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.     

Influence of amiodarone on QT dispersion in patients with life-threatening ventricular arrhythmias and clinical outcome

Increased QT dispersion, defined as the difference between the maximum and minimum QT interval on the standard 12-lead electrocardiogram, is assumed to reflect regional inhomogeneity of ventricular repolarization and has been shown to be associated with an increased risk of arrhythmic events. The purpose of the present study is to examine the influence of amiodarone on QT dispersion in patients with life-threatening ventricular arrhythmias and to evaluate the predictive value of QT dispersion after amiodarone therapy for further arrhythmic events. ECG's were obtained in 47 patients 1–2 days before and 6–8 weeks after amiodarone was started. All patients had coronary artery disease with a mean EF of 34±14%. The QT interval was measured in each lead of a digitized ECG displayed on a high resolution monitor (250 mm s⁻¹). Amiodarone therapy resulted in a significant increase in the maximal QT_c interval (476±44 to 505±44 ms, p<0.001). However, measurement of QT dispersion (70±34 vs 73±29 ms) and Qtc dispersion (78±37 vs 77±31 ms) revealed no significant difference before and after amiodarone. During a one year follow-up period 26 patients were free of arrhythmic events and 7 patients developed further arrhythmic events. The remaining 14 patients were excluded from the one year follow-up analysis because of drug discontinuation (n=8), death due to heart failure (n=1), medical intervention (n=3) and incomplete follow-up (n=2). No measure of QT dispersion was predictive of recurrent arrhythmic events during treatment with amiodarone.

Conclusion: Treatment with amiodarone results in significant QT prolongation without altering QT dispersion. Measurements of QT dispersion were not predictive of amiodarone efficacy in this patient population.     

Continuous QT Interval Measurements from 24-Hour Electrocardiography and Risk after Myocardial Infarction

Objectives: The aim of this study was to examine the clinical value of QT analysis from Holter recordings in patients after myocardial infarction (Ml). Background: Prolongation and dispersion of QT intervals in the 12-lead standard ECG have been proposed as indicators of risk for arrhythmic events. However, the value of QT and T wave measurements from Holter recordings has yet to be established. Methods: Intervals from Q to the peak and to the end of T were determined every 30 seconds from 24-hour Holter recordings and corrected for cycle length (QTc). The duration of late repolarization was calculated as QT end minus QT peak. 24-hour QT variability was determined as the standard error of estimate from the linear regression analysis of QT and RR intervals. In a case control design, 51 post-MI patients suffering from subsequent cardiac death within 1 year were compared to 51 post-MI patients with an uncomplicated follow-up. Results: QTc intervals as well as 24-hour QT variability did not differ between post-MI patients with favorable and unfavorable clinical outcome. However, there was a prolonged interval from the peak to the end of the T wave in cardiac death victims (mean ± SE: 110 ± 4 ms) as compared to controls (95 ± 3ms, P < 0.001). Conclusions: Prolongation of the late repolarization phase seems to be associated with an increased risk of cardiac death after Ml. Standard QT measurements from ambulatory ECG recordings have no predictive value in post-MI patients.     

Amiodarone reduces QT dispersion in patients with hypertrophic cardiomyopathy.

To compare QT interlead variability (dispersion) in patients who receive a class III antiarrhythmic with those not on antiarrhythmic therapy, we measured QT in all 12 leads of a standard ECG in 24 patients with hypertrophic cardiomyopathy, 12 (50%) of whom were on amiodarone monotherapy and 12 (50%) who were not on amiodarone or other cardioactive medication which could affect QT. Age, functional class, chamber dimension or the degree of left ventricular hypertrophy expressed by maximal wall thickness (21 +/- 5 vs 20 +/- 4 mm; p = NS) was not different between the amiodarone and the non-amiodarone group. Maximal corrected QT (QTc) was greater in patients receiving (488 +/- 25 ms) compared to those not receiving amiodarone (451 +/- 23 ms) (p less than 0.001). However, QTc dispersion defined as the difference of maximum minus minimum QTc was decreased in the amiodarone (48 +/- 10 ms) compared to the non-amiodarone group (78 +/- 17 ms) (p less than 0.001). We conclude that in patients with hypertrophic cardiomyopathy, amiodarone prolongs QTc but reduces QTc dispersion. These results agree with expected changes in ventricular recovery time in patients who receive Class III antiarrhythmic agents and provide further support to the theory that QTc dispersion reflects regional differences in ventricular recovery time.     

