QT间期延长综合征

ＱＴ间期延长综合征是心肌复极障碍所致的疾病 ,临床以ＱＴ间期延长 ,Ｕ波异常 ,反复发作晕厥 ,多形性室速和心源性猝死为主要特点。ＱＴ间期延长综合征可以分为先天性长ＱＴ间期综合征和继发性长ＱＴ间期综合征两种类型。1　先天性ＱＴ间期延长综合征先天性ＱＴ间期延长综合征     

肝硬变患者QT间期延长及QT间期离散度的临床意义

目的探讨肝硬变患者QT间期及QT间期离散度 (QTd)的变化与临床意义。方法测量 13 8例病毒性肝炎肝硬变患者的同步 12导联心电图 ,分析QT间期及QTd ,并与其他消化系疾病的 5 0例住院患者进行对照。结果肝硬变患者中QT间期延长发生率非常显著高于对照组 (P <0 .0 1) ,QTd也显著高于对照组 (P <0 .0 5 ) ;肝硬变患者Child PughA、B、C3级中QT间期延长发生率逐步升高 ,QTd增加也逐渐明显 (均为P <0 .0 5 ) ;肝硬变患者中死亡者的QT间期非常显著长于存活者 ,QTd也非常显著增加 (均为P <0 .0 1)。结论肝硬变患者QT间期延长发生率高 ,QTd增加明显 ,且与肝硬变严重程度相平行。提示QT间期延长及QTd可以作为肝硬变严重程度的指标之一。     

低血糖昏迷所致QT间期延长1例

<正>患者,女,64岁,主因昏迷3h于2013-3入院。患者于入院前2天,当地化验血糖7.8mmol/L,给予口服降糖药物,格列本脲片(每次2.5 mg,3次/d),家属诉共服用2次,1天前开始出现意识不清,伴出汗,呼之不应,当地诊所考虑"低血糖",     

QT间期延长综合征长期误诊为癫

1　 病例资料男 ,13岁。因反复晕厥、抽搐 8年入院。 8年前无明显诱因突然倒地 ,双眼球上翻 ,颜面发绀 ,呼之不应 ,双上肢痉挛屈曲 ,持续数秒自行缓解。此后每间隔 3个月～ 1年发作 1次 ,先后求治于多家医院 ,4次查脑电图均未见样放电 ,2 4小时动态脑电图仅枕区见异常慢活动 ,2次脑CT检查未见异常。按癫予苯妥英钠治疗不能控制发作。 3年前曾因癫持续状态 ,在某院查心电图示尖端扭转型室性心动过速 ,考虑为癫、药物中毒性心肌炎。停用苯妥英钠 ,改为卡马西平、地西泮等药物治疗 ,仍不能控制发作。既往未服用奎尼丁、索他洛尔、红霉…     

心脏起搏患者QT间期延长伴扭转型室速的识别和处理

目的：探讨安置起搏器患者中发生ＱＴ间期延长伴尖端扭转型室速（ＬＰＴｓ－ＴｄＰ）的早期诊断和治疗。方法：对本文报道的６例患者进行综合分析其病因，机制，临床特点及心电图变化。结果：被抢救的６例患者，３例为典型性ＬＰＴｓ－ＴｄＰ，３例为非典型性，ＬＰＴｓ－ＴｄＰ，６例中５例抢救成功，１例失败。结论：有晕厥发作史的起博患者应警惕合并存在ＬＱＴｓ－ＴｄＰ。     

家庭性特发性QT间期延长伴昏厥

1 病例介绍 患者，女，35岁，以昏厥原因待查收入院。入院查心电图示，窦性心律，62次／min，室性早搏3次／min，QTc=0．52s，ST—T未见异常。超声心动图及心脏像正常，电解质在正常范围。自诉：头晕、心悸、乏力。以往也有因体力劳动、激烈运动或情绪波动之后出现头晕、眼前发黑、心跳加速等。其兄弟姐妹六人，其中，其姐及其妹也述说过有相同表现。     

甲状腺功能减退致使QT间期延长1例

1 病例 患者，女性，60岁。反复头晕头痛半年入院。患者于40岁停经。近半年来反复出现发作性头晕头痛，每次发作时持续数秒，发作前无异常刺激先兆，并且与体位无关。入院后发作二次，每次持续5分钟～7分钟左右，并且伴有抽搐，大汗及大小便失禁等，呼叫她不答应，醒后无胸痛胸闷、无肢体障碍等。体格检查：血压11／9Kpa，心率75次／分，神志清楚。     

