急性心肌梗死早期溶栓治疗对QT离散度及恶性室性心律失常的影响

研究急性心肌梗死（ＡＭＩ）后溶栓治疗对ＱＴ离散度（ＱＴｄ）及恶性室性心律失常（ＭＶＡ）事件的影响。回顾性选择分析ＡＭＩ患者７５例（溶栓治疗组４３例、未溶栓组３２例）,通过测量入院时及入院后２４ｈ常规心电图计算ＱＴｄ、校正ＱＴｃ（ＱＴｃｄ）,并在入院后一周内心电监护观察ＭＶＡ事件发生情况。溶栓再通组ＱＴｄ、ＱＴｃｄ较溶栓前显著缩短（４２．６±１４．３ｍｓｖｓ７１．７±１６．９ｍｓ,４５．９±１７．４ｍｓｖｓ７４．８±１８．５ｍｓ,Ｐ均＜０．０１）;溶栓未通组、未溶栓组入院２４ｈ期间ＱＴｄ、ＱＴｃｄ无明显变化（Ｐ＞０．０５）。ＱＴｄ、ＱＴｃｄ≥９０ｍｓ者ＭＶＡ事件明显高于＜９０ｍｓ者（７０．６％ｖｓ１０．２％,Ｐ＜０．０１）,溶栓再通组ＭＶＡ事件与溶栓未通组比较趋于减少（１１％ｖｓ２８％）。结论：ＡＭＩ后成功的溶栓治疗可以缩短心室复极的ＱＴｄ,从而可能减少ＡＭＩ后早期ＭＶＡ的发生;无效的溶栓治疗对ＡＭＩ近期预后无任何影响。     

心肌缺血和冠状动脉病变对QTc离散度的影响

为探讨ＱＴｃ离散度（ＱＴｃｄ）与心肌缺血和冠状动脉（简称冠脉）病变程度的关系，分析２８例冠脉正常和５７例冠心病患者１２导联心电图的ＱＴｃｄ。结果示：冠心病组ＱＴｃｄ较冠脉正常组显著增大（４６．７±１２．６ｍｓｖｓ２６．３±１０．９ｍｓ，Ｐ＜０．０１）；不稳定型心绞痛ＱＴｃｄ明显大于稳定型心绞痛者（５４．６±１３．７ｍｓｖｓ４２．３±１４．１ｍｓ，Ｐ＜０．０５）；双支病变与单支病变以及三支病变与双支病变相比，ＱＴｃｄ均有显著增大（４８．７±１３．２ｍｓｖｓ３５．７±１１．９ｍｓ及５９．６±１５．１ｍｓｖｓ４８．７±１３．２ｍｓ，Ｐ均＜０．０５）。提示心肌缺血是引起冠心病患者ＱＴｃｄ增大的主要原因之一，ＱＴｃｄ的变化对于判断心肌缺血和冠脉病变程度有一定价值。     

美托洛尔对冠心病患者QT离散度的影响

为探讨β－受体阻断剂美托洛尔（Ｍｅｔｏｐｒｏｌｏｌ）对冠心病（ＣＡＤ）患者ＱＴ离散度（ＱＴｄ）的影响，采用随机分组、单盲处理、前瞻性研究的方法，观察６２例ＣＡＤ患者Ｍｅｔｏｐｒｏｌｏｌ治疗前、后ＱＴｄ及ＲＲ间期、心率校正ＱＴ间期离散度（ＱＴｃｄ）、最大ＱＴ间期（ＱＴｍａｘ）、最小ＱＴ间期（ＱＴｍｉｎ）的变化。试验组Ｍｅｔｏｐｒｏｌｏｌ治疗后ＣＡＤ患者ＱＴｍｉｎ延长（３８６±３１．８ｍｓｖｓ３５２±２２．４ｍｓ，Ｐ＜０．０１），而ＱＴｍａｘ无明显改变（４３０±３５．６ｍｓｖｓ４２３±３４．９ｍｓ，Ｐ＞０．０５），ＱＴｄ、ＱＴｃｄ则显著缩小（分别为４４±１２．９ｍｓｖｓ７１±２８．６ｍｓ，４５±１１．５ｍｓｖｓ７９±３４．９ｍｓ，Ｐ均＜０．０１）。对照组治疗前、后ＱＴｄ、ＱＴｃｄ、ＱＴｍａｘ、ＱＴｍｉｎ均无改变（Ｐ＞０．０５）。表明Ｍｅｔｏｐｒｏｌｏｌ通过显著延长ＣＡＤ患者的ＱＴｍｉｎ缩小心肌复极化离散的程度，使心肌复极化趋向同步，这有利于防止恶性室性心律失常的发生     