Assessment of QT dispersion in symptomatic patients with congenital long QT syndromes.

It has been suggested that QT dispersion recorded on the surface electrocardiogram may be a predictor of arrhythmic events in patients with congenital QT prolongation. To evaluate this, 9 patients (6 female, mean age 17.6 years) with congenital long QT syndromes, all of whom had syncope and documented torsades de pointes, were studied. Patients were studied off treatment and during therapy with beta-blocking agents. Three patients were also studied after left stellate ganglionectomy. An age-matched control group was also studied. Good quality 12-lead electrocardiograms were recorded from all patients. For each lead, QT and RR intervals were measured, and QTc value was calculated. QT and QTc dispersions were calculated for each patient. Patients had a significantly longer mean QT interval compared with that of the control group (450 +/- 100 vs 359 +/- 63 ms; p = 0.015) at similar mean RR intervals (736 +/- 231 vs 783 +/- 289 ms), with a longer mean QTc value (0.53 +/- 0.08 vs 0.41 +/- 0.02 s1/2; p = 0.004). Patients also had longer QT and QTc dispersions compared with those of the control group (110 +/- 45 vs 43 +/- 12 ms [p = 0.004], and 0.108 +/- 0.03 vs 0.05 +/- 0.02 s1/2 [p = 0.002], respectively). QT and QTc dispersions on and off beta-blocking agents were not significantly different. Comparing patients with frequent and those with infrequent symptoms, there was no difference in QT or QTc dispersion either off treatment or during therapy with beta-blocking agents.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

The effects of halothane and sevoflurane on QT dispersion

QT dispersion is defined as the difference between QT (max) and QT (min) in the 12-lead surface ECG. It has been shown to reflect regional variations in ventricular repolarization and is significantly greater in patients with arrhythmic events than in those without them. The aim of this study was to examine the effects of halothane and sevoflurane on QT and QTc dispersion during inhalational induction of anaesthesia. The effects on QT and QTc dispersion of halothane and sevoflurane have been investigated during induction of anaesthesia. Forty-six ASA (American Society of Anaesthesiologists) physical status I-II patients, aged 16-50 years, undergoing general anaesthesia were randomly allocated to receive either halothane or sevoflurane. The mean baseline values for QT and QTc dispersion were not significantly different between the two groups (P > 0.05). QT dispersion was increased with halothane compared with baseline values (50 +/- 16 ms vs. 29 +/- 9 ms, P < 0.01) and after sevoflurane compared with baseline (48 +/- 15 vs. 33 +/- 8 ms, P < 0.01). Also, QTc dispersion was increased with halothane compared with baseline values (48 +/- 13 ms vs. 31 +/- 9 ms, P < 0.001) and after sevoflurane compared with baseline (50 +/- 14 vs. 40 +/- 11 ms, P < 0.01). The QTc interval did not change by both sevoflurane (443 +/- 7 vs. 431 +/- 21 ms, P > 0.05) and halothane (419 +/- 33 vs. 431 +/- 19 ms, P > 0.05) compared with baseline. Both halothane and sevoflurane cause myocardial repolarisation abnormalities in man in terms of increased QTc dispersion. This may be relevant in the aetiology of arrhythmias in patients during anaesthesia with halothane or sevoflurane.     

