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Albuquerque, NM
Dr. Chen is a Cardiology Fellow for the Department of Medicine, University of New Mexico. Dr. Kusumoto is Associate Professor of Clinical Medicine, Cardiology Division, Department of Medicine, University of New Mexico, and Director of Electrophysiology and Pacing Service, Cardiology Department, Lovelace Medical Center.
Correspondence to: Fred M. Kusumoto, MD, Electrophysiology and Pacing Service, Cardiology Department, Lovelace Medical Center, 5400 Gibson Blvd SE, Albuquerque, NM 87108; e-mail: fred.kusumoto{at}lovelacesandia.com
The QT interval, in its basic form, is a seemingly simple concept. Defined as the interval from the beginning of the QRS complex to the end of the T wave on a surface ECG, the QT interval represents the period of global ventricular depolarization and subsequent repolarization.1 Prolongation of the QT interval due to inherited ion channel abnormalities or due to drugs or metabolic abnormalities has been associated with an increased incidence of ventricular arrhythmias. In addition, experimental studies234 have demonstrated that regional differences in repolarization facilitate reentry and the development of ventricular arrhythmias. Heterogeneous ventricular repolarization was recognized from surface ECGs as early as 1934.5 Over a decade ago, the difference between the longest and shortest QT intervals on a standard 12-lead ECG (QT dispersion) was forwarded as a simply measured marker for vulnerability to ventricular arrhythmias and risk for sudden cardiac death.6 A number of publications followed, and currently there are > 1,000 articles in the literature on QT dispersion. However, the exact physiologic mechanism and true clinical utility of QT dispersion have been the subject of intense debate over the past several years.789
QT dispersion is measured as the difference between the maximal and minimal QT intervals.6910 While the definition is straightforward, its accurate measurement becomes quite complex. First determining the end of the T wave can often be difficult, particularly if the T wave is of relatively low amplitude. Five "experts" were asked to measure the onset of the QRS complex and the end of the T wave in 250 ECGs from both normal and abnormal hearts without QT interval prolongation or bundle-branch block.11 The interexpert variation for the QRS onset was 6.5 ms, but the variation for the end of the T wave was 30.6 ms with an intraindividual variability of 8 ms. Several computer algorithms have been developed to accurately and reproducibly localize the end of the T wave, but have not been associated with any significant improvement in reproducibility over manual techniques.1213 Unfortunately, increasing paper speed or amplifying the signals do not aid in measuring the T wave end point.14 In general, interobserver and intraobserver variability of QT dispersion measurements can be as much as 30 to 40%.915 Second, it is not clear whether QT dispersion measurements must be corrected for rate. Several large studies1617 have demonstrated the potential clinical utility of QTc dispersion, but a recent clinical study18 in 35 patients demonstrated that QT dispersion is independent of heart rate. Since elevated heart rate itself is associated with increased risk of death in the general population, analysis of QT dispersion should probably not be rate corrected to eliminate the influence from an additional variable.1819 Third, the specific number of leads required for measurement of QT dispersion has not been formally defined. Initial studies in QT dispersion used body surface potential mapping (BSPM) with 100 to 200 unipolar precordial ECGs to identify differences in ventricular repolarization. A subsequent study by Cowan et al10 found that the values obtained from the surface 12-lead ECG were similar to those obtained by BSPM. However, since only two of the six frontal plane leads are actually recorded while the other four are derived mathematically, many clinical studies have used only six unipolar precordial leads or eight leads (two frontal plane leads and six precordial leads). The T wave generally shortens and decreases in amplitude from precordial leads V2 to V6 to reach minimal values in aVL due to tissue attenuation from air in the lungs. Recent studies suggest that using a specific combination of "quasiorthogonal" leads (aVF, V1, and V4; I, aVF, V2, and V4) may provide sufficient QT dispersion data for analysis.20 However, at this time no standardized method for acquiring QT dispersion exists.
Even if consistent and standardized measures could be obtained, it is also clear that QT dispersion provides only a correlate of global ventricular repolarization rather than directly identifying small regions of heterogeneous repolarization. An experimental study21 has demonstrated that the peak of the T wave rather than the end of the shortest QT interval coincides with initial ventricular repolarization. The shape of the T wave and the interval between the peak of the T wave and the end of the T wave contain most of the information on differences in regional ventricular depolarization. QT dispersion correlates with but is not a direct measure of heterogeneous ventricular action potential durations.22 An analysis23 suggests that the shape of the T wave vector of repolarization is the main determinant of QT dispersion.