不同临床类型冠心病的QTc离散度

分析１０９例经冠状动脉（简称冠脉）造影证实的不同类型冠心病患者ＱＴｃ离散度（ＱＴｃｄ），以４１例临床疑有冠心病而冠脉造影正常者作对照。结果显示：冠心病各组ＱＴｃｄ均明显大于对照组（６２．２９±２２．１９ｍｓ、７３．４４±２３．７７ｍｓ、１００．００±２０．１９ｍｓｖｓ３５．１９±１４．１８ｍｓ），Ｐ均＜０．００１。陈旧性心肌梗塞组的ＱＴｃｄ明显大于心绞痛组（７３．４４±２３．７７ｍｓｖｓ６２．２９±２２．１９ｍｓ），Ｐ＜０．０５；陈旧性心肌梗塞合并室壁瘤组ＱＴｃｄ显著大于陈旧性心肌梗塞组（１００．００±２０．１９ｍｓｖｓ７３．４４±２３．７７ｍｓ），Ｐ＜０．００１。前壁与下壁心肌梗塞患者ＱＴｃｄ比较无显著性差异（７３．５０±２４．３４ｍｓｖｓ７３．３３±２３．８７ｍｓ，Ｐ＞０．０５）。冠脉单支、双支及三支病变者ＱＴｃｄ（分别为７６．１８±２４．２５ｍｓ、７８．００±２８．５８ｍｓ和８０．２１±２５．１４ｍｓ）比较无显著性差异，Ｐ＞０．０５。提示不同临床类型冠心病患者心肌复极存在明显差异，陈旧性心肌梗塞伴室壁瘤形成者ＱＴｃｄ增大最显著，ＱＴｃｄ与梗塞部位及冠脉病变支数无关。     

高血压病QT离散度及美托洛尔的影响

目的：测定高血压患者ＱＴ离散度及美托洛尔对其影响。方法：１２０例高血压患者和３０例健康人作ＱＴ离散度测定，患者中随机抽取５０例进行美托洛尔治疗，并和未治疗组７０例作为对照。结果：（１）高血压患者的ＱＴ离散度明显高于健康人（３９．４８±７． ９２ ｍｓ ｖｓ ３４．３５±１０． ６２ ｍｓ， Ｐ＜０．０５）；（２）左室肥厚者的ＱＴ离散度明显高于无左室肥厚者（５８．４３±８．９４ ｍｓ ｖｓ ３９．９１± １０． １３ ｍｓ，Ｐ＜０． ０１）；（３）高血压患者伴心率失常者明显高于无心律失常者（５５．３６±９．３３ ｍｓ ｖｓ ３８．７１±７．９６ ｍｓ，Ｐ＜０．０５）；（４）经美托洛尔治疗后其ＱＴ离散度明显缩短。结论：高血压左室肥大和心律失常者ＱＴ离散度明显增加。美托洛尔治疗使ＱＴ离散度明显缩短，有利于防止恶性心律失常。     