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

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

T‐Wave Morphology in Short QT Syndrome

Background: Short QT syndrome (SQTS) is an inherited disorder characterized by a short QT interval and vulnerability to ventricular tachyarrhythmias. The diagnostic criteria for this syndrome are not well defined, since there is uncertainty about the lowest normal limits for the corrected QT (QTc) interval. Objective: The aim of this study was to determine whether T‐wave morphology parameters are abnormal in short QT subjects and whether those parameters can help in the diagnosis of SQTS. Methods and Results: We describe three families (10 patients) with short QT intervals (QTc 310 ± 32 ms). Seven subjects had suffered serious arrhythmic events and three were asymptomatic. T‐wave morphology was assessed using the principal component analysis (PCA). QTc was significantly shorter and T‐wave amplitude in lead V₂ higher in the short QT subjects compared to healthy controls (n = 149), (P < 0.001 for both). The total cosine of the angle between the main vectors of the QRS and T‐wave loops (TCRT) was markedly abnormal among the symptomatic patients with short QT syndrome (n = 7) (TCRT –0.14 ± 0.55 vs 0.36 ± 0.51, P = 0.019). None of the three asymptomatic patients with short QT but without a history of arrhythmic events had an abnormally low TCRT. Conclusion: Our observations suggest that patients with a short QT interval and a history of arrhythmic events have abnormal T‐wave loop parameters. These electrocardiogram (ECG) features may help in the diagnosis of SQTS in addition to the measurement of the duration of QT interval from the 12‐lead ECG.     

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.     

Prognosis in myocardial infarction survivors with left ventricular dysfunction is predicted by electrocardiographic RR interval but not QT dispersion

OBJECTIVES: The aim of the study was to assess if QT dispersion and RR interval on the standard 12-lead electrocardiogram (ECG) predict cardiac death and late arrhythmic events in postinfarction patients with low left ventricular ejection fraction (LVEF). QT dispersion on a standard electrocardiogram (ECG) is a measure of repolarization inhomogeneity, but its prognostic meaning in myocardial infarction (MI) survivors is unclear, especially in patients with left ventricular dysfunction. RR interval has been shown to predict mortality in post-MI patients, but its prognostic power has not been compared with other noninvasive risk factors. METHODS: Retrospective cohort study. Ninety patients were identified, from a series of 547 consecutive postinfarction patients admitted to our institution for phase II cardiac rehabilitation, as having a LVEF of <0.40 at two-dimensional echocardiography (mean LVEF 0.35+/-0.04; range 0.20-0.39). QT dispersion and RR interval were analyzed on the admission 12-lead electrocardiogram, 20+/-10 (range 8-45) days after MI, using specially designed software. Additional risk markers were collected from clinical variables, signal-averaged ECG and Holter recording. RESULTS: During 24+/-18 (range 1-63) months of follow-up, 10 of 90 patients (11%) died, all from cardiac causes, and there were 18 late arrhythmic events, defined as sudden death or the occurrence of a sustained ventricular arrhythmia > or =5 days after the index MI. QT interval and dispersion were not significantly prolonged in patients who died compared to survivors and not significantly different between patients with and without arrhythmic events. Mean RR interval from standard ECG was significantly shorter in patients with both cardiac death (682+/-99 vs. 811+/-134 ms; P=0.004) and arrhythmic events (720+/-100 vs. 818+/-139 ms; P=0.006). A Cox proportional hazards model identified RR interval from standard ECG (P<0.001) and a history of more than one MI (P=0.002) as significant predictors of cardiac death independent of thrombolytic therapy, LVEF, filtered QRS complex duration at signal-averaged ECG, mean RR and its standard deviation at 24-h Holter monitoring. CONCLUSIONS: Measurement of QT interval and dispersion 3 weeks after MI has no prognostic power in patients with LV dysfunction after a recent MI. RR interval on standard 12-lead ECG is as good a prognostic indicator as other, more expensive, noninvasive markers. These findings may be relevant in this era of limited health care resources.     

