亚临床甲状腺功能减退对QT间期和心率变异性的影响

目的 通过分析亚临床甲状腺功能减退(简称亚临床甲减)患者QT间期和心率变异性,探讨亚临床甲减对心脏电活动的影响.方法 收集55例亚临床甲减患者为试验组,54例甲状腺功能正常者为对照组,进行常规体检,检测促甲状腺激素(TSH)、游离三碘甲状腺原氨酸(FT3)和游离甲状腺素(FT4),行24小时长程心电图检查(当天上午9时～次日上午9时),比较两组研究对象的一般资料、心率(HR)、R-R间期、QT和QTc间期、心率变异性(时域性指标:SDNN、SDANN、rMSSD和pNN50;频域性指标:LF、HF和LF/HF)和心律失常发生率的差异.结果 与对照组相比,试验组(1)TSH水平较高,FT4水平较低,差异均有统计学意义;(2)R-R间期、QT和QTc间期明显延长,差异均有统计学意义;(3)总的心率变异性较低:SDNN、SDANN、rMSSD、pNN50和HF较小,而LF/HF较大,差异均有统计学意义;(4)心律失常发生率差异无统计学意义.结论 亚临床甲减增加QT离散度,降低心脏迷走神经节律,增加心脏交感神经节律,使心脏电活动紊乱.     

直立倾斜试验期间心室复极化指标、血浆腺苷水平与血管迷走性晕厥关系的研究进展

晕厥是临床上常见的症状,其中又以血管迷走性晕厥最为常见。引发晕厥的病因很多,其机制复杂,主要与自主神经功能障碍有关。直立倾斜试验是目前诊断血管迷走性晕厥的“金标准”,已被广泛应用于临床科室。心电图检查应用广、价格低,可发现具体或潜在的晕厥原因,是对晕厥进行初步评估的有效方法之一。正常心肌细胞电活动包括去极化和复极化,其中复极化过程尤为重要,而自主神经通过对离子通道的控制影响复极化过程,自主神经张力增高或减低均会对心室复极化产生影响。除此之外,血浆腺苷水平作为重要的生化指标对血管迷走性晕厥的诊断亦起着至关重要的作用。本文通过回顾相关文献,重点分析了直立倾斜试验期间心室复极化指标[包括QT间期（QT）、校正QT间期（QTc）、QT间期离散度（QTd）、T波峰-末间期（Tp-Te）、Tp-Te/QT、Tp-Te/QTc、JT间期、校正JT间期（JTc）、JT间期离散度（JTd）、JT延长指数（JTI）]、血浆腺苷水平与血管迷走性晕厥的关系。     

冠状动脉慢血流对心肌电活动的影响

目的分析校正后QT间期(QTc)、QT离散度(QTd)、T波峰-末间期(Tp-Te)与冠状动脉慢血流(CSF)现象的相关性,寻找预测CSF患者室性心律失常和心脏性猝死风险增加的指标。方法入选2017年1月至2019年12月因怀疑冠心病行冠脉造影检查,结果示冠状动脉无明显狭窄且存在CSF的老年患者,随机选择71例为实验组,在冠状动脉无明显狭窄且血流正常的患者中随机选择65例为对照组,对比两组临床资料、实验室数据及心肌电活动各指标情况。结果两组性别、年龄、吸烟、高血压、心率、糖尿病、体重指数(BMI)、血脂、超敏C反应蛋白(hsCRP)、血浆利钠肽(NT-proBNP)差异无统计学意义(P0.05);实验组QTc、QTd、Tp-Te明显长于对照组(P0.05)。结论当体表心电图提示QTc、QTd、Tp-Te延长时,表明CSF患者可能存在心室肌复极化不均一性和更明显的电不稳定性,早期干预可改善患者预后,提高CSF患者生活质量。     

心电图Tp-Te间期、Tp-Te/QT比值与恶性室性心律失常的关系

目的探讨心电图T波峰末间期(Tp-Te)、Tp-Te/QT比值对恶性室性心律失常(MVA)的诊断价值。方法连续入选2017年1月1日至2018年1月1日于保定市第一中心医院西院心电图、脑电图二室行24 h 12导联动态心电图检查的患者412例为研究对象。根据是否发生恶性室性心律失常分为两组:恶性室性心律失常组72例;无恶性室性心律失常组340例。分别测定两组患者Tp-Te间期、QT间期,计算出Tp-Te间期、QTc间期及Tp-Te/QT比值,并对两组患者Tp-Te间期、QTc间期及Tp-Te/QT比值进行统计学分析。结果恶性室性心律失常组的Tp-Te间期、Tp-Te/QT比值均较非恶性室性心律失常组明显增加(P0.001)。结论 Tp-Te间期、Tp-Te/QT比值增加对于恶性室性心律失常的发生均有预测价值。     