对QT离散度实质的探讨

为探讨ＱＴ离散度（ＱＴｄ）的真实意义，观察１３９例急性心肌梗死（ＡＭＩ，ＡＭＩ组）及１０９例正常人（对照组）的最长ＱＴ间期（ＱＴｍａｘ）、校正ＱＴｍａｘ（ＱＴｃｍａｘ）及ＱＴｄ的变化。结果：①ＡＭＩ组的ＱＴｍａｘ、ＱＴｃｍａｘ和ＱＴｄ均显著高于对照组（分别为４２２．６０±３０．５１ｍｓｖｓ３８２．４６±２３．４０ｍｓ、４６０．２１±２８．９６ｍｓｖｓ３８８．５１±２０．１５ｍｓ、５９．８０±２８．４０ｍｓｖｓ３９．４３±１２．２１ｍｓ，Ｐ均＜０．００１）。②ＡＭＩ组中发生严重室性心律失常（ＶＡ）患者（１１４例）的ＱＴｍａｘ、ＱＴｃｍａｘ、ＱＴｄ与无ＶＡ的患者（２５例）相比，均有显著差异（分别为４４８．５８±３３．４０ｍｓｖｓ４１６．１０±３５．３０ｍｓ、４８１．４３±３５．１７ｍｓｖｓ４３９．６０±２７．１０ｍｓ、６６．９０±２０．７２ｍｓｖｓ４８．３２±２３．６１ｍｓ，Ｐ均＜０．００１）。认为ＡＭＩ时ＱＴｄ系Ｔ向量环在不同导联上的“投影”差异所引起的，其异常的本质是ＱＴ间期延长     

经皮冠状动脉成形术改善冠脉狭窄患者的QT离散度

目的　评价冠状动脉成形术（ＰＴＣＡ） 对心肌复极电生理的影响。方法　连续测量了８９ 例冠状动脉狭窄患者ＰＴＣＡ 术前术后体表心电图的ＱＴ间期与ＱＴ离散度,并与４７ 例无狭窄对照组比较。结果　冠状动脉狭窄组较无狭窄组ＱＴ间期明显延长,ＱＴ离散度（ＱＴＤ） 明显增加［ＱＴｍａｘ：（４４５±５０）ｖｓ（３９０±３４） ;ＱＴｃｍａｘ ：（４８２±４５） ｖｓ （４３６±３９） ;ＱＴＤ：（７５±３４） ｖｓ （２７ ±１６）; ＱＴｃＤ：（７９ ±３７）ｖｓ （３１ ±１８）ｍｓ;Ｐ＜０－０１］ ;ＰＴＣＡ使ＱＴ间期缩短,ＱＴＤ 缩小［ＱＴｃｍａｘ：术前（４４５ ±５０） ｖｓ 术后１ 周（４５３±３６） ;ＱＴｃＤ：术前（７９ ±３７） ｖｓ 术后２４ ｈ内（６５±３０）及术后１ 周（５９±２９） ;ＱＴＤ：术前（７５±３４） ｖｓ 术后２４ ｈ 内（５９±２８） 及术后１ 周（５５±２９） ｍｓ,Ｐ＜ ０－０５］。结论　心肌灌注增加能改善心肌复极电生理,有助于减少心律失常的发生。     

经皮冠状动脉腔内成形术对不稳定型心绞痛患者心率变异的影响

应用长程心电图分析系统对１６例不稳定型心绞痛患者（ＵＡＰ组）入院后第２日、经皮冠状动脉腔内成形术（ＲＴＣＡ）后第１，３，３０日以及１４８例健康中、老年人（对照组）２４ｈ心电图进行心率变异（ＨＲＶ）分析。结果：ＵＡＰ组２４ｈ连续正常ＲＲ间期的标准差（ＳＤＮＮ）、２４ｈ内连续５ｍｉｎ节段平均正常ＲＲ间期的标准差（ＳＤＡＮＮｉ）、相邻ＲＲ间期差的均方根（ｒＭＳＳＤ），相邻两个正常心动周期差值大于５０ｍｓ个数占总搏数的百分比（ＰＮＮ５０）、低频功率（ＬＦ）及高频功率（ＨＦ）均明显低于对照组（分别为９２．７±１４．３ｍｓｖｓ１２８．９±１７．８ｍｓ、７８．８±１０．６ｍｓｖｓ１１８．６±１９．１ｍｓ、１９．３±７．７ｍｓｖｓ２９．８±１２．７ｍｓ、３．６±１．７％ｖｓ６．５±５．５％、３１７．２±１４８．３ｍｓ２ｖｓ４７６．５±２８７．３ｍｓ２，Ｐ均＜０．０５），而ＬＦ／ＨＦ高于对照组（３．５±１．３ｖｓ２．４±１．１，Ｐ＜０．０５）。ＰＴＣＡ术后３０天ＵＡＰ患者ＨＲＶ逐渐恢复正常。结果提示ＵＡＰ患者交感神经和迷走神经张力下降，而以后者更明显；ＰＴＣＡ后ＨＲＶ逐渐恢复，说明ＰＴＣＡ能改善ＵＡＰ患者的ＨＲＶ。     

