New Insight into Repolarization Abnormalities in Patients with Congenital Long QT Syndrome: the Increased Transmural Dispersion of Repoiarization

There is evidence from experimental studies that the time interval from the peak to the end of T-wave reflects the transmural dispersion in repolarization (electrical gradient) between myocardial "layers" (epicardial, M-cells, endocardial). Since Congenital Long QT Syndrome (LQTS) is considered to be classical disease or repolarisation abnormalities, we performed the present study to assess the transmtiral dispersion of repolarization in LQTS patients. The study group consisted of 17 patients: 7 LQTS pts and 10 pts from the control group. In each patient the 24-hour ECG recording was performed on magnetic tape. The interval from the peak to the end of the T-wave (TpTo) was automatically measured by Holter system during every hour as a measure of transmural dispersion of repolarisation. Thereafter the mean TpTo from 24-hours was calculated. In addition the spatial QT dispersion was measured from 12 lead ECG and 3 channel Holter tape as a difference between the shortest and the longest QT interval between leads. The values were compared between groups using the Anova test.
TpTo was 79,6±9,6 ms (72–92 ms) in LQTS group and 62,4±7,5 ms (51–70) in the control group (p< 0.001). In LQTS group TpTo was significantly longer at night hours 72,5±2 when compared to day hours 87,4±8 (p<0.01). The spatial QT dispersion was significantly higher in LQTS patients when compared to control, both in 12-lead standard and Holter ECG.
Congenital long QT syndrome is associated with increase in both transmural and spatial dispersion of repolarization. The extent of prolongation of the terminal portion of QT in patients with congenital long QT syndrome is greater at night sleep hours compared to daily activity.     

Analysis of the Corrected QT Before the Onset of Nonsustained Ventricular Tachycardia in Patients with Hypertrophic Cardiomyopathy

BARANOWSKI, R., et al .: Analysis of the Corrected QT Before the Onset of Nonsustained Ventricular Tachycardia in Patients with Hypertrophic Cardiomyopathy. This study examined ventricular repolarization before the onset of 37 episodes of nonsustained ventricular tachycardia (NSVT) in 26 untreated patients with hypertrophic cardiomyopathy (HCM). Fourteen episodes were recorded in patients with a history of cardiac arrest or patients who died suddenly during follow-up. The QT interval was measured beat-by-beat on 24-hour ambulatory electrocardiograms. Mean 24-hour, hourly QTc and QTc of the last 10 beats prior to NSVT, consisted of 4–50 cycles (mean   9 ± 10   ), at the fastest rates of 100–175 beats/min (mean 122 ± 22) were analyzed. NSVT was more prevalent during nighttime (23 episodes), than during daytime (14 episodes,   P < 0.05   ). No significant differences were observed between mean 24-hour, mean hourly QTc during the hour with NSVT, and QTc of the last 10 cycles prior to onset of NSVT. QTc was significantly longer in patients with a history of sudden cardiac death (SCD) or who died suddenly during follow-up than in survivors. The 24-hour QT variability was higher in nonsurvivors than in survivors (   -39 ± 6   vs   33 ± 6 ms, P = 0.03   ). Episodes of NSVT in untreated patients with hypertrophic cardiomyopathy were more frequent during the nighttime. The 24-hour QT variability was higher in nonsurvivors than in survivors. (PACE 2003; 26[Pt. II]:387–389)     

Circadian and Sex-Dependent QT Dynamics

The dynamic QT relationship between the QT and RR intervals in normal individuals, including sex differences, has not been well examined. The aim of this Holter monitor-based study was to assess circadian and sex-related variations in QT dynamics in healthy subjects. The study population consisted of 50 healthy volunteers (mean age = 32 ± 6 years, 25 men), in whom 24-hour digital Holter monitoring and QT interactive, beat-by-beat analyses were performed. The mean lengths of QT and RR intervals were measured from the 24-hour recordings. In order to assess QT dynamics, QT/RR linear regression was performed, and the slope was calculated over 24 hour and for day and night periods, and both genders separately. In the whole population, the mean QT interval was 356.5 ± 19.2 ms and RR interval was 785.9 ± 80.7 ms. The mean value of the slope over 24 hour was 0.17 ± 0.03, though significantly steeper during the day (0.13 ± 0.03) than at night (0.09 ± 0.03, P < 0.001). The analysis of QT/RR dynamics over 24 hour revealed a significantly steeper slope in women (0.18 ± 0.03) than in men (0.16 ± 0.03, P = 0.006), as well as during daytime (0.14 ± 0.03 vs 0.12 ± 0.03, P = 0.04). Circadian variations and sex differences were observed in QT dynamics. The latter may explain the greater susceptibility of women to torsades de pointes during treatment with drugs that prolong repolarization.     

