调整性别因素影响，两者仍无差异。（３）ＨＬＶＨ组复杂室性早搏（ＣＶＡ）发生率明显比ＳＨＴ组高，而ＳＬＶＨ组与ＳＨＴ组相比，ＣＶＡ发生率无差异，ＬＶＨＩ组ＣＶＡ发生率明显比ＳＬＶＨ组与ＳＨＴ组高。（４）ＬＶＨＩ组内ＣＶＡ发生与无ＣＶＡ两亚组间年龄和ＬＶＭＩ无显著差异。结论：ＨＬＶＨ患者心肌缺血发生率达４１．９％，而且大部分为无症状性心肌缺血；其ＣＶＡ发生率主要与心肌缺血存在及程度相关；左心室肥厚程度在心肌缺血及ＣＶＡ发生中不起重要作用     

老年前期和老年高血压病患者心律失常特点及其与左室肥厚的关系

分析老年前期８２例、老年期１２４例高血压病患者和健康老年前期４６例、老年期６３例的２４小时动态心电图心律失常特点。结果显示老年前期高血压组总房性心律失常和总室性心律失常发生率分别为９０．２％和５９．８％，老年高血压组分别是９８．４％和７５．０％，差异显著（均Ｐ＜０．０１）；老年前期对照组分别为８０．４％和４５．７％，与同期高血压组比较差异不显著（均Ｐ＞０．０５）；老年对照组分别为８７．３％和５２．３％。与同期高血压组比较差异显著（均Ｐ＜０．０１）。老年高血压组中伴左室肥厚（ＬＶＨ）者（６６例）其总室性心律失常和Ｌｏｗｎ’ｓ分级≥３级室性心律失常发生率分别是８４．８％和３６．４％，均高于不伴ＬＶＨ者（５８例）的６３．８％和１３．８％（Ｐ＜０．０１）。在老年前期高血压组中伴ＬＶＨ者其Ｌｏｗｎ’ｓ分级≥３级室性心律失常发生率为１９．０％，高于不伴ＬＶＨ者的２．５％（Ｐ＜０．０５）．提示室性心律失常的发生与ＬＶＨ密切相关。     

老年收缩期高血压左室肥厚与心肌缺血,心律失常,心衰间相关性探讨

本文检测了１００例单纯性收缩压升高（ＩＳＨ）老年人，根据ＥＣＧ，Ｘ线ＵＣＧ的结果，分为有和无左室肥厚（ＬＶＨ）两组，结果显示ＬＶＨ组的缺血性ＳＴ－Ｔ改变，心衰发生率，室性心律失常与无ＬＶＨ组比较有显著性差异（Ｐ＜０．０１），提示ＩＳＨ－ＬＶＨ与心肌缺血、心衰发生率、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。     

高血压左室肥厚的室性心律失常与QT间期离散度的关系

目的 探讨高血压左室肥厚（ＬＶＨ）与非左室肥厚（ＮＬＶＨ）患者的室性心律失常与ＱＴｃｄ的关系。方法 对１００例有或无左室肥厚高血压患者行ＱＴｃｄ与２４小时动态心电图监测,结果 ＬＶＨ组ＱＴｃｄ室性心律失常,复杂室性心律失常明显高于ＮＬＶＨ组（Ｐ〈０．０１）,并发现ＬＶＨ组有ＱＴｃｄ〉６０ｍｓ者室性心律失常检出率明显高于ＬＶＨ而ＱＴｃｄ〈６０ｍｓ者（０．０５≥Ｐ〉０．０１）。结论 高血压ＬＶＨ组ＱＴ     

高血压患者左心室肥厚对心脏功能的影响

高血压是最常见的心血管疾病。长期血压升高可导致左心室肥厚（ＬＶＨ）,ＬＶＨ又可引起心肌缺血,影响左室收缩和舒张功能,诱发室性心律失常。为观察高血压患者ＬＶＨ对心脏功能的影响,作者对６９例高血压患者进行彩超多普勒（Ｄｏｐｐｌｅｒ）和２４ｈ动态心电图（ＤＣＧ）检查,按有无ＬＶＨ进行分组对比。１　对象与方法　　按ＷＨＯ／ＩＳＨ１９９３年高血压诊断标准。选择６９例均系本院住院患者,其中男４３例,女２６例,高血压病程０．５年～２５年,平均９．４±９．０年。６９例患者均给予Ｄｏｐｐｌｅｒ检查,测出舒张末期室…     