Tp-Te间期及Tp-Te/QT比率对心功能不全患者的临床应用价值

【摘要】目的 探讨反应心室跨壁复极离散(transmural dispersion of repolarization,TDR)的相关指标T波峰-末间期（Tpeak-Tend interval,Tp-Te）和T波峰-末间期/QT间期比率(Tp-Te/QT)在心功能不全患者中的临床意义及应用价值。方法 105例心功能不全患者及100例正常对照组纳入研究,记录所有入选者的体表心电图Tp-Te间期及Tp-Te/QT比率,以及心率、年龄、BNP等相关临床指标。按照纽约心功能分级(NYHA)将病例组分为低危组(NYHA I-II)及高危组(NYHA III-IV),将高危组中治疗后BNP下降≥30%的患者纳入治疗有效组。分别比较心功能不全患者与正常人相较,心功能不全严重程度不同的患者之间相较,以及高危心功能不全患者治疗前后相较,Tp-Te间期及Tp-Te/QT比率的差异。结果 （1）心功能不全患者与对照组相较Tp-Te间期及Tp-Te/QT比率均明显增加（P＜0.05）;（2）高危心功能不全患者较低危患者的Tp-Te间期及Tp-Te/QT比率明显增大（P＜0.05）;（3）高危心功能不全患者治疗后与治疗前相较Tp-Te间期差距无统计学意义（P＞0.05）,而Tp-Te/QT比率有所降低（P＜0.05）。结论 Tp-Te间期及Tp-Te/QT比率可作为反应心功能不全患者病情严重程度及治疗效果的临床心电学指标。     

心电图T波峰末间期及其在动脉粥样硬化性心血管病中研究进展

<正>T波代表心室快速复极时的电位变化,T波峰末间期(Tpeak-Tend interval,Tp-Te间期)是指心电图中T波峰值至末端的时限,即整个T波降支的时间,反应了心室跨壁复极离散度。多项研究发现,Tp-Te间期、Tp-Te/QT比值是预测恶性室性心律失常的心电图指标,且与引起心源性猝死的各种心血管疾病的发生密切相关。动脉粥样硬化性心血管病是引起恶性室性心律失常的常见原因,缺血性室性心律失常亦是动脉硬化性心血管病患者发生猝死的重要因素。本文重点介绍Tp-Te间期及Tp-Te/QT比值与动脉粥样硬化性心血管病的联系,进一步了解Tp-Te间期及Tp-Te/QT比值意义。     

延续性护理干预对亚临床甲状腺功能减退症患者血脂、促甲状腺激素及预后的影响

正甲状腺功能减退症又被称为甲减,是由多种因素导致的TH(甲状腺激素)分泌、合成或生物效应不足引发的一系列内分泌疾病~[1]。若FT_4(血清游离甲状腺素)、FT_3(血清游离三碘甲腺原氨酸)水平正常,仅有TSH(促甲状腺激素)轻度上升,且患者仅有轻微甲减症状或无甲减症状,则为亚临床甲状腺功能减退症,又被称为亚临床甲减、潜伏期型甲减、轻微型甲减,为临床常见内分泌代谢类疾病,有研究~[2,7,8]指出,对亚     

亚临床甲状腺功能减退症与相关疾病的研究进展

亚临床甲状腺功能减退症(简称亚临床甲减)是常见的内分泌代谢性疾病,其定义为血清促甲状腺素(TSH)升高,游离三碘甲腺原氨酸(FT3)、游离甲状腺素(FT4)正常,大部分患者无明显临床症状.目前,随着TSH放射免疫测定技术的不断改进,对亚临床甲减诊断率越来越高.     