QT Variability Before and After Episodes of Nonsustained Ventricular Tachycardia in Patients with Hypertrophic Cardiomyopathy

This study examined the changes in QT dynamics occurring during 5-minute intervals sampled immediately before and 1 hour after episodes of nonsustained ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HCM). Twenty-four hour Holter recordings were performed in 10 patients with HCM in the absence of antiarrhythmic medications and processed by the ELA Medical QT analysis software. All sinus complexes were averaged over 30-second segments and 2,880 templates were created. For each template, a mean corrected QT_ec (time interval between the onset of QRS and the end of the T wave) and QT_ac (time interval between the onset of the QRS and the peak of the T wave) were calculated, with their standard deviations (SDQT_e and SDQT_a) taken as indices of QT variability. The slopes of the regression line for the QT_e and QT_a against the corresponding RR also were calculated. Forty 5-minute segments were analyzed immediately before (sample A) and 1 hour after (sample B) 20 episodes of nonsustained VT. QT_ac was significantly longer in group A than in group R (321 ± 20 vs 312 ± 22, P < 0.0001) and SDQT_a was significantly lower (2.8 ± 1.2 vs 4.7 ± 3.7, P < 0.03). There were no significant differences in QT_ec, SDQT_e, QTe/RR and QT_a/RR before and after the episodes. Our data indicate that in patients with HCM, the averaged QT_ac is significantly longer and the QT_a variability significantly lower before episodes of nonsustained VT.     

Polymorphous Ventricular Tachycardia and Atrioventricular Block

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during atrioventricular (AV) block. There were five men and four women with a mean age of 80 +/- 9 years. Five patients had organic heart disease and the remaining four had primary conduction disease (bundle branch block). AV block was complete in four patients (2:1 in three, and paroxysmal in two). The mean ventricular cycle length (of the AV block rhythm) was 1567 +/- 203 ms. The mean QT interval was 0.64 +/- 0.09 s and the mean QTc was 0.51 +/- 0.06 s. When compared to a similar control group with AV block but without PMVT, the ventricular cycle length was similar but the QT and QTc were significantly longer. PMVT was usually of short duration (eight beats to 12 s) and in seven of these nine patients, frequent premature ventricular beats (PVBs) were recorded at various times from the occurrence of PMVT. This is in contrast to the control patients in whom PVBs were detected in one patient only. In conclusion, patients with AV block who develop PMVT usually have longer QT intervals and have detectable PVBs on routine ECGs, unlike similar patients with AV block but without PMVT. In a patient with AV block, a QT interval above 0.60 s and PVBs on the ECG seem to indicate an increased risk for the development of PMVT.     

Electrocardiographic changes during steady mild hypothermia and normothermia in patients with poikilothermia.

1. ECG changes observed in short-term induced and accidental hypothermia are well known. To assess the influence of steady-state spontaneous hypothermia on the ECG, we subjected four patients with acquired poikilothermia (severe thermolability) to 24 h ECG recording, exercise testing and thermal stress. 2. Twenty-four hour Holter monitoring showed a significant reduction in heart rate and a prolongation of the QT interval during steady-state mild hypothermia (rectal temperature 33.9 +/- 0.7 degrees C, mean +/- SD) compared with during normothermia; no significant changes occurred in the PR interval, QRS complex and QTc interval (QT interval corrected for heart rate). 3. Unlike during normothermia, during steady hypothermia atrioventricular Wenckebach blocks were observed in two patients, whereas another patient showed markedly more atrioventricular Wenckebach blocks during hypothermia. 4. During steady hypothermia the heart rate variability was significantly enhanced in comparison with normothermia. 5. Exercise tolerance was similar during mild hypothermia and normothermia. 6. Heat exposure (ambient temperature 40 degrees C) induced significantly greater changes in rectal temperature, heart rate and PR interval, QRS complex and QT interval in the patients than in the control subjects (n = 8). 7. The present study reveals that even mild steady spontaneous hypothermia can elicit ECG changes, presumably mediated by relatively enhanced cardiac vagal tone. Hence, spontaneous abnormalities in core temperature should be taken into account in interpreting the ECG in clinical practice.     