左室肥厚与单纯收缩,舒张或双期血压增高的关系

目的研究高血压病患者单纯收缩期（ＩＳＨ）、单纯舒张期（ＩＤＨ）或双相高血压（ＴＨ）上左室肥厚的关系。方法根据２４小时动态血压将病人分为４组：１．对照组（ｎ＝２７）平均收缩压＜１４０ｍｍＨｇ，平均舒张压＜９０ｍｍＨｇ；２．ＩＳＨ组（ｎ＝１６）平均收缩压＞１４０ｍｍＨｇ，平均舒张压＜９０ｍｍＨｇ；３．ＩＤＨ组（ｎ＝３１）平均收缩压＜１４０ｍｍＨｇ，平均舒张＞９０ｍｍＨｇ；４．ＴＨ组（ｎ＝１９）平均收缩压＞１４０ｍｍＨｇ和平均舒张压＞９０ｍｍＨｇ。超声心动图检测或计算舒张末期左室内径（ＥＤＤ）、室间隔及左室后壁厚度（ＬＶＳＴ，ＬＶＰＷＴ）、左室重量指数（ＬＶＭＩ）。结果ＩＳＨ、ＩＤＨ及ＴＨ组ＬＶＭＩ明显大于对照组Ｐ＜０．００１。ＩＳＨ和ＩＤＨ间、ＩＤＨ和ＴＨ组间无明显统计学差异。结论２４小时动态血压监测诊断为高血压病的患者ＬＶＭＩ明显大于偶测血压增高者。双期血压均高者左室肥厚最重。     

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。     

苯那普利对高血压左室肥厚与QTc离散度的影响

目的:探讨苯那普利对高血压左室肥厚（ＬＶＨ）与ＱＴｃ离散度（ＱＴｃｄ）的影响。方法原发性高血压６０例用苯那普利治疗６个月,测定治疗前后左室重量指数（ＬＶＭＩ）和ＱＴｃｄ。结果ＬＶＨ组患者治疗后ＬＶＭＩ明显减少（Ｐ＜０．００１）,ＬＶＨ逆转率７２％。ＬＶＨ组ＱＴｃｄ治疗前显著高于无ＬＶＨ组（６９．１±１７．３比４０．６±１１．６ｍＳ,Ｐ＜０．００１）,治疗后明显降低（６９．１(１７．３比４３．９(１２．６ｍｓ,Ｐ＜０．００１）,而无ＬＶＨ组治疗前后ＱＴｃｄ无明显变化（Ｐ＞０．０５）。ＬＶＨ组中ＬＶＨ逆转者ＱＴｃｄ明显小于未逆转者（３８．２±１０．４比６０．０±１６．１ｍｓ,Ｐ＜０．００１）。ＬＶＭＩ与ＱＴｃｄ之间呈正相关（ｒ＝０．６７８,Ｐ＜０．００１）。结论高血压ＬＶＨ时ＱＴｃｄ增大,苯那普利长期治疗使ＬＶＭＩ减少的同时ＱＴｃｄ也明显降低。     