Given the methodologic problems associated with QT dispersion measurements, it is not surprising that normal values for QT dispersion have not been well defined. Generally values between 30 ms and 60 ms are considered normal. In an analysis9 of 8,455 healthy subjects from 51 studies, mean QT dispersion ranged from 11 ± 10 to 71 ± 7 ms. The weighted mean (± SD) from all of the studies was 33 ± 20 ms. Several large prospective studies have evaluated the use of QT dispersion in well-defined populations without recognized cardiac disease. In the Rotterdam Study,16 5,812 adults > 55 years old were followed up for 4 years. Subjects with QTc dispersion > 60 ms had a twofold risk for cardiac death or sudden death and a 40% increased mortality risk when compared to those subjects with a QTc dispersion < 30 ms. In the Strong Heart Study17 of 1,839 American Indians aged 45 to 74 years, QTc dispersion > 58 ms was identified in 4.1% of the population and was associated with a 3.4-fold increased risk for cardiovascular death.
Several studies have evaluated the use of QT dispersion in specific patient populations with hyperlipidemia, coronary artery disease, heart failure, and diabetes mellitus. The West of Scotland Coronary Prevention Study24 evaluated 6,595 middle-aged men with moderately raised cholesterol but no prior myocardial infarction; QT dispersion > 44 ms was associated with a 36% increased risk death or nonfatal myocardial infarction, but because the sensitivity was 8.8% and the specificity was 93.8%, the cut-off provided little predictive value. Although retrospective studies2526 have suggested that QT dispersion provides prognostic information after myocardial infarction, in the only prospective study27 to date QT dispersion provided no prognostic information in 280 patients after myocardial infarction. The prognostic value of QT dispersion has also been evaluated in patients with congestive heart failure with mixed results.28293031 In a retrospective study29 of 2,265 patients with an ejection fraction < 0.40 a QT dispersion > 35 ms was associated with a 5-year mortality rate of 58%, compared to 45% in patients with a QT dispersion of < 35 ms. The Losartan Heart Failure Survival Study30 evaluated 3,152 patients > 60 years old, New York Heart Association class II-IV, and ejection fraction < 0.40. In the 986 patients with interpretable ECG tracings, baseline QT dispersion was 86 ± 31 ms. Using a prespecified QT dispersion cutoff of > 80 ms, no prognostic information was obtained from QT dispersion measurements. In a retrospective study32 of 219 patients with diabetes mellitus, increased QT dispersion was associated with an increased incidence of myocardial ischemia and left ventricular hypertrophy.
The possible relationship between QT dispersion and pulmonary disease has been previously described. In a small study,33 patients with COPD had higher QT dispersion values than age-matched control subjects (COPD, 58 ± 10 ms; control subjects, 38 ± 8 ms). In addition, COPD patients with episodes of nonsustained ventricular tachycardia had higher QT dispersion values (67 ± 10 ms) than those without ventricular tachycardia (55 ± 8 ms). Nakamura and colleagues (see page 2107) extend this relationship by their finding that QT dispersion in patients with obstructive sleep apnea is significantly increased during sleep when compared to awake (sleep, 65 ± 15 ms; awake, 51 ± 13 ms; p < 0.0001). In addition, treatment with continuous positive airway pressure (CPAP) significantly decreased QT dispersion (awake, 56 ± 13 ms; CPAP, 51 ± 11 ms). Although the findings are statistically significant, as is common in many studies evaluating QT dispersion, the individual data points overlap significantly, thus limiting the clinical utility of QT dispersion measurements.
Obstructive sleep apnea can be associated with both bradyarrhythmias and tachyarrhythmias.323334 In a study34 of 458 patients undergoing sleep studies, arrhythmias were noted in 58% of patients with apneic episodes compared to 42% in patients without apnea. Two studies3536 have demonstrated that ventricular ectopy is particularly common in patients with sleep apnea and left ventricular dysfunction. In a study of 47 patients with left ventricular ejection fraction 
0.40 and sleep apnea, > 25 episodes of nonsustained ventricular tachycardia were observed in those patients with severe sleep apnea during 24-h ambulatory ECG monitoring.35 In a prospective study36 of 29 men with severe sleep apnea, left ventricular ejection fraction 0.45, and treated with continuous positive airway pressure, the 16 "responders" had a significant reduction in the frequency of premature ventricular contractions (66 ± 117/h vs 18 ± 20/h) and couplets (3.2 ± 6/h vs 0.2 ± 0.21/h).
The mechanism for increased ventricular irritability associated with obstructive sleep apnea and the salutary effects of CPAP are not known. Nakamura and colleagues provide intriguing data that heterogeneity of ventricular repolarization may be a possible mechanism for this finding. However, the vagaries of QT dispersion measurement prevent any fundamental conclusions to be reached. It may be that other measures of repolarization such as microvolt T wave alternans, T wave repolarization vectors, or direct measurement of regional monophasic action potentials will confirm that regional ventricular repolarization differences are an important pathophysiologic mechanism for the close relationship between ventricular arrhythmias and sleep disorders.
References
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