Epinephrine-induced QT interval prolongation: a gene-specific paradoxical response in congenital long QT syndrome

OBJECTIVE: To determine the effect of epinephrine on the QT interval in patients with genotyped long QT syndrome (LQTS). PATIENTS AND METHODS: Between May 1999 and April 2001, 37 patients (24 females) with genotyped LQTS (19 LQT1, 15 LQT2, 3 LQT3, mean age, 27 years; range, 10-53 years) from 21 different kindreds and 27 (16 females) controls (mean age, 31 years; range, 13-45 years) were studied at baseline and during gradually increasing doses of intravenous epinephrine infusion (0.05, 0.1, 0.2, and 0.3 microg x k(-1) x min(-1)). The 12-lead electrocardiogram was monitored continuously, and heart rate, QT, and corrected QT interval (QTc) were measured during each study stage. RESULTS: There was no significant difference in resting heart rate or chronotropic response to epinephrine between LQTS patients and controls. The mean +/- SD baseline QTc was greater in LQTS patients (500+/-68 ms) than in controls (436+/-19 ms, P<.001). However, 9 (47%) of 19 KVLQT1-genotyped LQT1 patients had a nondiagnostic resting QTc (<460 milliseconds), whereas 11 (41%) of 27 controls had a resting QTc higher than 440 milliseconds. During epinephrine infusion, every LQT1 patient manifested prolongation of the QT interval (paradoxical response), whereas healthy controls and patients with either LQT2 or LQT3 tended to have shortened QT intervals (P<.001). The maximum mean +/- SD change in QT (AQT [epinephrine QT minus baseline QT]) was -5+/-47 ms (controls), +94+/-31 ms (LQT1), and -87+/-67 ms (LQT2 and LQT3 patients). Of 27 controls, 6 had lengthening of their QT intervals (AQT >30 milliseconds) during high-dose epinephrine. Low-dose epinephrine (0.05 microg x kg(-1) x min(-1)) completely discriminated LQT1 patients (AQT, +82+/-34 ms) from controls (AQT, -7+/-13 ms; P<.001). Epinephrine-triggered nonsustained ventricular tachycardia occurred in 2 patients with LQTS and in 1 control. CONCLUSIONS: Epinephrine-induced prolongation of the QT interval appears pathognomonic for LQT1. Low-dose epinephrine infusion distinguishes controls from patients with concealed LQT1 manifesting an equivocal QTc at rest. Thus, epinephrine provocation may help unmask some patients with concealed LQTS and strategically direct molecular genetic testing.     

Noninvasive ventilation in children with spinal muscular atrophy types 1 and 2

OBJECTIVE: Our aim was to assess the efficacy of noninvasive ventilation (NIV) for the treatment of thoracoabdominal asynchrony during sleep in children with spinal muscular atrophy (SMA) types 1 and 2. DESIGN: Nine subjects underwent assessment for sleep apnea/hypopnea index (AHI), mean oxyhemoglobin saturation (SpO2), oxygen desaturation index, transcutaneous carbon dioxide tension (tcpCO2), and mean phase angle during sleep as a measure of thoracoabdominal coordination. A second sleep study was performed with use of NIV. RESULTS: The nine patients (7 mos of age, range 2-33) had a baseline AHI of 2.1 events per hour (range 0.5-55.8), oxygen desaturation index of 3.7 events per hour (range 1.6-46.1), mean tcpCO2 of 46 mm Hg (range 37-60), and phase angle of 127 degrees (range 72.7-151.7). Comparing baseline and NIV sleep studies, we found significant improvement in oxygen desaturation index (P < 0.010), mean tcpCO2 (P < 0.001), and phase angle (P < 0.001). For five patients, phase-angle improvement became significant when using high-span bilevel positive airway pressure (PAP). CONCLUSIONS: NIV improved sleep breathing parameters and thoracoabdominal coordination during sleep in SMA types 1 and 2. Phase-angle improvement correlated with bilevel PAP pressures. Phase angle may be useful for the evaluation and monitoring of therapeutic interventions such as NIV.     