QT Dispersion as a Marker for Response to Quinidine in Patients with Ventricular Tachyarrhythmias

Objective: This study was undertaken to measure the effect of quinidine on QT dispersion and to determine whether changes in QT dispersion are associated with the acute response to quinidine in patients with ventricular tachycardia. Methods: In 36 patients with inducible ventricular tachycardia during programmed electrical stimulation (PES), QT and JT intervals were measured in all 12 leads of electrocardiograms recorded at baseline and after quinidine. QT/JT dispersion was calculated by subtracting the smallest from the largest interval; QTc and JTc dispersion were also calculated. Response to therapy was defined as the inability to induce a ventricular tachyarrhythmia during a repeat PES study. Results: Quinidine significantly prolonged the QTc and JTc intervals in the patients who responded to quinidine (n = 12) and in the nonresponders (n = 24). At baseline, QTc dispersion was similar in responders and nonresponders. However, quinidine increased QTc dispersion in nonresponders (from 78 ± 28 to 113 ± 40 ms, P < 0.05) but not in responders (from 81 ± 26 to 83 ± 42 ms). A similar pattern was seen for QT dispersion, JT dispersion, and JTc dispersion. Conclusion: QT dispersion increases in nonresponders, but not in responders to quinidine for ventricular tachycardia. This QT dispersion profile is distinct from the Class III antiarrhythmics and may explain results from large clinical trials and delineate a new safety and efficacy marker.     

Short QT syndrome presenting as syncope: How short is too short?

We report the case of a 52-year-old man who presented to our emergency department (ED) after three episodes of syncope in the seven hours before admission. During his stay in the ED he had recurrent ventricular tachycardia (VT) requiring external electrical cardioversion. A 12-lead electrocardiogram (ECG) showed a short QT (SQT) interval (270 ms, QTc 327 ms), with frequent R-on-T extrasystoles triggering sustained polymorphic VT. After exclusion of other precipitating causes, the patient was diagnosed as having SQT syndrome (SQTS) according to the Gollob criteria. To our knowledge, this is the first known documentation of an SQT-caused arrhythmic episode on a 12-lead ECG, as well as the first reported case of SQTS in Portugal. The patient received an implantable cardioverter-defibrillator and was discharged. At a follow-up assessment 14 months later he was symptom-free, interrogation of the device showed no arrhythmic events, and the ECG showed a QT interval of 320 ms (QTc 347 ms).     

Effects of Epinephrine and Phenylephrine on QT Interval Dispersion in Congenital Long QT Syndrome

Objectives. Measurement of QT interval dispersion during pharmacologic adrenergic stimulation was used to assess the effect of alpha- and beta-adrenergic stimulation on arrhythmic vulnerability in familial long QT syndrome (LQTS).Background. Nonhomogeneity in the ventricular action potential duration causes electrical instability leading to life-threatening ventricular arrhythmias and is markedly increased in LQTS. QT interval dispersion measured from the electrocardiogram (ECG) can be used as an index of nonhomogeneous ventricular repolarization.Methods. Sixteen symptomatic patients with LQTS and nine healthy control subjects were examined at baseline and during epinephrine (mainly beta-adrenergic agonist, 0.05 μg/kg body weight per min) and phenylephrine infusions (alpha-adrenergic agonist, mean 1.4 μg/kg per min). QT interval dispersion was determined from a 12-lead ECG as interlead range and coefficient of variation measured to the end (QT_end) and apex (QT_apex) of the T wave.Results. At baseline QT_enddispersion was greater in patients with LQTS compared with control subjects (mean [±SD] 68 ± 34 vs. 36 ± 7 ms, p = 0.001). QT_enddispersion was markedly increased in patients with LQTS by use of epinephrine (from 68 ± 34 to 90 ± 36 ms, p = 0.002), but remained unchanged in control subjects. Phenylephrine did not affect QT dispersion in either group (all p = NS). Atrial pacing to achieve comparable heart rates during baseline and epinephrine and phenylephrine infusions did not influence the magnitude of QT dispersion in either group. QT_apexdispersion analysis gave congruent results.Conclusions. Epinephrine but not phenylephrine increased QT dispersion, suggesting that beta-adrenergic stimulation provokes arrhythmias in patients with LQTS by aggravating nonhomogeneity of ventricular repolarization, whereas alpha-adrenergic stimulation is less important for arrhythmic vulnerability. The results also suggest that rapid pacing may not reduce vulnerability to arrhythmias in congenital LQTS.     

Is QT Dispersion Associated with Sudden Cardiac Death in Patients with Hypertrophic Cardiomyopathy?

