Impact of electrocardiogram recording format on QT interval measurement and QT dispersion assessment

The aim of this study was to determine the effect of recording conditions on the operator dependent measures of QT dispersion in patients with known and/or suspected repolarization abnormalities. Among several methods for risk stratification, QT dispersion has been suggested as a simple estimate of repolarization abnormalities. In a cohort of high and low risk patients, different components of the repolarization process were assessed in the 12-lead ECG using three different paper speeds and amplifier gains. To assess measurement error and reproducibility, a straight line was repeatedly measured. The operator error was 0.675 +/- 0.02 mm and the repeatability of the measurement error was 31 +/- 6%. The QT interval was most frequently measurable in V2-V5. Depending on the lead selected for analysis, the incidence of visible U waves was greatest in the precordial leads with high amplifier gain and low paper speed, strongly affecting QT interval measurement. The timing of the onset of the QRS complex (QRS onset dispersion) or offset of the T wave was strongly dependent on the paper speed. Paper speed, but not amplifier gain, had a significant shortening effect on the measurement of the maximum QT interval. As QT interval measurement in each ECG lead incorporates QRS onset and T wave offset (depending on the number of visible U waves), the dispersion of each of these parameters significantly affected QT dispersion. Thus, QT dispersion appears to reflect merely the presence of more complex repolarization patterns in patients at risk of arrhythmias.     

Comparative Reproducibility of QT, QT Peak, and T Peak-T End Intervals and Dispersion in Normal Subjects, Patients with Myocardial Infarction, and Patients with Hypertrophic Cardiomyopathy

Abnormal repolarizaiion is associated with arrhythmogenesis. Because of controversies in existing methodology, new computerized methods may provide more reliable tools for the noninvasive assessment of myocardial repolarization from the surface electrocardiogram (ECC). Measurement of the interval between the peak and the end of the T wave (TpTe interval) has been suggested for the detection of repolarization abnormalities, but its clinical value has not been fully studied. The intrasubject reproducibility and reliability of automatic measurements of QT, QT peak, and TpTe interval and dispersion were assessed in 70 normal subjects, 49 patients with acute myocardial infarction (5th day; MI), and 37 patients with hypertrophic cardiomyopathy (HC). Measurements were performed automatically in a set of 10 ECCs obtained from each subject using a commercial software package (Marquette Medical Systems, Milwaukee, WI, U.S.A.). Compared to normal subjects, all intervals were significantly longer in HC patients (P < 0.001 for QT and QTp; p < 0.05 for TpTe); in MI patients, this difference was only significant for the maximum QT and QTp intervals (P < 0.05). In both patient groups, the QT and QTp dispersion was significantly greater compared to normal subjects (P < 0.05) but no consistent difference was observed in the TpTe dispersion among all three groups. In all subjects, the reproducibility of automatic measurement of QT and QTp intervals was high (coefficient of variation, CV, 1%-2%) and slightly lower for that of TpTe interval (2%–5%; p < 0.05). The reproducibility of QT, QTp, and TpTe dispersion was lower (12%–24%, 18%–28%, 16%–23% in normal subjects, MI and HC patients, respectively). The reliability of automatic measurement of QT, QTp, and TpTe intervals is high but the reproducibility of the repeated measurements of QT, QTp and TpTe dispersion is comparatively low.     

Assessment of the Coupling Between RTapex and RR Interval as an Index of Temporal Dispersion of Ventricular Repolarization

To evaluate the dynamic characteristics of the relationlship between the RT and RR intervals we analyzed the RR/RT_apex variability interaction with a dynamic parametric model whose parameters can be directly estimated from the beat-to-beat series RR and RT_opex intervals. The model is designed to separate the fraction of RT_apex variability driven by RR changes from that independent of RR variations and to quantify the gain and phase of the relationship between RR and RT_apex intervals. The percentage of RT_apex variability driven by RR variability was significantly greater in young normal subjects in comparison with postmyocardial infarction patients as well as with agematched control subjects. This new approach based on the quantification of the RT_apex variability dependent and independent of beat-to-beat RR interval changes could be used to quantify the degree of uncoupling between the two signals thus providing a new and noninvasive index of temporal dispersion of ventricular repolarization.     