Tp-Te间期的细胞电生理基础和临床价值

T波峰末间期(Tp-Te间期)是指心电图T波顶点至T波终末的时间间期。Tp-Te间期与中层心肌细胞独特的电生理特性有关。Tp相当于心外膜复极结束,Te相当于中层心肌细胞复极结束。最新研究显示,Tp-Te间期反映了跨室壁复极离散度,该指标在一些疾病如Brugada综合征、长QT综合征、短QT综合征等发生恶性心律失常的预测评估中有临床价值。     

高血压左心室肥大患者T波峰-末间期的检测

目的:检测高血压左心室肥大患者的T波峰一末间期(Tp-Te间期)TL心率校正的Tp-Te/√R-R间期,并探讨其可能的临床意义.方法:依据超声心动图测定的左室重量指数(LVMI)分为正常组和左室肥大组.比较正常组与高血压左室肥大组Tp-Te间期及Tp-Te/√R-R间期的差异.结果:正常组男性Tp-Te间期及Tp-Te/√R-R间期长于女性(P＜0.05);左室肥大组男、女性Tp-Te间期及Tp-Te/√R-R间期均比正常组明显延长(P＜0.05,P＜0.01).结论:高血压左心室肥大患者的Tp-Te间期及Tp-Te/√R-R间期比正常人明显延长,可能成为预测此类患者发生心律失常事件的临床指标之一.     

Predictive Value of QT Dispersion for Ventricular Tachyarrhythmias in Patients with Implantable Cardioverter Defibrillator

Background: QT dispersion, measured as interlead variability of QT intervals in the surface electrocardiogram, has been demonstrated to provide an indirect measurement of the inhomogeneity of myocardial repolarization as a potential substrate for ventricular arrhythmias. Methods: QT dispersion was measured in the standard 12-lead ECG in 51 patients at the time of implantation of a third generation implantable cardioverter defibrillator (ICD) with automatic electrogram storage capability for electrical events triggering device therapy. In addition, QT dispersion was measured in 100 age- and sex-matched healthy controls. All 5 1 study patients with ICD were prospectively followed to determine possible associations between QT dispersion at implant and subsequent spontaneous ICD shocks for ventricular tachyarrhythmias (VT). Results: Rate-corrected QT dispersion and adjusted QTc dispersion, which takes account of the number of leads measured, were significantly greater in ICD patients compared to controls (76 ± 25 ms vs 46 ± 11 ms, and 24 ± 7 ms vs 14 ± 3 ms respectively, P < 0.0 1). During 15 ± 8 months follow-up, ventricular tachyarrhythmias occurred in 23 (45%) of 51 ICD patients. QTc dispersion and adjusted QTc dispersion were not significantly different between ICD patients with ventricular tachyarrhythmias and ICD patients without ventricular tachyarrhythmias during follow-up (74 ± 19 ms versus 77 ± 29 ms, and 23 ± 6 ms vs 25 ± 8 ms respectively). Conclusion: Increased QT dispersion measured in the 12-lead standard ECG does not appear to be a useful marker for future arrhythmic events in a mixed patient population with ICD.     

The effect of electroconvulsive therapy on QT dispersion

Electroconvulsive therapy (ECT) is used frequently in psychiatric practice and various electrocardiographic (ECG) changes have been described during ECT. QT dispersion (defined as maximal QT interval minus minimal QT interval) as assessed on the surface electrocardiogram has been demonstrated to reflect regional inhomogeneity of ventricular repolarization. The aim of this study is to examine the effect of electroconvulsive therapy on QT dispersion. We studied 27 patients (age range 24-42 y, mean age 34 y, 11 men) without heart disease who were treated with ECT. Structural heart disease was eliminated with routine clinical examination and laboratory tests, echocardiography, and exercise treadmill test. QT interval and corrected QT (QTc) dispersion was measured on a 12-lead ECG before and just after ECT. QTc dispersion increased from 28.9 +/- 7.4 ms at baseline to 81.4 +/- 12.8 ms after the procedure (P < 0.0001). This result demonstrated that QTc dispersion increased significantly during ECT. This finding may explain that increased inhomogeneity of ventricular repolarization is associated with enhanced vulnerability to arrhythmias during ECT.     

Effects of azithromycin on ventricular repolarization in children with COVID-19

IntroductionAzithromycin is used to treat pediatric COVID-19 patients. It can also prolong the QT interval in adults. This study assessed the effects of azithromycin on ventricular repolarization in children with COVID-19.MethodThe study prospectively enrolled children with COVID-19 who received azithromycin between July and August 2020. An electrocardiogram was performed before, one, three, and five days post-treatment. Using ImageJ®, the following parameters were measured: QT max, QT min, Tp-e max, and Tp-e min. The parameters QTc max, QTc min, Tp-ec max, Tp-ec min, QTcd, Tp-ecd, and the QTc/Tp-ec ratio were calculated using Bazett's formula.ResultsThe study included 105 pediatric patients (mean age 9.8±5.3 years). The pretreatment heart rate was higher than after treatment (before 92 [79–108]/min vs. Day 1 82 [69–108)]/min vs. Day 3 80 [68–92.2]/min vs. Day 5 81 [70–92]/min; p=0.05).ConclusionAzithromycin does not affect the ventricular repolarization parameters on ECG in pediatric COVID-19 cases.     