Tp-e Interval, Tp-e/QT Ratio, and Tp-e/QTc Ratio are Prolonged in Patients with Moderate and Severe Obstructive Sleep Apnea

Background: Prolongation of the peak and the end of T wave (Tp-e) has been reported to be associated with ventricular arrhythmias. Tp-e/QT ratio and Tp-e/QTc ratio are used as an index of ventricular arrhythmogenesis. An increased incidence of ventricular arrhythmias has been reported in patients with obstructive sleep apnea (OSA). The aim of this study was to assess ventricular repolarization in patients with OSA by using Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio. Methods: We have studied 72 patients who underwent overnight polysomnography (PSG) between the years 2010-2011 at our institution. Patients with moderate and severe OSA (23 patients; mean age: 45±10), according to the apnea-hypopnea index, constituted the study group. Patients with normal PSG (23 patients; mean age: 42±11) were used as the control group. In all patients, Tp-e interval, Tp-e/QT ratio, Tp-e/QTc ratio, as well as some other electrocardiogram intervals were measured. Independent samples t-tests were used for comparison of continuous and categorical variables and correlations were calculated by Spearman rank correlation. Results: Although QT and QTc intervals were not different between the groups, mean Tp-e interval (81.6±11.1 msn; 63.9±7.3 msn; respectively; P < 0.001), Tp-e/QT ratio (0.21±0.03; 0.17±0.02; respectively; P < 0.001), and Tp-e/QTc ratio (0.20±0.03; 0.16±0.02; respectively; P < 0.001) were prolonged in the study group compared to the control group. Correlation analysis showed a significant positive correlation between the presence of moderate and severe OSA and Tp-e interval (r = 0.72; P < 0.001), Tpe/QT ratio (r = 0.70; P < 0.001), and Tp-e/QTc ratio (r = 0.70; P < 0.001). Conclusions: Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio are prolonged in patients with moderate and severe OSA patients. There is a positive correlation between the presence of OSA and Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio. (PACE 2012; 35:966-972).     

Electrocardiographic and Clinical Predictors of Torsades de Pointes Induced by Almokalant Infusion in Patients with Chronic Atrial Fibrillation or Flutter: A Prospective Study

The aim of this study was to identify predictors of torsades de pointes (TdP) in patients with atrial fibrillation (AF) or flutter exposed to the Class III antiarrhythmic drug almokalant. TdP can be caused by drugs that prolong myocardial repolarization. One hundred patients received almokalant infusion during AF (infusion 1) and 62 of the patients during sinus rhythm (SR) on the following day (infusion 2). Thirty-two patients converted to SR. Six patients developed TdP. During AF, T wave alternans was more common prior to infusion (baseline) in patients developing TdP (50% vs 4%, P < 0.01). After 30 minutes of infusion 1, the TdP patients exhibited a longer QT interval (493 ± 114 vs 443 ± 54 ms [mean ± SD], P < 0.01), a larger precordial QT dispersion (50 ± 74 vs 27 ± 26 ms, P < 0.05), and a lower T wave amplitude (0.12 ± 0.22 vs 0.24 ± 0.16 mV. P < 0.01). After 30 minutes of infusion 2, they exhibited a longer QT interval (672 ± 26 vs 489 ± 74 ms, P < 0.001), a larger QT dispersion in precordial (82 ± 7 vs 54 ± 52 ms, P < 0.01) and extremity leads (163 ± 0 vs 40 ± 34 ms, P < 0.001), and T wave alternans was more common (100% vs 0%, P < 0.001). Risk factors for development of TdP were at baseline: female gender, ventricular extrasystoles, and treatment with diuretics; and, after 30 minutes of infusion: sequential bilateral bundle branch block, ventricular extrasystoles in bigeminy, and a biphasic T wave. Patients developing TdP exhibited early during almokalant infusion a pronounced QT prolongation, increased QT dispersion, and marked morphological T wave changes.     