QT Interval and QT Dispersion Measured with the Threshold Method Depend on Threshold Level

Various computerized methods with multiple parameter options for measurements of the QT interval now are available. The optimum parameter setting for most algorithms is not known. This study evaluated the influence of the threshold level applied on the T wave differential on the QT interval and its dispersion measured in normal and abnormal electrocardiograms (ECGs). Seven hundred sixty ECGs recorded in 76 normal subjects and 630 in 63 patients with hypertrophic cardiomyopathy (HCM) (10 consecutive recordings in each individual) were analyzed. In each lead of each ECG, the QT interval was measured by the threshold method applied to the first differential of the T wave. The threshold level was varied between 5% and 30% of the T wave maximum in 1% steps, resulting in 26 different choices of QT measurements. With each choice the maximum QTc and the QT dispersion (QTd, standard deviation of the QT in all 12 leads) were obtained for each recording. The maximum QTc was significantly longer in HCM patients than in normal subjects (P < 0.001) at all threshold levels except between 5% and 7%. The QTd was significantly greater in HCM patients at all threshold levels. The QTc and QTd changed significantly with the threshold level. The maximum QTc varied up to 60 ms in normal subjects and up to 70 ms in HCM patients, depending on the threshold level. Thus, the QT intervai and its dispersion measured with the threshold method applied to the first T wave differential depended significantly on the threshold level in both normal and diseased hearts. All programmable options of available automatic instruments should be examined carefully before any study, and all algorithmic details should be systematically presented.     

Magnetocardiographic QT Interval Dispersion in Postmyocardial Infarction Patients with Sustained Ventricular Tachycardia: Validation of Automated QT Measurements

T dispersion is a measure of heterogeneity in ventricular repolarization. Increased ECG QT dispersion is associated with life-threatening ventricular arrhythmias. We studied if magnetocardiographic (MCG) measures of QT dispersion can separate postmyocardial infarction patients with and without susceptibility to sustained VT. Manual dispersion measurements were compared to a newly adapted automatic QT interval analysis method. Ten patients with a history of sustained VT (VT group) and eight patients without ventricular arrhythmias (Controls) were studied after a remote myocardial infarction. Single-channel MCGs were recorded from 42 locations over the frontal chest area and the signals were averaged. QT dispersion was defined as maximum — minimum or standard deviation of measured QT intervals. VT group showed significantly more QT and JT dispersion than Controls. QT_apex dispersions were 127 ± 26 versus 83 ± 21 ms (P = 0.004) and QT_end dispersions 130 ± 37 versus 82 ± 37 ms (P = 0.013), respectively. Automatic method gave comparable values. Their relative differences were 9% for QT_apex and 27% for QT_end dispersion on average. In conclusion, increased MCG QT interval dispersion seems to be associated with a susceptibility to VT in postmyocardial infarction patients. MCG mapping with automated QT interval analysis may provide a user independent method to detect nonhomogeneity in ventricular repolarization.     

QT Interval in Children with Sensory Neural Hearing Loss

EL HABBAL, M.H., et al. : QT Interval in Children with Sensory Neural Hearing Loss. Long QT syndrome was first described in children with congenital sensory neural hearing loss (SNHL). The deafness was attributed to abnormalities in potassium ion channels of the inner ear. Similar channels are present in the heart and its dysfunction causes long QT syndrome. Whether congenital SNHL is associated with prolonged QT is unknown. This study examined 52 patients (median age 8.35 years, range 0.21–17.42 years) with SNHL and compared them to 63 healthy children (median age 10.2 years; range 0.67–19 years). An observer, who was blinded from the presence or absence of SNHL, measured QT, QTc intervals and dispersions from a standard 12‐lead electrocardiogram. To assess the cardiac autonomic enervation, power spectral analysis of heart rate variability was determined using a 24‐hour ambulatory heart rate monitor and was expressed as high (HF) to low frequency (LF) ratio. Left ventricular size and functions were evaluated by using two‐dimensional echocardiography. The medians (and ranges) of QT intervals were 340 ms (230–420 ms) in patients and 320 ms (240–386 ms) in the control group (P < 0.01 ). The QTc was longer in patients with SNHL (median 417 ms, range 384–490 ms) than in controls (median 388 ms, range 325–432 ms, P < 0.001 ). QT dispersions in SNHL were higher (median .038 ms, range 00–11 ms) than controls (median 27 ms, range 00–52 ms, P < 0.001 ). T wave inversion (n = 16 ) and alternans (n = 3 ) occurred in patients with SNHL. Heart rates were similar in both groups. Some deaf patients (n = 8 ) had dizzy episodes with a QTc > 440 ms. The HF:LF ratio was 1.32 (0.516–2.33) in deaf patients and 1.428 (0.67–2.3) in the control group (P > 0.1 ). Left ventricular size and functions were similar and normal in deaf patients and controls. In children, congenital SNHL is associated with a prolonged QT interval.     