血液透析对QT间期和左室功能的影响

慢性肾功能衰竭 (CRF)患者血液透析 (血透 )中心血管并发症常为致死原因之一。观察 2 0例 CRF患者血透前后心电图 QT间期和超声心动图左室功能的变化 ,旨在探讨血透对心律失常和左室功能的影响。1　资料与方法1.1　病例 :维持性血透治疗 CRF患者2 0例中男 6例 ,女 14例 ;年龄 2     

心脏起搏患者QT间期延长伴扭转型室速的识别和处理

探讨安置起搏器患者中发生QT间期延长伴尖端扭转型室速 (LPTs -TdP)的早期诊断和治疗。方法 :对本文报道的 6例患者进行综合分析其病因 ,机制 ,临床特点及心电图变化 ,结果 :被抢救的 6例患者 ,3例为典型性LPTs -TdP ,3例为非典型性LPTs-TdP ,6例中 5例抢救成功 ,1例失败。结论 :有晕厥发作史的起搏患者应警惕合并存在LQTs -TdP。     

QT间期延长和尖端扭转型室性心动过速的临床对策

TdP是一种与QT间期延长相关联的恶性心律失常,临床对策有别于普通室性心动过速。本文扼要介绍了近年来在TdP临床对策方面所取得的进展。     

QT Interval Variability and Adaptation to Heart Rate Changes in Patients with Long QT Syndrome

Background: Increased QT variability (QTV) has been reported in conditions associated with ventricular arrhythmias. Data on QTV in patients with congenital long QT syndrome (LQTS) are limited.
Methods: Ambulatory electrocardiogram recordings were analyzed in 23 genotyped LQTS patients and in 16 healthy subjects (C). Short-term QTV was compared between C and LQTS. The dependence of QT duration on heart rate was evaluated with three different linear models, based either on the RR interval preceding the QT interval (RR₀), the RR interval preceding RR₀ (RR_-1), or the average RR interval in the 60-second period before QT interval (mRR).
Results: Short-term QTV was significantly higher in LQTS than in C subjects (14.94 ± 9.33 vs 7.31 ± 1.29 ms; P < 0.001). It was also higher in the non-LQT1 than in LQT1 patients (23.00 ± 9.05 vs 8.74 ± 1.56 ms; P < 0.001) and correlated positively with QTc in LQTS (r = 0.623, P < 0.002). In the C subjects, the linear model based on mRR predicted QT duration significantly better than models based on RR₀ and RR_-1. It also provided better fit than any nonlinear model based on RR₀. This was also true for LQT1 patients. For non-LQT1 patients, all models provided poor prediction of QT interval.
Conclusions: QTV is elevated in LQTS patients and is correlated with QTc in LQTS. Significant differences with respect to QTV exist among different genotypes. QT interval duration is strongly affected by noninstantaneous heart rate in both C and LQT1 subjects. These findings could improve formulas for QT interval correction and provide insight on cellular mechanisms of QT adaptation.     

Comparison of Formulae for Heart Rate Correction of QT Interval in Exercise Electrocardiograms

The study investigated the differences in five different formulae for heart rate correction of the QT interval in serial electrocardiograms recorded in healthy subjects subjected to graded exercise. Twenty-one healthy subjects (aged 37+/-10 years, 15 male) were subjected to graded physical exercise on a braked bicycle ergometer until the heart rate reached 120 beats/min. Digital electrocardiograms (ECG) were recorded on baseline and every 30 seconds during the exercise. In each ECG, heart rate and QT interval were measured automatically (QT Guard package, Marquette Medical Systems, Milwaukee, WI, USA). Bazett, Fridericia, Hodges, Framingham, and nomogram formulae were used to obtain QTc interval values for each ECG. For each formula, the slope of the regression line between RR and QTc values was obtained in each subject. The mean values of the slopes were tested by a one-sample t-test and the comparison of the baseline and peak exercise QTc values was performed using paired t-test. Bazett, Hodges, and nomogram formulae led to significant prolongation of QTc intervals with exercise, while the Framingham formula led to significant shortening of QTc intervals with exercise. The differences obtained with the Fridericia formula were not statistically significant. The study shows that the practical meaning of QT, interval measurements depends on the correction formula used. In studies investigating repolarization changes (e.g., due to a new drug), the use of an ad-hoc selected heart rate correction formula is highly inappropriate because it may bias the results in either direction.     