经皮球囊二尖瓣成形术对心率变异的影响

为了解经皮球囊二尖瓣成形术（ＰＢＭＶ）对风湿性心脏病二尖瓣狭窄病人心率变异（ＨＲＶ）的影响，自同期行ＰＢＭＶ的７１例病人中选择窦性心律者作为观察对象。于术前二日和术后第三日记录５ｍｉｎ的心搏数，经短时ＨＲＶ软件分析。结果表明术后ＲＲ间期均值标准差（３３．１８±１０．４２ｍｓｖｓ４２．８０±１５．８４ｍｓ，Ｐ＜０．０５）、相邻ＲＲ间期差值的均方根（２９．６１±１３．３８ｍｓｖｓ３７．５２±２６．０８ｍｓ，Ｐ＜０．０５）、相邻ＲＲ间期差值大于５０ｍｓ的百分比（６．７６±７．４９％ｖｓ９．０３±１０．２３％，Ｐ＜０．０１）、高频能谱（６１５．５８±４８５．６２ｂｐｍ２ｖｓ７０１．９７±６４９．９６ｂｐｍ２，Ｐ＜０．０５）均明显增大或升高。而平均心率（７４．３２±１１．３７ｂｐｍｖｓ６５．８８±７．７３ｂｐｍ，Ｐ＜０．０１）、最大心率（９５．６８±２８．６８ｂｐｍｖｓ７６．１４±８．５３ｂｐｍ，Ｐ＜０．０１）、低频能谱（４３８．２２±４０９．３１ｂｐｍ２ｖｓ２４０．１８±１９８．６８ｂｐｍ２，Ｐ＜０．０１）、极低频能谱（９７１．７４±５２９．５３ｂｐｍ２ｖｓ７２１．４３±５６４．０９ｂｐｍ２，Ｐ＜０．０１）均明显降?     

老年人急性心肌梗塞后心室颤动与QTc离散度关系的探讨

回顾性单盲分析老年人急性心肌梗塞发病２４小时内首次心电图ＱＴｃ离散度（ＱＴｃｄ）。心室颤动（简称室颤）组（ｎ＝１０）ＱＴｃｄ为７５．１±４５．２ｍｓ，非室颤组（ｎ＝６０）则为３２．０±１５．３ｍｓ，健康对照组（ｎ＝２０）为２７．２±７．１ｍｓ。室颤组与后两组比较，差异有高度显著性（Ｐ＜０．０１）。前壁心肌梗塞者（ｎ＝３０）ＱＴｃｄ为３６．３±３１．１ｍｓ，下壁心肌梗塞者（ｎ＝４０）则为３９．５±２２．５ｍｓ。ＱＴｃｄ≥４０ｍｓ２５例，发生室颤９例（３６％），而ＱＴｃｄ＜４０ｍｓ且ＱＴｃ＜４４０ｍｓ的２９例中，无一例发生室颤。结果提示老年人急性心肌梗塞后室颤的发生与ＱＴｃｄ明显增加有关。     

