Beat‐to‐Beat QT Interval Variability Is Primarily Affected by the Autonomic Nervous System

Background : Beat‐to‐beat QT interval variability is associated with life‐threatening arrhythmias and sudden death, however, its precious mechanism and the autonomic modulation on it remains unclear. The purpose of this study was to determine the effect of drugs that modulate the autonomic nervous system on beat‐to‐beat QT interval. Method : RR and QT intervals were determined for 512 consecutive beats during fixed atrial pacing with and without propranolol and automatic blockade (propranolol plus atropine) in 11 patients without structural heart disease. Studied parameters included: RR, QTpeak (QRS onset to the peak of T wave), QTend (QRS onset to the end of T wave) interval, standard deviation (SD) of the RR, QTpeak, and QTend (RR‐SD, QTpeak‐SD, and QTend‐SD), coefficients of variation (RR‐ CV, QTpeak‐CV, and QTend‐CV) from time domain analysis, total power (TP; RR‐TP, QTpeak‐TP, and QTend‐TP), and power spectral density of the low‐frequency band (LF; RR‐LF, QTpeak‐LF, and QTend‐LF) and the high‐frequency band (HF; RR‐HF, QTpeak‐HF and QTend‐HF). Results : Administration of propranolol and infusion of atropine resulted in the reduction of SD, CV, TP, and HF of the QTend interval when compared to controlled atrial pacing (3.7 ± 0.6 and 3.5 ± 0.5 vs 4.8 ± 1.4 ms, 0.9 ± 0.1 and 0.9 ± 0.1 vs 1.2 ± 0.3%, 7.0 ± 2.2 and 7.0 ± 2.2 vs 13.4 ± 8.1 ms², 4.2 ± 1.4 and 4.2 ± 1.2 vs 8.4 ± 4.9 ms², respectively). Administration of propranolol and atropine did not affect RR interval or QTpeak interval indices during controlled atrial pacing. Conclusions : Beat‐to‐beat QT interval variability is affected by drugs that modulate the autonomic nervous system.     

T wave “humps” as a potential electrocardiographic marker of the long QT syndrome

Objectives. This study attempted to determine the prevalence and electrocardiographic (ECG) lead distribution of T wave “humps” (T2, after an initial T wave peak, T1) among families with long QT syndrome and control subjects.Background. T wave abnormalities have been suggested as another facet of familial long QT syndrome, in addition to prolongation of the rate-corrected QT interval (QTc), that might aid in the diagnosis of affected subjects.Methods. The ECGs from 254 members of 13 families with long QT syndrome (each with two to four generations of affected members) and from 2,948 healthy control subjects (age ≥ 16 years, QTc interval 0.39 to 0.46 s) were collected and analyzed. Tracings from familes with long QT syndrome were read without knowledge of QTc interval or family member status (210 blood relatives and 44 spouses).Results. We found that T2 was present in 53%, 27% and 5% of blood relatives with a “prolonged” (≥ 0.47 s), “borderline” (0.42 to 0.46 s) and “normal” (≤0.41 s) QTc interval, respectively (p < 0.0001), but in only 5% and 0% of spouses with a borderline and normal QTc interval, respectively (p = 0.06 vs. blood relatives). Among blood relatives with T2, the mean [±SD] maximal T1T2 interval was 0.10 ± 0.03 s and correlated with the QTc interval (p < 0.01); a completely distinct U wave was seen in 23%. T2 was confined to leads V₂and V₃in 10%, whereas V₄, V₅, V₆or a limb lead was involved in 90% of blood relatives with T2. Among blood rotatives with a borderline QTc interval, 50% of those with versus 20% of those without major symptoms manifested T2 in at least one left precordial or limb lead (p = 0.05). A T2 amplitude > 1 mm (grade III) was observed, respectively, in 19%, 6% and 0% of blood relatives with a prolonged, borderline and normal QTc interval with T2 in at least one left precordial or limb lead. Among the 2,948 control subjects, 0.6% exhibited T2 confined to leads V₂and V₃, and 0.9% had T2 involving one or more left precordial lead (but none of the limb leads). Among 37 asymptomatic adult blood relatives with QTc intervals 0.42 to 0.46 s, T2 was found in left precordial or limb leads in 9 (24%; 5 with limb lead involvement) versus only 1.9% of control subjects with a borderline QTc interval (p < 0.0001).Conclusions. These findings are consistent with the hypothesis that in families with long QT syndrome, T wave humps involving left precordial or (especially) limb leads, even among asymptomatic blood relatives with a borderline QTc interval, suggest the presence of the long QT syndrome trait.     