The Relationship Between Heart Rate and QT Interval During Atrial Stimulation

The relationship between heart rate and QT interval was investigated during atrial stimulation (intrinsic effect of heart rate) in ten healthy male volunteers prior to and after administration of sotaloI. The QT interval in the ECG (paper speed 200 mm/s) was determined at rates of 70, 85, 100, 115, 130, 145, and 160 beats/min and at pacing periods of 180 s each at 30, 60, 120, and 180 s. After a 15-minute period, 2.0 mg sotalol/kg body weight were administered iv and the stimulation protocol was repeated. The analysis of QT interval behavior reveals contradictions to the mathematical implications of Bazett's equation     , so that the relationship between heart rate and QT interval is not adequately described under the given conditions. After examination of approaches reported in the literature and our own approaches, the expression QT = a e^−b(HR-60) is used as a possibility differentially to describe the data by nonlinear regression. The parameters a and b may be interpreted as QT reference value and shortening parameter. The QT reference value a, a parameter in reference to heart rate of 60 beats/min, has a comparable significance to the expression QT, in the Bazett equation. A reduction in the shortening parameter b indicates whether substances influencing the QT interval additionally produce overproportional shortening of the QT interval with increasing heart rate. After administration of sotalol, an increase can be observed in both the QT reference value and also in the shortening parameter. The suggested approach is an attempt to provide a more precise assessment of the QT interval under different conditions.     

Electrophysiologic Effects of Beta-blocking Agent, Tilisolol, on Isolated Guinea Pig Ventricular Myocytes

BACKGROUND: Electrophysiologic effects of a beta-blocking agent, tilisolol, were studied with isolated guinea pig ventricular myocytes using the whole cell patch clamp technique. METHODS AND RESULTS: Tilisolol at 10 μM or higher concentrations prolonged action potential duration (APD) at 90% repolarization (APD(90)) and at 100 μM or higher concentrations shortened APD at 20% repolarization (APD(20)) without changes in resting membrane potential. At 10 μM concentration tilisolol prolonged APD(90) from 236.6 +/- 55.3 ms in the control to 253.4 +/- 52.4 ms (n = 16; P <.01), while APD(20) was unaffected. At 100 μM tilisolol, APD(20) was shortened from 143.6 +/- 15.7 ms in the control to 133.7 +/- 22.6 ms (n = 8; P <.05). Under voltage clamp, tilisolol decreased the delayed rectifier K(+) current (I(K1)). Applications of 10 μM and 100 μM tilisolol reduced the maximal conductance of I(K) by 35.7 +/- 3.5% and 47.4 +/- 3.5% of the control, respectively, without changes in voltage dependence (n = 10). Tilisolol at 100 μM decreased the L-type Ca(2+) current (I(Ca.L)) by 22.0 +/- 9.8% (n = 6) of the control, and the inactivation curve was shifted to a hyperpolarizing direction. CONCLUSIONS: Tilisolol has a direct membrane action to depress I(K) and I(Ca.L), in addition to its beta-receptor blocking action.     

Beat-To-Beat Behavior of QT Interval During Conducted Supraventricular Rhythm in the Normal Heart

To assess beat-to-beat behavior of QT interval under different conditions, high resolution recordings and computerized beat-to-beat analysis of the electrocardiogram were performed at rest, during recovery after short exercise, and during atrial pacing. Beat-to-beat variations of QT interval during sinus rhythm at rest and after short exercise were measured in ten healthy men. In an additional three patients with supraventricular tachycardia, beat-to-beat QT changes were studied after abrupt sustained acceleration and deceleration of heart rate by atrial pacing. Beat-to-beat changes in RH interval at rest are followed by minimal changes of the QT interval. The measured proportional change of the QT interval compared with the change in HR interval (Δ QT/A BR) was 0.02. This value represents 10% of the value expected for QT changes from Bazett's formula. Following short exercise QT interval did not change for 15 seconds and reached a maximal value 30 seconds later as compared to the RR interval (192 vs 115 sees, P < 0.001). The steady state of the QT interval during sustained atrial pacing was achieved after 132, 135, and 133 seconds for pacing intervals of 600, 500, and 600 msec, respectively. Our data indicate a relatively slow adaptation of the QT interval to changes in heart rate.     