直接经皮腔内冠状动脉成形术对急性心肌梗死早期24小时心电稳定性的干预

为探讨直接经皮腔内冠状动脉成形术 (P PTCA)对急性心肌梗死 (AMI)早期 2 4h心电稳定性的影响 ,对发病≤ 6h并接受P PTCA治疗的 2 2例AMI患者 (P PTCA组 )进行动态心电图监测 ,持续观察其 2 4hQT间期值 (QT)和室性心律失常等心电指标变化 ,并与 15例梗死相关动脉 (IRA)未通患者 (对照组 )作对比。结果 :①P PTCA组的QT 2 4h内逐渐延长 ,其最小值 (术前 1h ,34 6± 16ms)与最大值 (术后第 2 3小时 ,391± 16ms)有显著性差异 (P <0 .0 1) ,与对照组的变化趋势类同。②P PTCA术前的心率校正QT(QTc)为 388± 15ms ,于术后开始迅速显著延长 ,至第 2小时达高值 (42 8± 17ms)后轻度缩短 ,然后又有逐渐延长趋势 ;对照组的QTc变化趋势与QT基本相同。③室性异位激动于P PTCA第 1小时 (5 31± 480次 )较术前 (185± 12 0次 )即迅速增加 ,主要见于术后的 3h内 ;对照组的室性异位激动在 2 4h内散在出现。提示AMI患者于P PTCA早期心电不稳定性增加 ,此为IRA开通和心肌再灌注损伤的临床强力指标之一。     

缬沙坦对急性心肌梗死患者早期QT间期离散度的影响

通过研究缬沙坦对急性心肌梗死 (AMI)患者早期QT间期离散度 (QTd)的影响 ,探讨缬沙坦对缺血心肌的保护作用。将 34例AMI患者随机分成缬沙坦 +基础治疗组 (治疗组 ,A组 ,17例 )和基础治疗组 (对照组 ,B组 ,17例 )。另设正常人 2 0例作对照组 (正常对照组 ,C组 )。在服药前、服药后 3,7天分别测量QTd及校正的QTd(QTcd) ,并观察服药前及服药 3天后室性心律失常的发生率。结果 :AMI患者的QTd及QTcd较正常人明显延长 (75 .9± 11.9vs 32 .7± 12 .6ms ,85 .5± 12 .8vs 36 .5± 13.2ms,P均 <0 .0 1) ;AMI患者中发生室性心律失常者 (19例 )的QTd及QTcd则较非室性心律失常者 (15例 )明显增加 (81.1± 11.1vs 6 9.3± 9.6ms,92 .0± 10 .5vs 73.6± 18.9ms ,P均 <0 .0 1) ;服药 7天后A组和B组的QTd及QTcd均明显减少 ,但A组比B组减少的更为显著 (41.5± 11.1vs 5 7.9± 10 .8ms,4 6 .9± 12 .3vs 6 5 .5± 12 .5ms ,P均 <0 .0 1) ;服药 3天后A组的QTd及QTcd较服药前也有明显的减少 ;服药 3天后A组中发生室性心律失常者 (2例 )明显减少 ,与治疗前 (10例 )有显著性差异 (P <0 .0 5 )。结论 :AMI患者早期QTd及QTcd较正常人增大 ,并且伴有室性心律失常的患者QTd及QTcd增大更为显著 ,AMI患者早期服用缬沙坦可降低QTd及     

心房颤动患者体表心电图QT间期的变化

探讨心房颤动(简称房颤)患者体表心电图QT间期的变化。入选81例房颤患者和71例对照者,测量Ⅰ导联和V2导联QT间期,根据Bazett公式计算QTc。结果:窦性心律时V2导联QT间期可测量性略高于Ⅰ导联,而房颤时相反。V2导联测得的QTc比Ⅰ导联长。房颤组与对照组比较,窦性心律时Ⅰ导联和V2导联的QTc两组间均无明显差异;房颤发作时Ⅰ导联QTc较对照组延长(429.01±43.08msvs408.50±31.93ms,P<0.05);V2导联QTc较对照组也延长(444.45±33.16msvs414.82±25.57ms,P<0.05)。房颤组房颤发作时与窦性心律时的自身对照比较,V2导联的QTc也延长(448.63±31.59msvs426.22±29.08ms,P<0.05)。结论:房颤患者在房颤发作时QTc延长,而房颤患者窦性心律时QTc与对照组无差异。     