Relationship Between QT Interval Duration and Electrical Induction of Ventricular Tachycardia

The relation of inducible ventricular tachycardia (VT) to QT interval duration of ventricular paced rhythm has not been evaluated. To clarify this relation we measured corrected QT interval duration (QT_C) during sinus rhythm and QT interval duration during ventricular paced rhythm (QT-V) in patients with coronary artery disease without (non-VT group = group B) and with inducible VT (VT group = group A). Duration of QT-V was greater in the VT group (n = 20) compared with non-VT group (n = 20) during ventricular pacing at cycle lengths of 600 ms (424 ± 26 vs 396 ± 19 ms, P < 0.01), of 500 ms (407 ± 20 vs 383 ± 21 ms, P < 0.01), and of 400 ms (390 ± 21 vs 362 ± 17 ms, P < 0.001). During sinus rhythm the mean values of QT_C were similar in both groups (408 ± 25 vs 413 ± 20 ms, NSJ. During ventricular stimulation the percentage of patients with values of QT-V exceeding 380 ms was 35% in non-VT group and 95% in VT group (P <0.01) at cycle length of 500 ms and 5% versus 60%, respectively, (P < 0.01), at cycle length of 400 ms. Thus, a trend toward longer QT values of ventricular paced rhythm exists in patients with inducible VT.     

Antiarrhythmic Effects of VVI Pacing at Physiologic Rates: A Crossover Controlled Evaluation

Ventricular pacing can prevent bradycardia-dependent ventricular ectopic activity (VEA) and is helpful in some cases of drug-refractory venfricuiar tachycardia (VT). This study is a prospective evaluation of VVI pacing for the control of VEA not related to underlying bradycardia, drug side-effects, or prolonged QT interval syndromes. Twenty-nine patients undergoing serial electrophysioiogic-pharmacoiogic testing for VT control were studied. Eighteen of these patients (12 men; meon age = 60.1) both completed ihe protocol and had sufficient VEA for analysis. Coronary disease was present in 13 patients, cardiomyopathy in two patients, and one patient each had myocarditis, mitral valve prolapse, and no structural heart disease. Ambulatory (Holter) monitor recordings during VVI pacing were compared with control recordings made in the absence of pacing, VVI pacing rates were 10–15 bpm above the mean daily heart rate (mean = 92 bpm; range = 63–110). Hours from paced recordings were paired with hours from control (prior to analysis) according to time of day to reduce the effects of spontaneous variability in VEA frequency. Overall, VVI pacing reduced ventricular premature complexes (VPGs) 26% from 331 to 245/hour (p < 0.001). During pacing, couplets (pairs, successive VPGs) were reduced from 6.95 to 1.03/hour (p < 0.000001) and VT (≥3 successive VPCs) from 0.89 to 0.045 episodes/hour (p < 0.003). Of 13 patients with couplets, 11 had ≥50% reduction and five had ≥90% reduction. Baseline VT was eliminated in four out of nine patients during pacing. Pacing did not increase VEA significantly in any patient. In this group of patients, reduction of VEA by VVI pacing was significant and was comparable to pharmacologic interventions. Higher forms of VEA fcouplets and VT) appeared to respond better than single VPCs. Further studies may define patients with VEA who can benefit from pacing     

Influence of cardiac autonomic neuropathy on heart rate dependence of ventricular repolarization in diabetic patients

OBJECTIVE: Prolongation of the QT interval and increased QT dispersion are associated with a poor cardiac prognosis. The goal of this study was to assess the long-term influence of the autonomic nervous system on the heart rate dependence of ventricular repolarization in patients with diabetic autonomic neuropathy (DAN). RESEARCH DESIGN AND METHODS: We studied 27 subjects (mean age 51.8 years) divided into three age- and sex-matched groups: nine control subjects, nine diabetic subjects with DAN (mostly at a mild stage; DAN+), and nine diabetic subjects without DAN (DAN-). DAN was assessed on heart rate variations during standard maneuvers (Valsalva, deep-breathing, and lying-to-standing maneuvers). No subject had coronary artery disease or left ventricular dysfunction or hypertrophy, and no subject was taking any drugs known to prolong the QT interval. All subjects underwent electrocardiogram and 24-h Holter recordings for heart rate variations (time and frequency domain) and QT analysis (selective beat averaging QT/RR relation, nocturnal QT lengthening). RESULTS: Rate-corrected QT intervals (Bazett formula) did not differ significantly between the three groups. The diurnal and nocturnal levels of low frequency/high frequency, an index of sympathovagal balance, were significantly reduced in DAN+ subjects. Using the selective beat-averaging technique, a day-night modulation of the QT/RR relation was evidenced in control and DAN- subjects. This long-term modulation was significantly different in DAN+ subjects, with a reversed day-night pattern and an increased nocturnal QT rate dependence. CONCLUSIONS: In diabetic patients with mild parasympathetic denervation, QT heart rate dependence was found to be impaired, as determined by noninvasive assessment using Holter data. Analysis of ventricular repolarization could represent a sensitive index of the progression of neuropathy. The potential prognostic impact of a reversed day-night pattern with steep nocturnal QT/RR relation still remains to be defined.     