缝隙连接对心肌肥厚兔室性心律失常的影响

目的研究兔慢性压力超负荷模型中缝隙连接(G J)对室性心律失常的影响。方法30只兔随机分为假手术组(Sham组)、心肌肥厚组(LVH组)和抗心律失常肽组(AAP10组)。LVH组和AAP10组通过缩窄腹主动脉制备兔左室压力超负荷心肌肥厚模型,Sham组仅游离腹主动脉未进行缩窄。动物饲养3个月后制备兔左室楔形心肌块的灌注模型,Sham组和LVH组灌流台氏液,AAP10组灌流含AAP10的台氏液,记录不同起搏周长下容积心电图、跨室壁离散度(TDR)及刺激反应间期(SR I),并观察早期后除极(EAD)及室性心律失常的发生率。结果在不同频率起搏下,LVH组SR I和TDR与Sham组比较均明显增加(P<0.05)。而AAP10组的SR I和TDR与LVH组比较明显减小(P<0.05)。Sham组无1例诱发EAD和室性心律失常;在5 000 m s起搏时LVH组和AAP10组EAD的发生率分别为10/10、3/10,室性心律失常发生率分别为4/10,1/10,两组比较差异有显著性(P<0.05)。结论G J激动剂AAP10减轻了心肌肥厚时SR I的延长和TDR增加,相应的减少了EAD和室性心律失常的发生率。     

老年高血压患者心律失常特点及其与左室肥厚的关系

分析原发性高血压病226例（老年组139例，非老年组87例）和80例健康老年人（对照组）24h动态心电图检测的心律失常。结果示总房性和室性心律失常发生率在高血压老年组为97％和77％，非老年高血压组为85％和53％，对照组为89％和59％；其中阵发房速、房颤和Lown's分级≥3的室性心律失常在高血压老年组达47％和40％，非老年组21％和22％，对照组30％和11％（P＜0．05～0．001）。在高血压老年组中62例伴左室肥厚（LVH），其总室住心律失常发生率和town's分级≥3者达92％和57％，均高于无LVH者的65％和27％（P＜0．001）。提示其发生与LVH密切相关。     

Ventricular arrhythmias in hypertensive left ventricular hypertrophy. Relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis

Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The relationships, however, between ventricular arrhythmias and coexistent coronary artery disease, left ventricular dysfunction and left ventricular fibrosis have not been examined in hypertensive LVH. We carried out coronary arteriography on fifteen hypertensive patients with LVH and nonsustained ventricular tachycardia (greater than or equal to 3 consecutive ventricular complexes) of whom nine (60%) were free of significant (greater than 50% stenosis) coronary disease. To identify other possible correlates of left ventricular arrhythmias, 28 patients with LVH, comprising 17 with ventricular tachycardia and 11 without ventricular arrhythmias, underwent quantitative assessment of left ventricular function (angiographic ejection fraction), left ventricular mass (echocardiography), and left ventricular fibrosis (endomyocardial biopsy). Ejection fraction was not significantly different between the two groups (53 +/- 8% v 62 +/- 2%, P = NS). However, left ventricular mass was significantly greater (442 +/- 28 g v 339 +/- 34 g, P less than .05) and percentage fibrosis significantly higher (19 +/- 4% v 3 +/- 1%, P less than .001) in those patients with ventricular tachycardia. Thus ventricular arrhythmias in hypertensive patients with LVH cannot be entirely attributed to coexistent coronary disease, nor to left ventricular dysfunction, but are related to the degree of cardiac hypertrophy and subendocardial fibrosis.     

老年人高血压左室肥厚与心律失常关系的研究

目的探讨老年人高血压左室肥厚(LVH)与心律失常的关系。方法对178例老年高血压患者进行超声心动图及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178例老年高血压患者并发LVH81例(45·5%),LVH组各种心律失常的发生率与非LVH组比较,差别均有显著性意义(P<0·01),LVH组复杂性室性心律失常(CVA)为39例(48·1%),显著高于无LVH组的17·5%(17例)(P<0·01)。结论老年人高血压LVH与心律失常的发生有密切关系,且与CVA成正相关。     