Effect of amiodarone on qt dispersion in the 12-lead standard electrocardiogram and its significance for subsequent arrhythmic events

Background and hypothesis: QT dispersion, measured as interlead variability of QT intervals in the surface electrocardiogram, has been demonstrated to provide an indirect measurement of the inhomogeneity of myocardial repolarization. The purpose of the present study was twofold: (1) to analyze the effect of amiodarone on QT dispersion measured in the 12-lead standard ECG, and (2) to examine the association between QT dispersion on amiodarone and subsequent arrhythmic events. Methods: To determine the effect of amiodarone on QT dispersion and its clinical significance for subsequent arrhythmic events, QT dispersion was measured in the 12-lead standard electrocardiogram (ECG) in 52 patients before and after administration of empiric amiodarone for ventricular tachyarrhythmias. Results: QT intervals increased from 401 ± 44 ms before amiodarone to 442 ± 53 ms after amiodarone therapy, and rate corrected QT intervals (QTc) increased from 452 ± 43 ms to 477 ± 37 ms, respectively (p<0.01). QT dispersion, QTc dispersion, and adjusted QTc dispersion, which take account of the number of leads measured, were not significantly different before and after initiation of amiodarone therapy (58 ± 24 ms vs. 61 ± 26 ms, 68 ± 29 vs. 66 ± 26 ms, and 22 ± 8 vs. 22 ± 8 ms, respectively, p = NS). During 31 ± 25 months follow-up after initiation of amiodarone therapy, arrhythmic events defined as sustained ventricular tachycardia, ventricular fibrillation, or sudden death occurred in 11 of 52 study patients (21%). QT dispersion, QTc dispersion, and adjusted QTc dispersion on amiodarone were not different between patients with and without arrhythmic events during follow-up (65 ± 14 vs. 59 ± 29 ms, 73 ± 15 vs. 64 ± 28 ms, and 25 ± 6 vs. 21 ± 8 ms, respectively, p=NS). Conclusions: We conclude that (1) amiodarone increases QT intervals and QTc intervals during sinus rhythm but does not significantly change measures of QT dispersion; and (2) QT dispersion measured in the 12-lead standard ECG after initiation of amiodarone therapy does not appear to be a useful marker for subsequent arrhythmic events.     

Cardiac repolarization interval in end-stage diabetic and nondiabetic renal disease

Background and hypothesis: QT interval length is influenced by autonomic nervous activity. In patients with diabetic autonomic neuropathy, both prolongation and shortening of ventricular repolarization has been reported. We studied diabetic and nondiabetic uremic patients to assess the effects of autonomic neuropathy on QT interval length. Methods: 24-hour electrocardiogram recordings were performed in 12 diabetic and 11 nondiabetic renal transplantation patients, and in 12 control patients. Mean and corrected QT interval (QTc) during the 24-h period and intervals at predetermined heart rates at day and night periods were determined. The degree of autonomic neuropathy was assessed with cardiovascular autonomic function tests and measurement of heart rate variability. Results: In the diabetic group, severe autonomic neuropathy was present; in nondiabetic uremic patients, abnormalities were less severe. Mean QTc interval during 24 h was 444 ± 24,447 ± 21, and 442 ± 19 ms in the diabetic and nondiabetic uremic patients, and in the control groups, respectively, without any between-group difference. QT and QTc interval length did not differ among the groups when measured at heart rates of 70, 80, 90, or 100 beats/min. Conclusions: In patients with autonomic failure caused by diabetes and/or uremia, QT interval length cannot be used as a diagnostic indicator of cardiac autonomic neuropathy.     