Dynamicity of Early and Late Phases of Repolarization in Patients with Remote Anterior Myocardial Infarction: The Interlead Differences

Background: Repolarization dynamicity (QT/RR) is supposed to be a prognostic marker in post‐MI patients. However, data on the relationships between early and late phases of QT and RR intervals (QT peak/RR and T peak–T end/RR) are insufficient, and which ECG lead should be used for the analysis is unclear. We analyzed repolarization dynamicity in patients after anterior MI with and without VT/VF history using two leads of Holter recordings‐ modified V₅ and V₃. The daytime and nighttime periods were also analyzed. Methods: Cohort of 88 patients after anterior MI (>6 months) consisted of 43 patients without VT/VF (33 males; 59 ± 12 years; LVEF: 41 ± 7%; NoVT/VF), and 45 patients with VT/VF history‐ ICD implanted as secondary prevention (40 males; 64 ± 10 years; LVEF: 32 ± 8%; VT/VF). QT/RR, QT peak/RR and T peak–T end/RR were calculated from 24‐hour ECG for the entire recording, daytime and nighttime periods, from V₅ and V₃ leads, respectively. Results: VT/VF patients had lower LVEF (P = 0.001). There were no differences in age and gender. VT/VF group had steeper QT/RR, QT peak/RR, and T peak–T end/RR in V₅: 0.233 ± 0.04 versus 0.150 ± 0.05, P = 0.0001, 0.181 ± 0.04 versus 0.120 ± 0.04, P = 0.0001, 0.052 ± 0.02 versus 0.030 ± 0.02, P = 0.0001, and in V₃: 0.201 ± 0.04 versus 0.149 ± 0.05, P = 0.0001, 0.159 ± 0.03 versus 0.118 ± 0.04, P = 0.0001, and 0.042 ± 0.02 versus 0.031 ± 0.02, P = 0.004; respectively. VT/VF patients had higher indices in V₅ than in V₃ lead (P = 0.001). QT/RR and QT peak/RR were steeper at daytime period in both leads. It was not found for T peak–T end/RR. Conclusions : Patients with VT/VF history are characterized by steeper relationships between repolarization duration and RR intervals. These findings are more evident in modified V₅ lead.     

Modulation of ventricular repolarization in patients with transient left ventricular apical ballooning: a case control study

Objective: Even though diffuse T wave inversion and prolongation of the QT interval in the surface electrocardiogram (ECG) have been consistently reported in patients with transient stress‐induced left ventricular apical ballooning (AB), ventricular repolarization has not yet been systematically investigated in this clinical entity. Background: AB, an emerging syndrome that mimics acute ST‐segment elevation myocardial infarction (MI), is characterized by reversible left ventricular wall motion abnormalities in the absence of obstructive coronary heart disease and significant QT interval prolongation. Methods: We prospectively enrolled 22 consecutive patients (21 women, median age 65 years) with transient left ventricular AB. A total of 22 age‐, gender‐, body‐mass‐index‐, and left‐ventricular‐function‐matched patients with acute anterior ST‐segment elevation MI undergoing successful direct percutaneous coronary intervention for a proximal occlusion of the LAD, as well as 22 healthy volunteers served as control groups. Beat‐to‐beat QT interval and QT interval dynamicity were determined from 24‐hour Holter ECGs, recorded on the third day after hospital admission. Results: There were no significant differences in baseline clinical characteristics, except higher peak enzyme release in MI patients. Compared with MI patients, AB patients exhibited significantly prolonged mean QT intervals and rate‐corrected QT intervals (QT: 418 ± 37 vs 384 ± 33 msec, P < 0.01; QTc_Bazett: 446 ± 40 vs 424 ± 35 msec, P < 0.05; QTc_Fridericia: 437 ± 35 vs 412 ± 31 msec, P < 0.05). Mean RR intervals tended to be higher in AB patients, without reaching statistical significance (877 ± 96 vs 831 ± 102 msec, P = NS). The linear regression slope of QT intervals plotted against RR intervals was significantly flatter in AB patients at both day‐ and nighttime (QT/RR slope_day: 0.18 ± 0.04 vs 0.22 ± 0.06, P < 0.01; QT/RR slope_night: 0.12 ± 0.03 vs 0.17 ± 0.05, P < 0.01). Conclusion: The present study is the first to demonstrate significant differences of QT interval modulation in patients with transient left ventricular AB and acute ST‐segment elevation MI. Even though transient AB is associated with a significant QT interval prolongation, rate adaptation of ventricular repolarization (i.e., QT dynamicity) is not significantly altered, suggesting a differential effect of autonomic nervous activity on the ventricular myocardium in transient AB and in acute MI.     