钙调蛋白激酶Ⅱ抑制剂对心肌肥厚兔室性心律失常的影响

目的观察钙调蛋白激酶Ⅱ抑制剂KN-93对心肌肥厚兔室性心律失常的影响。方法雌性新西兰大白兔随机分为4组：假手术组（Sham组）、心肌肥厚组（LVH组）、心肌肥厚＋KN-93组（KN-93组）、心肌肥厚＋KN-92组（KN-92组）,每组10只。LVH、KN-93及KN-92组通过缩窄腹主动脉制备兔心肌肥厚模型,Sham组仅游离腹主动脉未进行缩窄。8周后制备兔左室楔形心肌块的灌注模型,同步记录心内、外膜动作电位及跨壁心电图,观察低钾（2mmol／L）、低镁（0．25mmol／L）台氏液灌流及慢频率刺激条件下各组早期后除极（EAD）和尖端扭转型室性心动过速（Tap）的发生率,并记录在不同起搏周期下QT间期、动作电位时程（APD）及跨室壁复极离散度（TDa）的变化。结果在低钾、低镁台氏液灌流及2000～4000hi8慢频率刺激下,Sham、LVH、KN-92组（0．5μmol／L）及KN-93组（0．5μmol/L）EAD的发生率分别为0／10、10／10、9／10和5／10,Tdp的发生率分别为0／10、5／10、4／10和1／10;当KN-92组及KN-93组中药物浓度增至1μmol／L时,EAD的发生率分别为9／10和3／10,Tdp的发生率分别为4／10和1／10。而且KN-93组、KN-92组对QT间期、APD及TDR无明显影响（P〉0．05）。结论钙调蛋白激酶Ⅱ特异性抑制剂KN-93能够有效抑制心肌肥厚兔室性心律失常的发生,其主要作用机制是通过减少EAD的发生来实现。     

老年高血压性左室舒张功能不全对房室性心律失常的影响

目的 研究老年高血压患者左室舒张功能不全对房、室性心律失常发生及其严重程度的影响.方法 入选老年原发性高血压患者210例,均经24 h动态心电图检查判定心律失常情况,和多普勒超声心动图检查评价心脏结构和功能.根据不同左室舒张充盈类型分为正常舒张充盈型(即左室舒张功能正常组)、松弛受损型、假正常充盈型、限制性充盈型(后3型为左室舒张功能不全组).结果 (1)共检出房性心律失常占70%,室性心律失常占49%,两组差异有统计学意义(χ2=19.975,P<0.05);(2)左室舒张功能不全组的房、室性心律失常发生率以及复杂房、室性心律失常发生率分别为89%、63%、49%、30%,均高于左室舒张功能正常组[40%、26%、13%、7%,χ2=56.723、28.359、28.076、15.9102,P<0.05];(3)不同左室舒张充盈类型间的房室性心律失常以及复杂房室性心律失常的发生率差异亦有统计学意义(P<0.05),其中以假正常充盈型和限制性充盈型的发生率最高,分别为93.6%和96.4%.结论 老年高血压患者左室舒张功能不全促进房、室性心律失常的发生,并影响其严重程度;左室舒张功能不全的假正常充盈型和限制性充盈型易发生复杂房、室性心律失常.     

QTc dispersion and complex ventricular arrhythmias in untreated newly presenting hypertensive patients.

Increased dispersion of ventricular repolarisation (increased QT dispersion) is believed to predispose to arrhythmias associated with sudden death in certain cardiac diseases. Hypertension is also associated with increased risk of sudden death, particularly in those with left ventricular hypertrophy (LVH). Therefore, the first aim of this study is to look into the possible pathogenic role of QT dispersion on the ventricular arrhythmias occurring in a group of never-treated hypertensive patients. The second aim is to look at other possible determinants of QT dispersion (ie, level of blood pressure, hypokalaemia, electrocardiographic LVH and presence or absence of strain pattern) in hypertensive patients, and their relevance to complex ventricular arrhythmias. QTc (corrected QT) was measured in 70 newly presenting (never-treated) hypertensive patients (47 male, 23 female, mean age 51.9 +/- 12.5 years) from a standard 12-lead surface electrocardiogram (ECG). Blood pressure measurements and 24-h ECG holter recordings were performed in all patients. Serum potassium level was measured in 51 of the patients. Ventricular arrhythmias were classified using a modified Lown's scoring system. Maximum QTc, minimum QTc and QTc dispersion for all patients were 442 +/- 30.3 ms, 380 +/- 26.7 ms and 61.5 +/- 21.6 ms respectively. High grade ventricular arrhythmias (Lown's score >/=3) were found in 43% of the patients. The QTc dispersion was strongly correlated with the Lown's classification of arrhythmia and the age of the patients. Patients with more severe ectopy (Lown's score >/=3) were significantly older (57.4 +/- 10.3 years) compared to those with score /=3 Lown's score compared to 39% in the group with LVH but without strain. In the presence of relative hypokalaemia, hypertensive patients with LVH showed more QTc dispersion (85.7 +/- 15.5 ms) and a greater tendency for complex ventricular arrhythmias (100% grade >/=3 Lown's score) compared to those with LVH and normal serum potassium levels (64.1 +/- 22.6 ms and 35%, QTc dispersion and Lown's score >/=3, respectively P = 0. 05). The level of blood pressure had no effect on either the QTc dispersion or the prevalence of complex ventricular arrhythmias. Prevalence of complex ventricular arrhythmias in hypertensive patients is strongly correlated with QTc dispersion and age. When hypertensive patients with LVH have low potassium levels the risk of developing complex ventricular arrhythmias is significantly increased.     