Circadian Profile of QT Interval and QT Interval Variability in 172 Healthy Volunteers

BONNEMEIER, H., et al .: Circadian Profile of QT Interval and QT Interval Variability in 172 Healthy Volunteers. The limited prognostic value of QT dispersion has been demonstrated in recent studies. However, longitudinal data on physiological variations of QT interval and the influence of aging and sex are few. This analysis included 172 healthy subjects (89 women, 83 men; mean age   38.7 ± 15   years). Beat-to-beat QT interval duration (QT, QTapex [QTa], T_end[Te]), variability (QTSD, QTaSD), and the mean R-R interval were determined from 24-hour ambulatory electrocardiograms after exclusion of artifacts and premature beats. All volunteers were fully active, awoke at approximately 7:00 am , and had 6–8 hours of sleep. QT and R-R intervals revealed a characteristic day-night-pattern. Diurnal profiles of QT interval variability exhibited a significant increase in the morning hours (6–9 am ; P < 0.01) and a consecutive decline to baseline levels. In female subjects the R-R and T_end intervals were significantly lower at day- and nighttime. Aging was associated with an increase of QT interval mainly at daytime and a significant shift of the T wave apex towards the end of the T wave. The circadian profile of ventricular repolarization is strongly related to the mean R-R interval, however, there are significant alterations mainly at daytime with normal aging. Furthermore, the diurnal course of the QT interval variability strongly suggests that it is related to cardiac sympathetic activity and to the reported diurnal pattern of malignant ventricular arrhythmias. (PACE 2003; 26[Pt. II]):377–382)     

Effect of Vicriviroc on the QT/Corrected QT Interval and Central Nervous System in Healthy Subjects

Vicriviroc is a CCR5 antagonist in clinical development for the treatment of HIV-1. Two phase I studies were conducted to assess the safety of vicriviroc. One study characterized the drug''s potential to prolong the QT/corrected QT (QTc) interval and to induce arrhythmia. In this partially blind, parallel-group study, 200 healthy subjects aged 18 to 50 years were randomized in equal groups to the following regimens: (i) placebo for 9 days and a single dose of moxifloxacin at 400 mg on day 10, (ii) placebo, (iii) vicriviroc-ritonavir (30 and 100 mg), (iv) vicriviroc-ritonavir (150 and 100 mg), and (v) ritonavir (100 mg). The second study characterized the effects of a range of vicriviroc doses on the central nervous system (CNS). In this third-party-blind, parallel-group study, 30 healthy subjects aged 18 to 48 years were randomized to receive a single dose of either vicriviroc at 200, 250, or 300 mg or placebo, followed by multiple (seven) once-daily doses of either vicriviroc at 150, 200, or 250 mg or placebo, respectively. In the first study, vicriviroc produced no clinically meaningful effect on the QT/QTc interval when administered at a supratherapeutic or therapeutic dose concurrently with ritonavir. In the second study, vicriviroc produced no observable seizure activity, nor was it held to be associated with any clinically relevant changes in brain waveforms in the final consensus of reviewers. These findings showed that vicriviroc produced no clinically relevant QTc prolongation cardiac or epileptogenic effects in healthy individuals at exposures as high as five times those expected for HIV-infected patients receiving therapeutic doses of vicriviroc in a ritonavir-boosted protease inhibitor-containing regimen.Vicriviroc maleate is a novel CCR5 antagonist that is currently in late-stage clinical development as part of a ritonavir-boosted protease inhibitor regimen for HIV-1-infected individuals. In clinical studies, vicriviroc has demonstrated potent and durable virologic suppression, immunologic activity, and generally favorable tolerability (5).The current report describes two phase I studies that investigated the cardiac and central nervous system (CNS) safety, respectively, of vicriviroc in normal healthy adult volunteers. The first study was performed in accordance with the standard guidance for industry, which requires a comprehensive evaluation of cardiac safety for the safe conduct of drug development programs and drug registration, including those for vicriviroc (9). These assessments characterize the potential for new agents to prolong the QT/corrected QT (QTc) interval and to induce cardiac arrhythmias, such as torsade de pointes (TdP) and other ventricular tachyarrhythmias (1, 2, 8). Vicriviroc was studied both at a supratherapeutic dose and at the intended clinical dose in comparison with a placebo (negative control) and moxifloxacin (positive control). The effect of vicriviroc was evaluated in the presence of ritonavir, since the intended clinical administration of vicriviroc is to be part of an antiretroviral regimen that includes a ritonavir-boosted protease inhibitor (PI).The second, independent study was performed to evaluate the CNS safety of vicriviroc, since the dose-limiting toxicity for vicriviroc in nonclinical safety evaluations was seizures, although no seizures have been seen clinically in any patient treated with vicriviroc and there has been no evidence of a clinically significant CNS effect in humans (4). Seizures observed in several animal species were characterized as tonic-clonic convulsions, occurred generally at the time of maximal plasma drug concentrations, were self-limiting, and were preventable with standard anticonvulsant therapy. The mechanism by which vicriviroc caused seizures in animals is not clear. Animal-to-human exposure multiples (based on the pharmacokinetic concentration value associated with seizure activity in the dog) are ≥10 based on the intended clinical usage of 30 mg of vicriviroc as part of a ritonavir-boosted PI-containing antiretroviral regimen. To further characterize vicriviroc, we performed clinical assessments of the safety of both single and multiple supratherapeutic doses of vicriviroc, including electroencephalogram (EEG) monitoring.     