Preconditioning Reduces QTc Value in Patients with First Non‐ST‐Segment Elevation Myocardial Infarction (NSTEMI)

Background: Preinfarction angina (PA) consists a strong clinical correlate to ischemic preconditioning (PC) and seems to occur in a bimodal time course. The aim of the study is to evaluate the impact of both forms of PC on QTc value representing myocardial electric stability, in patients with a first NSTEMI. Methods: Forty‐eight patients, with first NSTEMI and poor or no collateral development were enrolled in the study. QTc at admission and discharge were recorded. All patients had comparable admission QTc values and were divided into three groups according to the absence or presence and exact timing of preinfarction angina. The first group consisted of 20 patients who did not report PA (PA?, representing no PC effect); the second group of 12 patients with reported PA within 12 hours prior to admission (12h PA+, representing the classic form of PC); and the third group of 16 patients reporting PA within 12 to 48 hours prior to admission (48‐hour PA+, representing the delayed form of PC). The primary outcome was determined as the effect of PA on QTc value at discharge. Results: Discharge QTc values were significantly reduced in both (PA+) groups compared to (PA?) group (412 ± 50 vs. 455 ± 53 ms, p = 0.015 and 417 ± 29 vs. 455 ± 53 ms, P = 0.033 , respectively). Both groups of (PA+) patients compared to (PA?) patients suffered no arrhythmic events during their hospitalization (0/12 vs. 6/20, P = 0.04 and 0/16 vs. 6/20, P = 0.02 ). Conclusions: Both forms of preconditioning, similarly and significantly reduce QTc value at discharge in patients experiencing a first NSTEMI, suggesting possible protection from future arrhythmic events.     

心肌梗死急性期QRS波增宽预测远期心脏性猝死发生的价值

目的探讨急性心肌梗死后早期无创性指标左心室射血分数(LVEF)、QRS波时限和QTc间期预测远期心脏性猝死(SCD)发生的价值。方法采集289例急性心肌梗死后存活患者在急性期(<30 d)超声测定LVEF、体表心电图测定QRS波时限和QTc间期的数据,临床随访观察远期(>1年)发生的SCD事件。LVEF降低的界值为35%,QRS波增宽的界值为110 ms,QTc间期延长的界值为450 ms(男)/460 ms(女)。根据随访结果将患者分为SCD组和幸存组。结果在心肌梗死后平均(15±3)个月内,15例(5.2%)患者发生SCD。与幸存组患者相比,SCD组患者的LVEF明显降低[35%(28%～52%)比50%(33%～60%),P<0.0001],QRS波时限明显延长[115(88～152)ms比105(91～126)ms,P=0.0222],而两组患者QTc间期差异无统计学意义[458(416～513)ms比450(394～493)ms,P=0.1836]。SCD组患者中LVEF降低、QRS波增宽和QTc间期延长的比率依次为40%、67%和60%。生存分析提示,LVEF降低(26.1%比3.4%,P<0.0001)和QRS波增宽(9.7%比2.7%,P=0.0098)患者远期SCD发生率增加。多元Logistic回归分析显示,LVEF降低[RR:6.0(2.0～17.8),P=0.0011]和QRS波增宽[RR:3.1(1.0～9.0),P=0.0345]均为SCD发生的独立危险因素。结论急性心肌梗死后早期QRS波增宽能独立预测远期SCD的发生。     