Effect of a single oral dose of moxifloxacin (400 mg and 800 mg) on ventricular repolarization in healthy subjects

BACKGROUND: Moxifloxacin is a new fluoroquinolone. In vitro studies have suggested that it could prolong ventricular repolarization. The main objective of this study was to measure the actual effect of single oral doses of moxifloxacin on QT interval duration in healthy volunteers. METHODS: Nine men and 9 women participated in a double-blind, randomized, placebo-controlled, crossover study. Each participant received single oral doses (400 mg and 800 mg) of moxifloxacin or placebo. At the time of expected moxifloxacin maximum concentration, several electrocardiographic recordings were obtained at rest and during the course of a submaximal exercise test. QT interval and the corresponding RR interval value were measured within a wide range of RR intervals in each subject. RESULTS: ANOVA showed that both moxifloxacin doses increased mean QT intervals compared with placebo. The mean QT interval duration at RR = 1000 ms was 379 +/- 24 ms during placebo, 394 +/- 33 ms during moxifloxacin 400 mg (P < .05), and 396 +/- 28 ms during moxifloxacin 800 mg (P < .05). Moxifloxacin-induced QT interval prolongation remained significant at all tested heart rates. The increase in QT interval duration relative to placebo remained between 2.3% +/- 2.8% and 4.5% + 3.8% across the range of RR intervals tested. CONCLUSION: Moxifloxacin prolongs QT interval duration. The amplitude of this effect is small, and the risk of moxifloxacin-induced torsades de pointes is expected to be minimal when the drug is administered at the recommended dose of 400 mg/d. However, moxifloxacin should not be used in patients with predisposing factors of torsades de pointes such as electrolyte disturbances and bradycardia or during coadministration of proarrhythmic drugs.     

Prolongation of the QT interval in heart failure occurs at low but not at high heart rates

Abnormal left ventricular structure and function as in, for example, left ventricular hypertrophy or chronic heart failure, is associated with sudden cardiac death and, when the ejection fraction is depressed, with prolongation of the QT interval. The dependence on heart rate of QT interval prolongation in these conditions, and the relationship of any abnormalities either to deranged autonomic nervous system function or to an adverse prognosis, has not been well studied. We therefore investigated (1) the dependence on heart rate of the QT interval, and (2) the relationship between both QT interval and the QT/heart rate slope and markers of adverse prognosis in these two conditions. The QT interval was measured at rest and during exercise in 34 subjects with heart failure, 16 subjects with left ventricular hypertrophy and 16 age-matched controls with normal left ventricular structure and function. QTc (corrected QT) intervals at rest were significantly longer in heart failure patients (471+/-10 ms) than in controls (421+/-6 ms) or in subjects with hypertrophy (420+/-6 ms) (P<0.05). At peak exercise, despite the attainment of similar heart rates, the QT intervals no longer differed from each other, being 281+/-7 ms for controls, 296+/-11 ms in hypertrophy and 303+/-10 ms in heart failure (no significant difference). The QT/heart rate slope was significantly increased in heart failure [2.3+/-0.1 ms.(beats/min)(-1)] compared with controls [1.55+/-0.06 ms.(beats/min)(-1)] and hypertrophy [1. 66+/-0.1 ms.(beats/min)(-1)] (P<0.001). In left ventricular hypertrophy, despite animal data suggesting that QT interval prolongation should occur, no abnormalities were found in QT intervals at rest or during exercise. The QT/heart rate slope did not relate to any markers for an adverse prognosis, except that of prolongation of QT interval. Long QT intervals were associated principally with impairment of left ventricular systolic function. Our data emphasize the dynamic nature of the QT interval abnormalities found in heart failure.     