Effect of Beta-Adrenergic Stimulation on the QT Interval of Children with Syncope

The effect of intravenous bolus doses (0.25. 0.5. 1.0 fig) of isopwterenol on the QT and BR intervals was reviewed in a group of 34 children undergoing autonomic testing for svncope. Twenty-one patients had a positive orthostatic test and 13 were negative. The two groups (positive and negative) were compared Baseline QT and RR intervals were similar. The RR interval was shortened by isoproterenol in both groups Isoproterenol shortened the QT interval in the negative group (as seen in normal persons), but produced QT prolongation in the positive group, although neither reached statistical significance when compared to baseline within the respective group. Comparing the values for RR and QT at each dose of isoproterenol (including baseline) between the two groups showed a significant difference in the QT interval after the 1.0-fxg dose of isoproterenol. Thus children with orthostatic positive neurocardiogenic syncope showed a different QT response to fi-adrenergic stimulation. This lends support to the theory of altered /3-adrenergic sensitivity being present in children with neurocardiogenic syncope.     

Circadian Rhythm of the Corrected QT Interval: Impact of Different Heart Rate Correction Models

SMETANA, P., et al .: Circadian Rhythm of the Corrected QT Interval: Impact of Different Heart Rate Correction Models . A reduced circadian pattern in the QTc interval has been repeatedly reported to provide prognostic information in cardiac patients. However, the results of studies in healthy subjects in which different heart rate correction formulas were used are inconsistent regarding the presence and extent of diurnal variations in QTc. This study compared the diurnal variations in QTc obtained with four frequently used heart rate correction models with those based on individually optimized heart rate correction. In 53 subjects (25 men aged 27 ± 7 years and 28 women aged 27 ± 9 years) 12-lead digital ECGs were obtained every 30 seconds during 24 hours. The QT interval was measured automatically by six different algorithms provided by a commercially available device. The QT/RR relation was estimated by four common heart rate correction models and by an individually optimized correction model, QTc = QT/RR^α. In each 24-hour recording, RR, QT, and QTc intervals of separate ECG samples were averaged over 10-minute intervals. Marked differences were found in the extent of the circadian pattern of QTc obtained with different formulas for heart rate correction. Under and overcorrection of the QT interval resulted in significant over- or underestimation of the circadian pattern. Thus, the extent of circadian variation in QTc depends highly on the heart rate correction formula used. To obtain proper insight regarding diurnal variation in QTc prolongation during pharmacologic therapy and/or to assess higher risk due to impaired autonomic regulation of ventricular repolarization, individualized heart rate correction is necessary. (PACE 2003; 26[Pt. II]:383–386)