Relation of complex ventricular arrhythmias to presenting features and prognosis in dilated cardiomyopathy

To evaluate whether complex ventricular arrhythmias relate to presenting features and prognosis of dilated cardiomyopathy, 104 patients were studied from 1977 to 1987. At diagnosis, the 19 patients with complex ventricular arrhythmias (18%), as compared to the 85 patients without (82%), had a higher incidence of palpitation (P less than 0.01), severe dyspnea (P less than 0.001) and atrial fibrillation (P less than 0.01). They showed also higher mean right atrial pressures (10 +/- 5 vs 6 +/- 4 mm Hg, P less than 0.001) and higher right ventricular end-diastolic pressures (11 +/- 4 vs. 7 +/- 4 mm Hg, P less than 0.001) than patients without complex ventricular arrhythmias. Histologic samples were collected from the 32 patients (31%) studied since 1984 and semiquantitatively graded. The 11 patients with complex ventricular arrhythmias showed a higher frequency of severe interstitial fibrosis than the 21 patients without (64% vs. 24%, P less than 0.05), but they were otherwise similar as to the frequency of marked myocellular hypertrophy, changes of myocardial regression, endocardial fibrosis, attenuation of myocytes, hyperplasia of smooth muscle cells and infiltration by inflammatory cells. During a follow-up of 3.8 +/- 3.5 years, 35 patients (34%) died. Mortality was 58% (11 out of 19) in patients with complex ventricular arrhythmias and 28% (24 out of 85) in patients without (P less than 0.025). These results show that complex ventricular arrhythmias in dilated cardiomyopathy are associated with impairment of function of the right heart and severe interstitial fibrosis of the left ventricle, rather than with left ventricular dysfunction. Presence of complex ventricular arrhythmias also seems to identify those at high risk for death.     

In which type of hypertension should ventricular hyperexcitability be suspected?]

The aim of the present study was to determine when a search for ventricular arrhythmias, by ambulatory electrocardiographic monitoring, is necessary in hypertensive patients. An electrocardiogram, an echocardiogram and a 24 hour Holter monitoring were recorded in 88 patients with essential hypertension. According to the results of electrocardiogram patients were subdivided into 4 groups: normal electrocardiogram, isolated left auricular hypertrophy (LAH), isolated left ventricular hypertrophy (LVH) and major ST-T wave changes. According to the degree of septal thickness (ST), patients were classed in 4 groups. [table; see text] For hypertensive patients with normal electrocardiogram, Holter monitoring is not necessary; in fact practically no complex arrhythmias is found in this group. On the contrary, for hypertensive subjects with ST-T waves changes, this investigation seems very interesting, nearly 75% of them present high-grade ventricular arrhythmias. For the patients with electrocardiographic isolated LAH or LVH, the realisation of an echocardiography permits to separate the subjects with mild LVH (ST less than 12 mm) where Holter monitoring is not necessary (81% Lown O-I) and the patients with mean or severe LVH (ST greater than or equal to 12 mm) where this investigation seems very interesting, nearly 65% of them present high-grade ventricular arrhythmias.