Sildenafil Citrate Does Not Alter Ventricular Repolarization Properties: Novel Evidence from Dynamic QT Analysis

Background: Sildenafil citrate may have direct cardiac electrophysiological effects, and is possibly responsible for some cardiac events. The aim of our study was to investigate the effects of sildenafil citrate on QT dynamicity properties with a new QT analysis program showing even small changes in ventricular repolarization. Methods: Twenty‐four‐hour Holter electrocardiographic recordings were used to obtain the data in the predrug phase (1‐hour rest position before drug administration), and in the postdrug phase (1‐hour rest position, which began 60 minutes after 50 mg oral sildenafil citrate administration). With the special QT analysis program (Verda, Reynolds Medical Ltd., UK); mean values of RR, QT, QT_o (corrected QT), J (the exponent of correction formula) and S (QT/RR plots slope) parameters together with QT variability indexes (QTVI) were calculated for study phases. Results: Mean ± SEM values for RR and QT were higher in postdrug phase than in predrug phase (RR: 845 ± 42 ms vs 816 ± 46 ms, P < 0.05; QT: 371 ± 8 ms vs 361 ± 9 ms, P < 0.05). However, sildenafil did not induce any significant change in mean ± SEM values for QT_o, J, and S in postdrug phase compared with predrug phase (408 ± 10 ms vs 406 ± 8 ms, 0.474 ± 0.030 vs 0.433 ± 0.025, 0221 ± 0.020 vs 0.198 ± 0.017, respectively; P > 0.05). QTVIs were also not different in each phase (predrug: ?0.874 ± 0.071 vs postdrug: ?0.997 ± 0.067, P = 0.109). Conclusions: Fifty milligrams sildenafil does not affect QT dynamicity properties. The cardiac events associated with sildenafil could not be explained with ventricular arrhythmias.     

Epinephrine Bolus Test in Detecting Long QT Syndrome Mutation Carriers with Indeterminable Electrocardiographic Phenotype

Background: In long QT syndrome (LQTS), prolonged and heterogeneous ventricular repolarization predisposes to serious arrhythmias. We examined how QT intervals are modified by epinephrine bolus in mutation carriers of three major LQTS subtypes with indefinite QT interval. Methods: Genotyped, asymptomatic subjects with LQTS type 1 (LQT1; n = 10; four different KCNQ1 mutations), type 2 (LQT2; n = 10; three different HERG mutations), and type 3 (LQT3; n = 10; four different SCN5A mutations), and healthy volunteers (n = 15) were examined. Electrocardiogram was recorded with body surface potential mapping system. After an epinephrine 0.04 μg/kg bolus QT end, QT apex, and T‐wave peak‐to‐end (Tpe) intervals were determined automatically as average of 12 precordial leads. Standard deviation (SD) of the 12 channels was calculated. Results: Heart rate increased 26 ± 10 bpm with epinephrine bolus, and similarly in all groups. QT end interval lengthened, and QT apex interval shortened in LQTS and normals, leading to lengthening of Tpe interval. However, the lengthening in Tpe was larger in LQTS than in normals (mean 32 vs 18 ms; P < 0.05) and SD of QT apex increased more in LQTS than in normals (mean 23 vs 7 ms; P < 0.01). The increase in Tpe was most pronounced in LQT2, and in SD of QT apex in LQT1 and LQT2. Conclusions: Abrupt adrenergic stimulation with a moderate dose of exogenous epinephrine affects ventricular repolarization in genotype‐specific fashion facilitating distinction from normals. This delicate modification may help in diagnosing electrocardiographically silent mutation carriers when screening LQTS family members. Ann Noninvasive Electrocardiol 2011;16(2):172–179     