房室结功能曲线连续性房室结折返性心动过速患者的射频消融终点初探

目的　探讨房室结功能曲线连续性房室结折返性心动过速 (AVNRT)患者的射频消融终点。方法　在AVNRT患者中 ,对心房 A1 A2 和 A1 A2 A3程序刺激房室结功能曲线均呈连续性者为 组 ,A1 A2 刺激房室结功能曲线呈连续性而 A1 A2 A3刺激呈不连续性者为 a组 ,房室结功能曲线均呈不连续性者为 b组。行慢径区域消融后 ,对组间的电生理参数进行比较。结果　 组非典型 AVNRT的诱发率高于 组 (2 7.3 % vs5 .6% ,P<0 .0 5 )。在 I组和 a组 ,消融后最长 A2 H2 间期 (A2 H2 m ax)均比消融前有所缩短 ,但无显著性差异 (P>0 .0 5 ) ,而 b组则显著缩短 (3 76± 73 ms vs2 0 6± 5 6ms,P<0 .0 1)。消融后 组、 a组和 b组的最长 A3H3间期 (A3H3m ax)均比消融前显著缩短 (2 74± 71ms vs 196± 45 ms,P<0 .0 5 ;3 62± 91m s vs 2 2 6± 72 m s,P<0 .0 1;3 85± 88ms vs 2 19± 61ms,P<0 .0 1)。结论　非典型 AVNRT与房室结功能曲线的连续性有关。对于房室结功能曲线连续性的 AVNRT患者 ,消融后 A3H3max的缩短可作为消融终点的指标之一     

Utility of a Simplified Lidocaine and Potassium Infusion in Diagnosing Long QT Syndrome among Patients with Borderline QTc Interval Prolongation

Background: Congenital long QT syndrome (LQTS) is caused by mutations in the cardiac Na⁺ or K⁺ channels that result in a prolonged QTc interval and increased QT dispersion. Na⁺ channel blockers and K⁺ can reverse the repolarization abnormalities in the Na⁺ channel variant (LQT3) and K⁺ channel variant (LQT1, LQT2), respectively. The phenotype of LQTS can be difficult to recognize, especially when the QTc interval is mildly prolonged. Additional noninvasive testing methods are needed to enhance the diagnosis of LQTS. This study compared the response of the QTc interval and QT dispersion to a sequential lidocaine/K⁺ infusion in LQTS patients with borderline QTc interval prolongation and control patients as a means of diagnosing LQTS. Methods: In this study, eight LQTS patients with borderline QTc, defined as QTc < 470 ms, and 10 healthy controls received sequential lidocaine/K⁺ infusion. Results: At baseline, LQTS patients had a longer QTc (446 ± 29 vs 416 ± 28 ms, P < 0.05) but similar QT dispersion (43 ± 14 vs 29 ± 10 ms) compared to controls. After lidocaine administration, baseline QTc and QT dispersion did not change in either LQTS or controls. One LQTS patient had a 54 ms (12%) reduction in his QTc but no change in QT dispersion. Following K⁺ infusion, baseline QTc and QT dispersion decreased by 9% (P < 0.005) and 45% (P < 0.005), respectively in LQTS. No effect was seen in control patients, where QTc and QT dispersion shortened by 1% (5 ± 14 ms) and 20% (6 ± 7 ms), respectively, compared to baseline. The combined lidocaine/K⁺ infusion had a sensitivity, specificity, and accuracy of 88%, 100%, and 94%, respectively, in diagnosing LQTS. Conclusions: A simplified sequential lidocaine/K⁺ challenge is accurate in diagnosing LQTS among patients with borderline QTc prolongation.     

QT Interval Length and Diabetic Autonomic Neuropathy

QT interval length was measured in ECG recordings from three groups of age-matched male subjects: 36 normal subjects, 41 diabetic patients without (DAN-ve), and 34 with (DAN+ve) autonomic neuropathy. ECG samples were selected from previously recorded 24-h ECGs on the basis of a clearly defined T wave and a steady RR interval over 2 min of around 750 ms (80 beats min^?1). There were no significant differences in RR interval between the groups. The two diabetic groups had slightly longer QT measurements (normal 365 ± 14 (±SD) ms, DAN-ve 373 ± 18 ms, DAN+ve 375 ± 23 ms, p = 0.05), and corrected QT (QTc) values (normal 423 ± 15 ms, DAN-ve 430 ± 20 ms, DAN+ve 435 ± 24 ms, p = 0.05). Ten diabetic patients fell above our defined upper limit of normal for QTc (>mean + 2SD). There was a significant correlation in the DAN-ve group between the QT indices and 24-h RR counts (QT r = ?0.38, p < 0.01; QTc r = ?0.40, p < 0.01). We conclude that there are some small alterations in QT interval length in the steady state in diabetic autonomic neuropathy. The changes appear to be due to autonomic impairment, rather than diabetes per se.     