QT dispersion and late potentials during doxorubicin therapy for non-Hodgkin's lymphoma

OBJECTIVES: To investigate effects of doxorubicin therapy on cardiac electrophysiology, with special emphasis on QT dispersion and late potentials, in lymphoma patients. DESIGN: Prospective study. SETTING: University hospital. SUBJECTS: Twenty-eight adult non-Hodgkin's lymphoma patients who received doxorubicin to a cumulative dose of 400-500 mg m-2. MAIN OUTCOME MEASURES: Standard 12-lead electrocardiogram (ECG) and signal-averaged ECG (SAECG) recordings were performed at baseline and after cumulative doxorubicin doses of 200, 400 and 500 mg m-2. RESULTS: Heart rate-corrected QT interval (QTc) increased from 402 +/- 4 to 416 +/- 5 ms (P = 0.002) during the study period. QT dispersion (variability in QT interval duration amongst the different leads of the standard 12-lead ECG) increased from 24.1 +/- 2.5 to 35.0 +/- 2.8 ms (P = 0.041) and QTc dispersion increased from 26.5 +/- 2.5 to 39.0 +/- 3.5 ms (P = 0.039). Five patients (18%) developed QT dispersion exceeding 50 ms. In addition, two patients (7%) developed late potentials during doxorubicin therapy. The changes in QTc duration, QT dispersion and late potentials occurred independently of the impairment of left ventricular function. CONCLUSIONS: Prolongation of QTc, increased QT dispersion and development of late potentials are indicative of doxorubicin-induced abnormal ventricular depolarization and repolarization. QT dispersion and late potentials are both known to be associated with increased risk of serious ventricular dysrhythmias and sudden death in various cardiac diseases. Thus, follow-up of these parameters might also be useful in assessing the risk of late cardiovascular events in cancer patients treated with anthracyclines.     

Enhanced Transmural Dispersion of Repolarization in Patients with J Wave Syndromes

J Wave Syndromes . Introduction: Recently, great attention has been paid to the risk stratification of asymptomatic patients with an electrocardiographic early repolarization (ER) pattern. We investigated several repolarization parameters including the Tpeak‐Tend interval and Tpeak‐Tend/QT ratio in healthy individuals and patients with J wave syndrome who were aborted from sudden cardiac death. Methods and Results: Ninety‐two subjects were enrolled: 12 patients with ventricular fibrillation associated with J waves, 40 healthy subjects with an uneventful ER pattern and 40 healthy control subjects (C) without any evident J waves. Using ambulatory electrocardiogram recordings, the average QT interval, corrected QT interval (QTc), Tpeak‐Tend (Tp‐e) interval, which is the interval from the peak to the end of the T wave, and Tp‐e/QT ratio were calculated. Using ANOVA and post hoc analysis, there was no significant difference in the average QT and QTc in all 3 groups (QT; 396 ± 27 vs 405 ± 27 vs 403 ± 27 m, QTc; 420 ± 26 vs 421 ± 21 vs 403 ± 19 milliseconds in the C, ER pattern and J groups, respectively). The Tp‐e interval and Tp‐e/QT ratio were significantly more increased in the J wave group than the ER Pattern group (Tp‐e: 86.7 ± 14 milliseconds vs 68 ± 13.2 milliseconds, P < 0.001, Tp‐e/QT; 0.209 ± 0.04 vs 0.171 ± 0.03, P < 0.001), but they did not significantly differ between the C and ER pattern groups (Tp‐e: 68.6 ± 7.5 vs 68 ± 13.2, P = 0.97, Tp‐e/QT 0.174 ± 0.02 vs 0.171 ± 0.03, P = 0.4). Conclusion: As novel markers of heterogeneity of ventricular repolarization, Tpeak‐Tend interval and Tp‐Te/QT ratio are significantly increased in patients with J wave syndromes compared to age and sex‐matched uneventful ER. (J Cardiovasc Electrophysiol, Vol. 23 pp. 1109‐1114, October 2012)     