QT dispersion is significantly greater in patients with hypertrophic cardiomyopathy (HCM) than that in healthy subjects. Few data exist regarding the prognostic value of QT dispersion in HCM. In this study, we retrospectively investigated the association between QT dispersion and sudden cardiac death in 46 patients with HCM (mean 33.1 ±; 15.5 years, 32 men). The case group consisted of 23 HCM patients who died suddenly, and the control group consisted of 23 HCM patients who survived uneventfully during follow‐up. Study patients were pair‐matched for age, gender, and maximum left ventricular wall thickness. QT dispersion (maximum minus minimum QT interval) was manually measured on early 12‐lead ECGs using a digitizing; board. An in‐house program was used for calculating QT interval, QT dispersion, JT interval, and JT dispersion (maximum minus minimum J point to T end interval). Patients in the case group tended to have shorter RR intervals than those in the control group (777 ±; 171 vs 856 ±; 192 ms, P = 0.08). Maximum corrected QT and JT intervals did not discriminate the case group from controls (489 ±; 29 vs 479 ±; 27 ms, P = NS; 375 ±; 36 vs 366 ±; 22 ms, P = NS, respectively). Greater QT dispersion and JT dispersion were found in the case group compared with controls (74 ±; 28 vs 59 ±; 21 ms, P = 0.02 and 76 ±; 32 vs 59 ±; 26 ms, P = 0.03, respectively). The measurements of maximum QT, JT, and T peak to T end intervals, precordial QT and JT dispersion, and T peak and T end dispersion were all comparable between the two groups (P = NS for all). No systematic changes in ECG measurements were found from late ECGs of the case group compared to those from early ECGs (P = NS). No correlation between maximum left ventricular wall thickness and QT dispersion, JT dispersion, maximum QTc or JTc intervals was observed (r < 0.29, P > 0.05 for all). Our results; show that increased QT dispersion and JT dispersion is weakly associated with sudden cardiac death in the selected patients with HCM. A.N.E. 2001; 6(3):209–215     

QT dispersion in nonischemic dilated cardiomyopathy. A long-term evaluation

BACKGROUND: In idiopathic dilated cardiomyopathy (IDC), the predictive value of QT dispersion is still under debate. AIMS: This study assessed the role of QT dispersion for the long-term risk of cardiac death and of major arrhythmic events in IDC. METHODS AND RESULTS: In 162 patients with IDC (age 52+/-12 years), the QT interval on a 12-lead ECG was measured manually. QT dispersion was evaluated with QT range and QT standard deviation, for both QT and QTc (Bazett formula). With a follow-up of 53+/-41 months, QT dispersion was not a predictor of cardiac death in univariate or in multivariate analysis, and was of similar value for patients with or without bundle branch block. Using multivariate analysis, increased pulmonary capillary wedge pressure (p=0.003), decreased heart rate variability (Standard deviation of all NN intervals, p=0.01) and non-sustained ventricular tachycardia (NSVT) (p=0.03) were predictors of cardiac death. Sudden death and/or major arrhythmic events were independently predicted by NSVT (p=0.005), decreased heart rate variability (p=0.01) and late ventricular potentials on signal averaged ECG (p=0.02). CONCLUSION: This study confirms the poor prognostic value of QT dispersion in patients with IDC. Other methods to assess repolarization abnormalities need to be evaluated in such patients.     

Impact of QT Variables on Clinical Outcome of Genotyped Hypertrophic Cardiomyopathy