U Wave Variability in the Surface ECG

A 72‐year‐old man with heart failure, left ventricular dysfunction (ejection fraction 20%), prior ischemic stroke, COPD, and exacerbation of chronic renal failure was admitted in our unit. Serum potassium was 6.1 mmol/L, calcium concentration was at the lower normal range 2.15 mmol/L, and NT‐pro‐BNP was 28,900 pg/mL. The surface 12‐lead electrocardiogram (ECG) showed sinus rhythm at 60 bpm, PR interval 160 ms, QRS duration 115 ms, QT interval 460 ms, and left ventricular hypertrophy criteria. Negative T waves in leads I, II, aVL, and V₄–V₆ were also seen. In leads V₄–V₆, negative U waves were observed in concordance with negative T waves. In all precordial leads, beat‐to‐beat U‐wave polarity variability was observed as a polarity variation from negative to positive with associated and stable negative T waves, in a beat‐to‐beat alternate morphology.     

Circadian Pattern of QT/RR Adaptation in Patients with and Without Sudden Cardiac Death after Myocardial Infarction

Background: Abnormalities in the adaptation of the QT interval to changes in the RR interval may facilitate the development of ventricular arrhythmias. Methods: This study sought to evaluate the dynamic relation between the QT and RR intervals in patients after acute myocardial infarction. The study population consisted of 14 patients after myocardial infarction (age 60 ± 7 years, 12 men) who died suddenly (SCD victims) within 1 year after the myocardial infarction and 14 pair-matched age, sex, left ventricular ejection fraction, infarct site, thrombolytic therapy) patients who remained event-free after myocardial infarction (Ml survivors) for at least 3 years. Fourteen normal subjects were studied as controls (age 55 ± 9 years, 11 men). QT and RR intervals were measured on a beat-to-beat basis automatically with a visual control from 24-hour ambulatory ECGs using Reynolds Pathfinder 700. Mean hourly values of the QT/RR slope (QT =α+βRR) and corrected QT interval at 1000 ms of RR interval (QT_1s) were derived for each subject using an inhouse program (QT_1s=α+1000β). The dynamics of the QT/RR slope and QT_1s were assessed on the basis of hourly mean values. The circadian rhythm of ventricular repolarization (QT_1s and QT/RR slope) was examined by harmonic regression analysis. Results: There was a trend towards a significant difference in 24-hour mean value of QT_1s between study groups (408 ± 26 ms vs 381 ± 43 ms and 386 ± 22 ms, P = 0.06), and a significant difference was found between SCD victims and normal subjects (408 ± 26 vs 386 ± 22 ms, P = 0.02). The QT_1s differed significantly between study groups (P = 0.038) only during the day time (09:00–19:00 hour), when QT_1s was significantly longer in SCD victims than in normal subjects (409 ± 33 vs 380 ± 27 ms, P = 0.02) and tended to be longer than in Ml survivors (409 ± 33 vs 379 ± 42 ms, P = 0.08). The 24-hour mean value of QT/RR slope was significantly different between study groups (P = 0.04), with a significantly steeper slope in SCD victims than in normal subjects (0.15 ± 0.07 vs 0.09 ± 0.02, P = 0.008). During day time, the QT/RR slope differed significantly between study groups (P = 0.04), while the difference was less marked at night (P = 0.08). The slope was significantly steeper in SCD victims than in normal subjects during both day and night (P < 0.05). A marked circadian variation of QT_1s was observed in normal subjects, which was blunted in Ml survivors and SCD victims. Conclusions: Abnormal repolarization behaviors, characterized by longer QT_1s and impaired adaptation of QT to variations in RR intervals, were found in SCD victims. Hence, lethal ventricular tachyarrhythmias might be provoked by the altered repolarization dynamics in patients after myocardial infarction. A.N.E. 1999;4(3):286–294     