QT的频率依赖性对心肌梗死后室性心动过速的预测价值

目的：探讨QT的频率依赖性对心肌梗死（MI）后室性心动过速（VT）发生率的相关性。方法：对52例有Q型AMI后3个月患者进行动态心电图检查，分别测定清醒阶段、睡眠阶段，苏醒阶段在不同RR间期（600ms、800ms,1000ms）时的QT间期，同时计算QT的频率依赖性，其中VT组27例，非VT组25例。结果：VT组患者的QT间期的频率依赖性明显高于非VT组患者（P均＜0．01），尤以苏醒阶段最显著。结论：QT的频率依赖性的变化可以较好的预测MI后VT发作。     

Circadian Variations of Heart Rate and STIMT Interval: Adaptation for Nighttime Pacing

In order to determine the optimal pacing rate for pacemaker patients at night, 150 normal subjects with regular sinus rhythm and free of manifest heart disease, were studied using 24-hour Holter monitoring. Minimum and average heart rates were analyzed on an hourly basis. The study group was divided into six age groups, 25 subjects each, ranging from 20-29 years to 60-69 years. The minimum heart rate during the night was found to be lower than 65 ppm for all groups. The youngest subjects showed the largest variation in the minimum heart rate. The results suggest that an automatic lowering of the pacing rate during the night would allow for longer periods of sinus rhythm, thereby improving hemodynamic performance and reducing pacemaker power consumption. Suitable sensors for automatic lowering of the pacing rate include inbuilt 24-hour clock systems and the QT interval that lengthens during sleep.     

An Analysis of Post-Pacing R-R Intervals During Atrial Fibrillation

Bursts of ventricular pacing at cycle lengths of 350-260 ms were introduced during atrial fibrillation in nine patients, and the post-pacing R-R intervals were compared to the R-R intervals of spontaneous QRS complexes. In eight of nine patients, the mean post-pacing R-R interval was 126-199 ms longer than the mean spontaneous R-R interval (p less than 0.005). Spontaneous runs of aberrantly conducted supraventricular complexes were recorded during atrial fibrillation in one patient. The mean R-R interval following the runs of aberrantly conducted supraventricular complexes was significantly longer than the mean R-R interval of spontaneous narrow QRS complexes (p less than 0.001), but not significantly different than the mean post-pacing R-R interval. The findings of this study suggest that the R-R interval that follows a wide-complex tachycardia during atrial fibrillation is unlikely to be of value in differentiating ventricular tachycardia from aberrantly conducted supraventricular complexes. Analysis of R-R intervals that follow bursts of ventricular pacing suggests that there is likely to be considerable overlap between the R-R intervals that follow runs of ventricular tachycardia and the spontaneous R-R intervals during atrial fibrillation. Furthermore, even when the post-tachycardia R-R interval clearly exceeds the longest spontaneous R-R interval during atrial fibrillation, this is still of little diagnostic value, because a long pause may occur after either a run of ventricular tachycardia or a run of aberrantly conducted QRS complexes of supraventricular origin.     

Effects of aging and gender on QT dispersion in an overtly healthy population

The objective of this study was to measure the normal variation of QT dispersion (QTd) with respect to age and gender. The QT interval is a measure of the duration of ventricular depolarization and repolarization, while the QTd is a measure of the variability of the ventricular recovery time. The QTd has been suggested as a means of identifying those patients at risk for sustained ventricular tachyarrythmias and sudden cardiac death (SCD). A total of 250 patients (120 women, 130 men; age range 20-86 years) were recruited for this study. The QT intervals were measured in each of the 12 standard leads of the electrocardiogram. Data are presented as mean (mu) +/- SD. The QTd did not vary significantly within the same gender. A significant difference (P < 0.001) was noted in QTd between men (age [mu] = 53.3 +/- 15.6 years, QTd = 0.044 +/- 0.019 s) and women (age [mu] = 52.1 +/- 15.1 years, QTd = 0.034 +/- 0.015 s). Overall, men had a greater QTd, while women had a longer QT. In conclusion, we found that men had a longer QTd, which may explain the increased risk of SCD. However, women have a longer QT interval with a smaller QTd. A longer QTmin, as opposed to a longer QTmax, is responsible for the shorter QTd in women. This longer QTmin in women may predispose to an increased risk of drug induced torsades de pointes.     

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。