Hyperthyroidism is associated with lengthening of ventricular repolarization

OBJECTIVE: Lengthened ventricular repolarization, as assessed by the QT interval on electrocardiogram (ECG), can predispose to an increased risk of cardiac dysrhythmias; no data are available on QT corrected for heart rate (QTc) in hyperthyroidism in vivo. DESIGN: QT and RR intervals from 24 h ambulatory ECG Holter recording were measured in patients with hyperthyroidism and again following pharmacological achievement of stable euthyroidism for at least 2 months. PATIENTS: We enrolled a total of 16 hyperthyroid patients with Graves' disease, six males and 10 females (mean age 47 +/- 4 years, mean +/- SEM); 13 healthy age- and sex-matched subjects were utilized as a control group. MEASUREMENTS: The QT analysis was carried out by a computerized algorithm (QTc was corrected by the heart rate by Bazett's formula). Serum total T4, total T3, free T4, free T3 and TSH concentrations were measured by a fully automated immunoenzymometric assay; plasma norepinephrine by automatized high-pressure liquid chromatography, potassium and chloride by a potentiometric method, magnesium and calcium by a colourimetric method. RESULTS: The 24-h average QTc in the hyperthyroid patients was significantly prolonged compared to controls (458 +/- 7 vs. 431 +/- 6 ms, P = 0.01) and it returned to normal after treatment of thyrotoxicosis (432 +/- 6 ms, P < 0.05 vs. time H, NS vs. controls). QTc positively correlated with FT3 (r = 0.63, P < 0.001) and with FT4 (r = 0.481, P < 0.02). Conversely, QTc did not correlate with plasma basal norepinephrine levels, nor with electrolytes. CONCLUSIONS: Hyperthyroidism is associated with prolonged QTc that normalizes once the patient becomes euthyroid. The strong positive correlation between FT3 and QTc supports the hypothesis of an important role of thyroid hormone on modulation of QTc lengthening.     

Diagnostic performance of QT interval variables from 24-h electrocardiography in the long QT syndrome

Aims The long QT syndrome is mainly defined by QT interval prolongation(QTc >0·44s). However, data obtained in genotyped patientsshowed that resting QTc measurement alone may be inaccuratefor ascertaining the phenotype. The aim of this study was toevaluate the diagnostic performance of QT interval rate-dependencein untreated chromosome 11-linked patients. Methods The study population consisted of 25 untreated longQT patients linked to chromosome 11 and 25 age- and gender-matchedcontrols. QTc intervals were measured on 12-lead resting ECGrecordings. From 24-h Holter recordings, the slope of the relationshipbetween ventricular repolarization and heart rate was studiedseparately day and night to assess neural modulation. Mean heartrates and rate-dependences of QT and Q-maximum of T (QTm) intervalswere compared between long QT patients and controls for bothtime periods. Results In both groups, the rate-dependences were modulatedby day–night influences. When compared to controls, longQT patients showed a significant increase at night in QT/RRslopes (0·158±0·05 vs 0·117±0·03,P=0·002)and QTm/RR slopes (0·163±0·05 vs 0·116±0·04,P=0·0006).Multivariate analysis, adjusting QTc interval on age and gender,discriminated between long QT patients and controls with a 76%sensitivity and a 84% specificity. A 96% sensitivity and a 96%specificity were reached by taking into account the QTm/RR slopeat night, the QTc interval and the mean heart rate during theday. Conclusion QT interval variables obtained from 24-h ECG recordingsimprove long QT syndrome diagnosis by showing an increased nocturnalventricular repolarization rate-dependence in genotyped chromosome11-linked patients.     

Dispersion of the QT Interval in Subjects with Frequent Nonsustained Ventricular Arrhythmias and No Underlying Heart Disease: Arrhythmogenic Substrate or Mechanoelectrical Feedback of Arrhythmias?

Background: QT dispersion (QTd) on the ECG is thought to reflect the temporal and spatial inhomogeneity of repolarization in the underlying myocardium. In myocardial infarction, ischemia, and long QT syndromes, an increased QTd is associated with a propensity for malignant ventricular arrhythmias and sudden cardiac death. We investigated this feature of the repolarization process in subjects with frequent ventricular arrhythmias and structurally normal hearts. Methods: Forty‐nine patients referred for frequent, nonsustained ventricular arrhythmias (45 ± 14 years, ×± SD, 61% female) had normal ventricular dimensions and function, no late potentials, and normal ECG. They were compared with 30 controls (42 ± 13 years, 50% female). QTd was measured as the difference between the longest and the shortest QT in the six precordial leads at a paper speed of 50 mm/s. Results: In patients, QTc was similar to that of controls: 395 ± 21 versus 386 ± 20. However, QTd was greater: 49 ± 20 ms versus 32 ± 14 ms, P < 001. Moreover, 18 patients (36%) had QTd exceeding 60 ms—a value superior to the mean normal value of 2 SD—compared to only 1 control (3%) (P < 0.01). Finally, patients with more frequent ventricular arrhythmias had larger QTd. Conclusions: In patients with frequent nonsustained ventricular arrhythmias and otherwise normal hearts, QT interval dispersion is increased. We speculate that, instead of representing a specific electrophysiological substrate of arrhythmias, QT dispersion in this specific population could result from arrhythmias themselves through a possible mechanoelectrical feedback.