QT interval abnormalities and heart rate variability in patients with cirrhosis

Background and study aimsWe aimed to assess the relationship of the QT interval and heart rate variability with the severity and aetiology of cirrhosis and determine the effect of propranolol on them.Patients and methodsThis prospective study included 44 patients with cirrhosis categorised into three groups based on the Child–Pugh score: groups 1, 2 and 3 (with 12, 15 and 15 patients, respectively). Demographic characteristics, propranolol administration, severity of cirrhosis evaluated by the Child–Pugh score, aetiology of cirrhosis, and serum sodium, potassium and calcium levels were evaluated. All patients underwent 24 h-Holter monitoring. Corrected QT interval (QTc), average heart rate, standard deviation of normal-to-normal intervals (SDNN) and corrected SDNN (cSDNN) were evaluated.ResultsThe average QTc was significantly longer in group 3 than in groups 1 and 2 (453.4 ± 17.4 vs 422.8 ± 18.6 and 428.9 ± 17.24 ms, p < 0.001). The median SDNN was 70 ms and was significantly lower in group 3 vs groups 1 and 2 (77; interquartile range [IQR], 67–89.5 vs 57; IQR, 38–68 and 75 ms; IQR, 61–81 ms, p = 0.003). cSDNN was significantly lower in group 3 vs groups 1 and 2 (200.0 ± 42.6 vs 254.5 ± 75.3 and 277.8 ± 110.6 ms, p = 0.022). Propranolol administration resulted in a significant increase in the average SDNN value but had no effect on cSDNN or QTc. QTc was associated with the Child–Pugh class (p < 0.001), viral aetiology (p = 0.009) and sex (p = 0.010); SDNN was associated with the mean heart rate (p = 0.015) and Child–Pugh class (p = 0.024).ConclusionQTc interval prolongation and decreased SDNN are common in cirrhosis. Their prevalence is closely associated with disease severity. Propranolol has no effects on cSDNN or QTc.     

An Evaluation of the Impact of Gender and Age on QT Dispersion in Healthy Subjects

Objectives: To determine if gender, age, and gender per age category, have an impact on QT and QTc dispersion in healthy volunteers. Methods: This study was undertaken in 150 patients (50 per age group, 75 males, 75 females). The age groups included young (20–40 years), middle‐aged (41–69 years) and elderly (> 70 years) subjects. The QT intervals on a 12 lead ECG were determined and Bazett's formula was used to derive the QTc intervals. The QT and QTc dispersion were determined by subtracting the shortest QTc interval from the longest on each 12‐lead recording. Results: Males had higher QT dispersion than females (50 ± 22 vs 42 ± 18 ms, P = 0.017) but QTc dispersion was not significantly changed. No significant differences were seen among the different age categories for QT or QTc dispersion. In elderly subjects, males had higher QT and QTc dispersion than females (54 ± 23 vs 42 ±15 ms, P = 0.039 and 63 ± 23.7 vs 48 ± 21 ms, P = 0.032, respectively). Conclusions: When evaluating the effect of gender in different age categories, elderly males have significantly greater QT and QTc dispersion than elderly female subjects. No other gender differences were noted for QT or QTc dispersion in the other two age categories. When evaluating a population of healthy volunteers, regardless of age, gender has an impact on QT dispersion but no significant interaction with QTc dispersion. Evaluating age without dividing the data by gender yields no significant differences in QT or QTc dispersion. A.N.E. 2001;6(2):129–133