Paradoxically Shortened QT Interval after a Prolonged Pause

We analyzed Holter ECG recordings in 15 patients with episodes of prolonged RR intervals > 2.5 seconds. In 13 patients, the QT interval showed a linear prolongation when RR interval was < 1.5 seconds and became relatively flat at longer RR intervals. In the remaining two patients, the QT and RR intervals were correlated within physiological range of RR intervals. However, at longer RR intervals, the QT interval was unexpectedly shortened and constant. The paradoxically shortened QT interval observed in the present 2 cases may indicate an abnormal adaptation of repolarization time to an abrupt increase in the preceding RR intervals.     

Determinant of QT Dispersion in Patients with Hypertrophic Cardiomyopathy

KAWASAKI, T., et al. : Determinant of QT Dispersion in Patients with Hypertrophic Cardiomyopathy. QT dispersion is thought to reflect a regional difference in repolarization process although QT interval is composed of depolarization and repolarization. This study was designed to investigate the effect of depolarization and repolarization on QT dispersion in hypertrophic cardiomyopathy. Standard 12-lead ECG was recorded in 70 hypertrophic cardiomyopathy patients with anteroseptal wall hypertrophy (HC-As), 8 patients with lateral wall hypertrophy (HC-L), 8 patients with diffuse hypertrophy (HC-D), and 46 normal controls. QRS, JTc, maximum and minimum QTc, and QTc dispersion were compared. The maximum QTc was greater in HC-As and HC-L than in the control; the minimum QTc was similar in all 3 groups; consequently, QTc dispersion was greater in HC-As and HC-L. In HC-D, the maximum QTc and the minimum QTc were greater than the control, which produced QTc dispersion similar to that in the control. JTc did not differ among 4 groups. In hypertrophic cardiomyopathy, both QTc and QRS duration were increased in the leads coinciding with the left ventricular portion of localized hypertrophy. We conclude that QTc dispersion depended on the heterogeneity of QRS duration or depolarization rather than repolarization, which in fact may be ascribed to the regionally different hypertrophy of the left ventricle in hypertrophic cardiomyopathy. (PACE 2003; 26[Pt. I]:819–826)     

Cycle Length-Associated Modulation of the Regional Dispersion of Ventricular Repolarization in a Canine Model of Long QT Syndrome

CHINUSHI, M., et al. : Cycle Length‐Associated Modulation of the Regional Dispersion of Ventricular Repolarization in a Canine Model of Long QT Syndrome. Previous tridimensional activation mapping showed that the development of functional conduction block at the onset of torsades de pointes was regionally heterogeneous; conduction block was frequently observed in the LV and the interventricular septum (IVS) but not in the RV, in the canine anthopleurin‐A (AP‐A) model of long QT syndrome (LQTS). This may be related to the distribution of myocytes with M celllike electrophysiological characteristics. To better understand the regional difference of arrhythmogenicity in LQTS, the authors investigated cycle length related modulation of ventricular repolarization among three different layers: the endocardium (End), mid‐myocardium (Mid), and epicardium (Epi) of the LV and RV and at two different areas: the Epi and septum (Sep) in the IVS. The LQT3 model was produced by AP‐A in dogs. Using constant pacing and single premature stimulation (S₁S₂), the ventricular repolarization pattern was analyzed from 256 unipo2 lar electrograms. Activation‐recovery intervals (ARIs) were used to estimate local repolarization. In seven experiments, AP‐A increased regional ARI dispersion to 88.1 ± 36.0 ms in the LV, to 72.9 ± 35.7 ms in the IVS, and to 23.0 ± 8.7 ms in the RV at the pacing cycle length (CL) of 1,000 ms. Development of the large ARI dispersion was due to greater ARI prolongation at the Mid site in the LV and at Sep site in the IVS. As the S₁S₂ interval was shortened, regional ARI dispersion decreased gradually, and finally, ARI dispersion showed a reversal gradient of repolarization between the Mid and Epi sites in the LV and between the Sep and Epi sites in the IVS. Two factors contributed to create the reversal gradient of repolarization: (1) a difference in restitution kinetics at the Mid site in the LV and at the Sep site in the IVS, characterized by a larger Δ ARI and slower time constant (τ), and (2) a difference in diastolic intervals at each site resulting in different input to restitution at the same CL. However, the RV showed small alteration in the transmural dispersion of repolarization in the S₁S₂ protocol. S₂ created heterogeneous functional conduction block in the LV and IVS but not in the RV. In the LQT3 model, the arrhythmogenicity of torsades de pointes is primarily due to dispersion of repolarization in the LV and IVS because of prominent distribution of M cells. The RV seems to participate passively in reentrant excitation during torsades de pointes.     