Background: Although QT variables such as its interval and/or dispersion can be clinical markers of ventricular tachyarrhythmia, few data exist regarding the role of QT variables in genotyped hypertrophic cardiomyopathy (HCM). Therefore, we analyzed QT variables in genotyped subjects with or without left ventricular hypertrophy (LVH). Methods: QT variables were analyzed in 111 mutation and 43 non‐mutation carriers who were divided into three groups: A, those without ECG abnormalities and echocardiographically determined LVH (wall thickness ≥13 mm); B, those with ECG abnormalities but LVH; and C, those with ECG abnormalities and LVH. We also examined clinical outcome of enrolled patients. Results: Maximal LV wall thickness in group C (19.0 ± 4.3 mm, mean ±SD) was significantly greater than that in group A (9.2 ± 1.8) and group B (10.4 ± 1.8). Under these conditions, maximum QTc interval and QT dispersion were significantly longer in group C than those in group A (438 ± 38 ms vs 406 ± 30 and 64 ± 31 vs 44 ± 18, respectively; P < 0.05). QTc interval and QT dispersion in group B (436 ± 50 and 64 ± 22 ms) were also significantly greater than those in group A. During follow‐up periods, four sudden cardiac deaths and one ventricular fibrillation were observed in group C, and two nonlethal ventricular tachyarrhythmias were observed in group B. Conclusions: Patients with HCM‐related gene mutation accompanying any ECG abnormalities frequently exhibited impaired QT variables even without LVH. We suggest that careful observation should be considered for those genotyped subjects.     

QT interval dispersion in North Indian children with Kawasaki disease without overt coronary artery abnormalities

Increased QT interval dispersion has been associated with an increased risk for ventricular arrhythmias and sudden cardiac events. We examined the QT interval dispersion in 20 North Indian children with Kawasaki disease (KD) with no coronary artery abnormalities on echocardiography compared the same with matched controls. The study population consisted of 20 children in convalescent phase of KD and 20 age and sex-matched healthy controls. Intervals were measured with the use of a digital caliper with least count of 0.01 mm by a single blinded observer. The QTc dispersion was calculated as the difference between the maximum and minimum corrected QT intervals in 12 and 8 leads (i.e. the 6 precordial leads, the shortest extremity lead, and the median of the 5 other extremity leads). Of the 480 leads obtained (12 per subject), 36 were excluded from analysis (15 because of poor T wave formation and 11 because of presence of U waves). Children with KD had significantly higher QTc dispersion in 12 lead (67.08 ± 17.72 ms compared to 47.63 ± 16.48 ms in controls P ≤ 0.001) as well as 8 lead (60.51 ± 18.54 ms compared to 42.92 ± 18.03 ms in controls P ≤ 0.001) analysis. There was no correlation between delay in IVIG therapy and QT interval dispersion. In conclusion, QT interval dispersion is significantly increased in North Indian children with KD. The dispersion is indicative of inhomogenous ventricular repolarization and may represent increased risk for developing ventricular arrhythmia in this population.     

Spatial features in body surface potential maps of patients with ventricular tachyarrhythmias with or without coronary artery disease.

Body surface potential maps (BSPM) from patients with coronary artery disease or no structural heart disease were analyzed with respect to their spatial features and QT/QTc dispersion in order to determine whether BSPM allows identification of patients with ventricular fibrillation. QRST integral maps and QT/QTc dispersion were acquired from simultaneous recordings of 62 ECG leads during sinus rhythm in patients with idiopathic ventricular fibrillation (n=13), ventricular fibrillation and coronary artery disease (n=22), coronary artery disease without ventricular fibrillation (n=21) and healthy controls (n=18). The Karhunen-Loeve transformation was applied to reduce the dimensionality of the data matrix of the QRST map to eight coefficients. Linear discriminant analysis allowed discrimination between idiopathic ventricular fibrillation patients and controls with high sensitivity (85%) and specificity (89%). However, discrimination between coronary artery disease patients with or without ventricular fibrillation was poor (68% and 67%, respectively). QTc dispersion calculated from BSPM was longer in idiopathic ventricular fibrillation patients than in controls (99+/-30 ms vs 70+/-14 ms, P=0.009) in contrast to QTc dispersion taken from 12-lead ECG (53+/-21 ms vs. 47+/-12 ms, P=n.s.). No significant difference was noted for coronary artery disease patients with or without ventricular fibrillation. In conclusion, repolarization disturbances detected by BSPM allow identification of ventricular fibrillation patients without structural heart disease. However, our results do not suggest a major impact of QT/QTc dispersion or QRST integral mapping for identification of ventricular fibrillation patients with coronary artery disease.