Three-Lead Measurement of QTc Dispersion

QTc Dispersion. Introduction: QTc dispersion has traditionally been calculated from all 12 leads of a standard electrocardiogram (ECG). It is possible that alternative, quicker methods using fewer than 12 leads could be used to provide the same information. Methods and Results: We have previously shown a difference in QTc dispersion from ECGs recorded at least 1 month after myocardial infarction between patients who subsequently died and long-term survivors. In the current study, we recalculated QTc dispersion in these ECGs using different methods to determine if the observed difference in QTc dispersion measurements between the two groups, as calculated from 12-lead ECGs, persisted when using smaller sets of leads. QTc dispersion was recalculated by four methods: (1) with the two extreme QTc intervals excluded: (2) from the six precordial leads; (3) from the three leads most likely to contribute to QTc dispersion (aVF, V₁V₄); and (4) from the three quasi-orthogonal leads (aVF, I, V). For each of the 270 12-lead ECGs examined, a mean of 9.9 leads (SD 1.5 leads) had a QT interval analyzed; the QT interval could not be accurately measured in the remaining leads. Using the standard 12-lead measurement of QTc dispersion, there was a difference in the fall in QTc dispersion from early to late ECG between the groups: 9.1 (SD 60.8) msec for deaths versus 34.4 (55.2) msec for survivors (P = 0.016). This difference in QTc dispersion between early and late ECGs was maintained using either three-lead method (quasi-orthogonal leads: -2.6 [56.2] msec for deaths vs 26.9 [54.3] msec for survivors [P = 0.003]; “likeliest” leads: 8.6 [64.9] msec vs 29.5 [50.2] msec [P = 0.05]), but not when using the other two methods (precordial leads: 19.1 [55.5] msec vs 22 [50.8] msec [P = 0.76]; extreme leads removed: 9.2 [50.1] msec vs 21.8 [42] msec [P = 0.13]). Conclusion: QTc dispersion calculated from three leads may be as useful a measurement as QTc dispersion calculated from all leads of a standard ECG. Its advantages over the standard measurement are its simplicity and the lack of problems with lead adjustment.     

Relation between Beat‐to‐Beat QT Interval Variability and T‐Wave Amplitude in Healthy Subjects

Objectives: Elevated beat‐to‐beat QT interval variability (QTV) has been associated with increased cardiovascular morbidity and mortality.The aim of this study was to investigate interlead differences in beat‐to‐beat QTV of 12‐lead ECG and its relationship with the T wave amplitude. Methods: Short‐term 12‐lead ECGs of 72 healthy subjects (17 f, 38 ± 14 years; 55 m, 39 ± 13 years) were studied. Beat‐to‐beat QT intervals were extracted separately for each lead using a template matching algorithm. We calculated the standard deviation of beat‐to‐beat QT intervals as a marker of QTV as well as interlead correlation coefficients. In addition, we measured the median T‐wave amplitude in each lead. Results: There was a significant difference in the standard deviation of beat‐to‐beat QT intervals between leads (minimum: lead V₃ (2.58 ± 1.36 ms), maximum: lead III (7.2 ± 6.4 ms), ANOVA: P < 0.0001). Single measure intraclass correlation coefficients of beat‐to‐beat QT intervals were 0.27 ± 0.18. Interlead correlation coefficients varied between 0.08 ± 0.33 for lead III and lead V₁ and 0.88 ± 0.09 for lead II and lead aVR. QTV was negatively correlated with the T‐wave amplitude (r =–0.62, P < 0.0001). There was no significant affect of mean heart rate, age or gender on QT variability (ANOVA: P > 0.05). Conclusions: QTV varies considerably between leads in magnitude as well as temporal patterns. QTV is increased when the T wave is small.     

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     

Enhanced Transmural Dispersion of Repolarization in Patients with J Wave Syndromes

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

QT Interval Length and Diabetic Autonomic Neuropathy

QT interval length was measured in ECG recordings from three groups of age-matched male subjects: 36 normal subjects, 41 diabetic patients without (DAN-ve), and 34 with (DAN+ve) autonomic neuropathy. ECG samples were selected from previously recorded 24-h ECGs on the basis of a clearly defined T wave and a steady RR interval over 2 min of around 750 ms (80 beats min^?1). There were no significant differences in RR interval between the groups. The two diabetic groups had slightly longer QT measurements (normal 365 ± 14 (±SD) ms, DAN-ve 373 ± 18 ms, DAN+ve 375 ± 23 ms, p = 0.05), and corrected QT (QTc) values (normal 423 ± 15 ms, DAN-ve 430 ± 20 ms, DAN+ve 435 ± 24 ms, p = 0.05). Ten diabetic patients fell above our defined upper limit of normal for QTc (>mean + 2SD). There was a significant correlation in the DAN-ve group between the QT indices and 24-h RR counts (QT r = ?0.38, p < 0.01; QTc r = ?0.40, p < 0.01). We conclude that there are some small alterations in QT interval length in the steady state in diabetic autonomic neuropathy. The changes appear to be due to autonomic impairment, rather than diabetes per se.     