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.     

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.     

Effects of intravenous magnesium in a prolonged QT interval model of polymorphic ventricular tachycardia focus on transmural ventricular repolarization

BACKGROUND: This study was performed to clarify the antiarrhythmic effects of magnesium sulfate (Mg(++)) in a prolonged QT interval canine model of polymorphic ventricular tachyarrhythmia (VTA). METHODS: In six experiments in a canine model of prolonged QT by anthopleurin-A, Mg(++) was administered in boluses of 0.2 mL/kg during repetitive episodes of self-terminating polymorphic VTA or frequent premature ventricular complexes (PVCs). The distribution of ventricular repolarization across the left ventricular(LV) wall and dispersion of transmural repolarization were analyzed before, and 30 and 120 seconds after Mg(++) administration, during ventricular pacing at 100 bpm. Transmural unipolar electrograms were recorded from multipolar needle electrodes, and local activation-recovery intervals (ARI) were measured. RESULTS: Mg(++) rapidly eliminated self-terminating polymorphic VTA and all isolated PVCs. During ventricular pacing at 100 bpm, Mg(++) caused modest shortening of ARI at all recording sites. Since the magnitude of ARI shortening was greater at mid-myocardial sites than at other ventricular sites, mean transmural ARI dispersion decreased from 80 +/- 22 to 45 +/- 18 ms within 30 seconds after Mg(++) injection. However, this effect was transient, and, at 120 seconds after Mg(++) administration, ARI had increased all sites and transmural ARI dispersion lengthened to 65 +/- 18 ms. Besides suppression of triggered premature activity, homogenization of transmural ventricular repolarization was associated with the antiarrhythmic effects of intravenous Mg(++) in this model. CONCLUSION: Since these effects were transient, a continuous intravenous infusion of Mg(++) is preferred to prevent recurrences of VTA.     

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)     

The JT Interval as a Depolarization Independent Measurement of Repolarization: Lessons from Catheter Ablation of the Wolff-Parkinson-White Syndrome

In patients with Wolff-Parkinson-White syndrome (WPW), preexcitation precludes accurate assessment of the ventricular repolarization by the QT_C. In patients with long QT syndrome, it has been demonstrated that the JT_C does not change when depolarization abnormalities develop. We hypothesized that this phenomenon should also be applicable to WPW patients. To test this, we assessed the surface ECG of 29 patients (16 males, 13 females) with WPW pre- and postablation. The QRS, QT, and JT intervals were measured pre- and postablation at 50 mm/s paper speed in leads II and V₂. QT_C and JT_C were calculated according to Bazett's formula. The average age was 12.8 ± 4.9 years (range 1.5–21). All patients had no residual preexcitation on postablation ECG. Early and late follow-up ECGs were obtained at 32 ± 34 days and 388 ± 197 days postablation, respectively. Both the QRS and the QT_C intervals shortened significantly on the postablation versus preablation ECGs (QRS: 115 ± 23 ms vs 89 ± 15 ms, respectively; P < 0.0001), (QT_C: 454 ± 26 vs 423 ± 23, respectively; P < 0.0001). The preablation JT_C interval did not change, postablation (319 ± 21 vs 323 ± 23, respectively; P > 0.2). Also, the JT_C interval did not change between early and late follow- up, postablation. JT_C: is an independent measure of repolarization, not related to depolarization. JT_C may be a useful tool in assessing repolarization in patients with WPW and other depolarization abnormalities.     

Cardiac repolarization properties during standardized exercise test as studied by QT,QT peak and terminated T-wave intervals

Summary. Changes in QT, QT peak (QT_p) and terminal T-wave, T_p–T_e (QT–QT_p) were studied in 11 apparently healthy subjects during and after a standardized exercise test. ECG was recorded at scalar lead positions. Averaged complexes were later analysed by computer for the different time intervals. QT and QT_p decreased in parallel with increasing heart rate with a ratio QT_p/QT of 0·80 ± 0.02 at rest and 0·74 ± 0·02 at maximal heart rate around 170. After exercise QT and QT_p prolonged disproportionately slower than heart rate, reaching the relation observed during exercise only 9·5 min post exercise. T_p–T_e was 75 ± 10 ms at rest and 65 ± 8 ms at maximal heart rate. The decrease was significant (P<0·001). The main part of the rate-associated shortening of the QT interval occurred in the QT_p interval where it was about six to seven times larger than in the T_p–T_e interval. In conclusion, QT and QT_p decreased similarly with heart rate during exercise. Post exercise there was an initial slower return of these intervals to the resting state than for heart rate. T_p–T_e changes were minimal.     

Dispersion of QT Intervals: A Measure of Dispersion of Repolarization or Simply a Projection Effect?

QT interval dispersion may provide little information about repolarization dispersion. Some clinical measurements demonstrate an association between high QT interval dispersion and high morbidity and mortality, but what is being measured is not clear. This study was designed to help resolve this dilemma. We compared the association between different clinical measures of QT interval dispersion and the ECG lead amplitudes derived from a heart vector model of repolarization with no repolarization dispersion whatsoever. We compared our clinical QT interval dispersion data obtained from 25 subjects without cardiac disease with similar data from published studies, and correlated these QT dispersion results with the distribution of lead amplitudes derived from the projection of the heart vector onto the body surface during repolarization. Published results were available for mean relative QT intervals and mean differences from the maximum QT interval. The leads were derived from Uijen and Dower lead vector data. Using the Uijen lead vector data, the correlation between measurements of dispersion and derived lead amplitudes ranged from 0.78 to 0.99 for limb leads, and using the Dower values ranged from 0.81 to 0.94 for the precordial leads. These results show a clear association between the measured QT interval dispersion and the variation in ECG lead amplitudes derived from a simple heart vector model of repolarization with no regional information. Therefore, measured QT dispersion is related mostly to a projection effect and is not a true measure of repolarization dispersion. Our existing interpretation of QT dispersion must be reexamined, and other measurements that provide true repolarization dispersion data investigated.     

QT Dispersion Does Not Predict Early Ventricular Fibrillation After Acute Myocardial Infarction

Ventricular arrhythmias may be associated with increased QT dispersion (difference between maximum and minimum QT on standard 12-lead ECG). We performed a case control study to determine if QT dispersion on the admission ECG could predict early VF after acute myocardial infarction. The cases were 24 patients with acute myocardial infarction (14 inferior, 8 anterior, and 2 lateral) with VF within 12 hours of admission. There were 24 control patients without VF matched for site of infarction and ST segment score (sum of ST segment elevation). VF occurred a median of 153 minutes (interquartile range 93–245) after onset of chest pain and 33 minutes (range 7–104) after initial ECG. QT (399 ± 37 and 394 ± 37), QT corrected (440 ± 38 and 429 ± 29), and QT dispersion (68± 20 and 66 ± 27) were similar in patients and controls. By design, ST score was similar (11 ± 9 vs 9 ± 5 mV), although a good match could not be obtained for three patients with extreme ST elevation. Patients with VF presented to the hospital earlier after the onset of chest pain (median 95 min [range 65–188] compared to 150 min [range 80–270], P= 0.05) and had a lower serum sodium (138 ± 2.4 vs 140 ± 2.5, P = 0.05) than controls. Thus, QT interval and QT dispersion, measured on the presenting ECG, did not predict early VF after myocardial infarction.     

Clinical Value of Electrocardiographic Parameters in Genotyped Individuals with Familial Long QT Syndrome

MOENNIG, G., et al. : Clinical Value of Electrocardiographic Parameters in Genotyped Individuals with Familial Long QT Syndrome. Rate corrected QT interval (QTc) and QT dispersion (QTd) have been suggested as markers of an increased propensity to arrhythmic events and efficacy of therapy in patients with long QT syndrome (LQTS). To evaluate whether QTc and QTd correlate to genetic status and clinical symptoms in LQTS patients and their relatives, ECGs of 116 genotyped individuals were analyzed. JTc and QTc were longest in symptomatic patients (  n = 28  ). Both QTd and JTd were significantly higher in symptomatic patients than in asymptomatic (  n = 29  ) or unaffected family members (  n = 59  ). The product of QTd/JTd and QTc/JTc was significantly different among all three groups. Both dispersion and product put additional and independent power on identification of mutation carriers when adjusted for sex and age in a logistic regression analysis. Thus, symptomatic patients with LQTS show marked inhomogenity of repolarization in the surface ECG. QT dispersion and QT product might be helpful in finding LQTS mutation carriers and might serve as additional ECG tools to identify asymptomatic LQTS patients.