The Prognostic Accuracy of Different QT Interval Measures

Background: The QT intervals accuracy for predicting arrhvthmic death varies between studies, possibly due to differences in the selection of the lead used for measurement of the QT interval. The purpose of this study was to analyze the prognostic accuracy of all known ways to select the lead. Methods and Results: Three institutions that used different methods for measuring QT intervals provided their QT databases. They included more than 3500 twelve‐lead surface ECGs. The data represented low‐ and high‐risk patients of the normal population (survivors vs dead from cardiovascular causes), acute myocardial infarction (survivors versus death from all causes) and remote myocardial infarction (with vs without a history of ventricular arrhythmia). The prognostic accuracy was defined as the area under the Receiver Operator Curve (ROC‐area). The most accurate standard leads were I and aVL and the least accurate was AVR. The most accurate precordial lead was V₄. The prognostic accuracy of the longest QT interval was higher than for any standard lead. The prognostic accuracv of the mean of the three longest QT intervals was equal to or slightly lower than for the longest QT interval. Conclusions: The highest prognostic accuracy is obtained with the longest QT interval. The accuracies of the lead selection methods are so different that it can explain a substantial part of the differences between otherwise similar studies in the literature. We recommend the use of the mean value of the three longest QT intervals. A.N.E. 2002;7(1):10–16     

Circadian and Gender Effects on Repolarization in Healthy Adults: A Study Using Harmonic Regression Analysis

Background: Sudden cardiac death and myocardial infarction have a circadian variation with a peak incidence in the early morning hours. Increased dispersion of repolarization facilitates the development of conduction delay necessary to induce sustained arrhythmia. Both QT‐dispersion and T‐wave peak to T‐wave end (TpTe) have been proposed as markers of dispersion of myocardial repolarization. Methods: Forty healthy adults (20 women), age 35–67 years old, with normal EKGs, echocardiograms, stress tests, and tilt‐table tests were analyzed during a 27‐hour hospital stay. EKGs were done at eight different time points. QT‐intervals, QT‐dispersion, and TpTe were measured at each time point. Harmonic regression was used to model circadian periodicity, P < 0.05 was considered significant. Results: The composite QT‐interval was longer in women than in men (416 ± 17 msec vs 411 ± 20 msec, respectively, P = 0.006). The QT‐dispersion among all leads was greater in men than women (37 ± 13 msec vs 30 ± 11 msec, respectively, P < 0.0001); a similar difference was found in the precordial leads. Harmonic regression showed that QT‐dispersion had a significant circadian variation, primarily in men. In men, the maximum QT‐dispersion occurred at 6 AM (45 ± 15 msec). TpTe also had a significant circadian variation that was not affected by gender in the majority of leads. Conclusions: A circadian variation exists in the dispersion of myocardial repolarization, as measured by both TpTe and QT‐dispersion. Men and women have a different circadian variation pattern. Further studies regarding the mechanisms and clinical implications are needed. Ann Noninvasive Electrocardiol 2010;15(1):3–10     

β-blockers protect against dispersion of repolarization during exercise in congenital long-QT syndrome type 1

Dispersion of Repolarization in LQT1. Introduction: β‐Blocker therapy reduces syncope and sudden death in long‐QT syndrome type 1 (LQT1), but the mechanism of protection is incompletely understood. This study tested the hypothesis that β‐blockade reduces QT prolongation and dispersion of repolarization, measured as the T peak‐to‐end interval (T_pe), during exercise and recovery in LQT1 patients. Methods and Results: QT and T_pe were measured in 10 LQT1 patients (33 ± 13 years) and 35 normal subjects (32 ± 12 years) during exercise tests on and off β‐blockade. In LQT1 patients, β‐blockade reduced QT (391 ± 25 milliseconds vs 375 ± 26 milliseconds, P = 0.04 during exercise; 419 ± 41 milliseconds vs 391 ± 39 milliseconds, P = 0.02 during recovery) and markedly reduced T_pe (91 ± 26 milliseconds vs 67 ± 19 milliseconds, P = 0.03 during exercise; 103 ± 26 milliseconds vs 78 ± 11 milliseconds, P = 0.02 during recovery). In contrast, in normal subjects, β‐blockade had no effect on QT (320 ± 17 milliseconds vs 317 ± 16 milliseconds, P = 0.29 during exercise; 317 ± 13 milliseconds vs 315 ± 14 milliseconds, P = 0.15 during recovery) and mildly reduced T_pe (69 ± 13 milliseconds vs 61 ± 11 milliseconds, P = 0.01 during exercise; 77 ± 19 milliseconds vs. 68 ± 14 milliseconds, P < 0.001 during recovery). Conclusion: In LQT1 patients, β‐blockers reduced QT and T_pe during exercise and recovery, supporting the theory that β‐blocker therapy protects LQT1 patients by reducing dispersion of repolarization during exercise and recovery. (J Cardiovasc Electrophysiol, Vol. 22, pp. 1141‐1146, October 2011)     

Spatial Properties of QT and the T‐Wave Morphology

Objective: To describe the relation between the QT interval and the T‐wave morphology. Material and methods: Frank orthogonal leads X, Y, Z of one subject and resting 12‐lead ECG of 40 subjects. QT was measured by the tangent method. The QT values are organized according to the anatomic orientation of the leads: I, ‐aVR, II, aVF, III, ‐aVL, ‐I, aVR, ‐II, ‐aVF, ‐III, aVL. and: V₁, V₂, V₃, V₄, V₅, V₆, ‐V₁ ‐V₂, ‐V₃, ‐V₄, ‐V₅, ‐V₆. The T‐wave amplitudes and QT were categorized according to QT into four groups with increasing mean QT. Results: Kruskal‐Wallis nonparametric test showed that the shortest and longest QT values are measured on the T wave with the smallest amplitudes (P < 0.001). Inspection of plots of QT and T waves reveals that the shortest and longest QT values are usually measured in leads with a small difference in orientation (neighbor leads). The mechanism behind these characteristics is mainly that the shortest and longest QT values are measured on T waves that are close to a lead orientation, whereas the T waves are flat or biphasic. We also observed an almost significant (P = 0.057) decrease in the T‐wave amplitude with increasing dispersion. Conclusion: The relation between T‐wave morphology and QT in the same cardiac plane is highly organized. The shortest and longest QT values are measured on the T wave with the smallest amplitudes (P < 0.001).     

QT dispersion and RR variations on 12-lead ECGs in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy

Increased QT dispersion, which has been proposed as a markerof ventricular repolarization inhomogeneity, may predisposeto ventricular arrhythmias. Data on QT disper sion in patientswith congestive heart failure are scarce. In this study, conventional12-lead ECGs were recorded in 135 consecutive patients withcongestive heart failure secondary to idiopathic dilated cardiomyopathy.Seventy-five patients were excluded from QT interval assessmentsdue to one or more of the following reasons: (1) low amplitudeof the T wave (n=3), (2) atrial fibrillation (n=26) and (3)bundle branch block (n=46). QT dispersion was calculated as(I) QT-range: the difference between the maximum and minimumQT intervals on any of the 12 leads and (2) QT-SD: the standarddeviation of the QT interval in all the 12 leads. RR intervalswere measured in leads II, aVL, V₂ and V₅ QT-SD (20·85± 5·00 ms) was significantly (r=0·8997,P<0·00l) related to QT-range (6565 ± l5 ms),but not to the QT interval. Neither QT-range nor QT-SD was significantlyrelated to age, left ventricular dimensions, left ventricularend diastolic pressure, left ventricular ejection fraction orleft ventricular wall thickness. There was no significant differencein QT dispersion between survivors and those who died (n=8)or were transplanted (n=9) during 34 ± 23 month follow-up.No significant difference in QT dispersion was observed betweenpatients with and without ventricular tachycardia ( three consecutivebeats) detected on 24-h Holter ECGs. RR interval variation wassignificantly lower in patients who died compared with survivors(standard deviation: 10·37 ± 3·61 vs 36·02± 35·03 ms, P<0·001; coefficient ofvariance: 1·87 ± 0·7 vs 4·50 ±4·9%, P=0 This was also true in patients with bundlebranch block. These observations suggest that QT dispersionin idiopathic dilated cardiomyopathy is not significantly relatedto either QT interval or cardiac size and function and doesnot predict death. The application of QT dispersion assessmentis limited by the commonly encountered atrial fibrillation andbundle branch block in this patient population. However, reducedRR variation on standard 12-lead ECGs has important prognosticimplications in these patients.