REVIEW ARTICLE
Year : 2019 | Volume : 8 | Issue : 2 | Page : 71-79
QT interval – Its measurement and clinical significance
Sita Ram Mittal DM (Cardiology)
Department of Cardiology, Mittal Hospital and Research Centre, Ajmer, Rajasthan, India
Date of Web Publication 3-Apr-2019
Correspondence Address:
Sita Ram Mittal
Xi/101, Brahmpuri, Ajmer - 305 001, Rajasthan
India
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Source of Support: None, Conflict of Interest: None
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DOI: 10.4103/JCPC.JCPC_44_18
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Abstract
QT interval extends from the beginning of QRS complex to the end of T wave. Thus, it includes the duration of ventricular depolarization (QRS) and repolarization (J point to end of T wave). It corresponds to the duration of cellular action potential. "long-" and "short"-QT intervals are considered as risk markers for cardiac arrhythmias and sudden death. In the last decade, there have been significant advances in our understanding about measurement and significance of QT interval. We have made an attempt to review the literature to find the limitations and queries surrounding the present status of measurement of QT interval and its significance as a risk marker for cardiac arrhythmias and sudden death.
Keywords: Arrhythmias, electrocardiography, repolarization heterogeneity, sudden cardiac death, torsades de pointes
How to cite this article:
Mittal SR. QT interval – Its measurement and clinical significance. J Clin Prev Cardiol 2019;8:71-9
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Introduction
Top
QT interval extends from the beginning of QRS complex to the end of T wave. It corresponds to the duration of action potential.[1]
(A) Measurement
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(a) Current understanding
At present, available electrocardiogram (ECG) machines can automatically measure QT interval and corrected QT (QTc) interval. Machines computing data from multiple leads give more accurate information than those which analyze only single lead. Automated measurement by ECG machines should, however, be confirmed by manual measurement, especially if there is difference between automated measurement and visual impression.[2] Such problem is likely to occur when T wave is notched, biphasic, or relatively flat.[3],[4],[5] QT interval is measured from the beginning of QRS to the end of T wave irrespective of whether the QRS complex begins with "Q" wave or "R" wave.[6] It is measured from the lead in which it is longest (usually leads V2 or V3).[1],[7] This is necessary because in some leads initial part of QRS and/or terminal part of T wave may be isoelectric[2] resulting in false shortening of QT interval. Mean of at least three beats is taken[8] in the same lead. Accurate measurement can be made only after a series of regular equal cycles[9] during stable sinus rhythm.[8]
At times, end of T wave and its junction with T-P segment is not sharp producing difficulty in defining exact end of T wave. In such situation, end of T wave is taken as the point where a tangent drawn from the steep portion of the downslope of T wave touches the isoelectric line.[10],[11]
(b) Controversies
(i) Measurement of end of T wave is not clear
There is no consensus regarding measuring of QT interval when a "U" wave fuses with the end of T wave masking the exact point of end of T wave. Some authors feel that the point where a tangent extending from the downslope of T wave touches the baseline should be taken as the end of T wave.[12] However, this might underestimate the QT interval.[2] Al-Akehar and Siddique[13] suggested that the "U" wave should be included in the QT measurement. However, this is likely to result in overestimation of QT interval. Further, there are no accepted reference values for the "normal" and prolonged QU interval.[8] Some authors have suggested measuring QT interval in leads in which a prominent U wave is absent (usually lead aVR and aVL).[1] However, this QT interval may not be the longest. Most of the authors feel that the point of notch between "T" and "U" wave can be taken as the end of T wave.[8],[9],[14],[15] This is not the true end-point of the T wave, but it does for practical purposes.[14]
If T wave is notched or bifid, end of the terminal wave can be taken to measure the QT interval. In tachycardia, end of T wave may fuse with the beginning ofPwave. In such a situation, junction of T andPwaves can be taken as the end of T wave for practical purposes.[9] However, there is no evidence that this is the true QT interval.
Due to above-mentioned differences in opinion, there can be considerable interobserver variability in manual measurement of QT interval.[16] Therefore, if the end of T wave is not clear, method used to determine the end of T wave should be mentioned in the report.
(ii) Measurement in the presence of broad QRS
There is currently no agreed consensus on how to measure the QT interval in patients with broad QRS, paced ventricular rhythm, or atrial fibrillation.[17] Measurement of J-T interval has been suggested for detection of prolonged repolarization in ventricular conduction defect. However, its use has not been validated. Further, J-T interval has strong correlation with ventricular rate.[18] Normal limits for rate adjusted J-T interval have not been established for ventricular conduction defect or for normal ventricular conduction. J-T interval, therefore, does not give correct information about QT interval in the presence of ventricular conduction defect. Bogossian et al.[19] suggested that in the presence of left bundle branch block (LBBB), native QT interval (QT interval before development of LBBB) can be calculated as measured QT interval −50% of LBBB duration. However, it can cause overcorrection of QT interval.[20] Further, this formula does not tell the correct QT interval in the presence of LBBB. This is especially important because factors that lead to the development of LBBB (e.g. myocardial ischemia) may also prolong QT. Finding native QT interval does not have much clinical significant once LBBB has developed. We should be able to determine QT interval after the development of LBBB. There is no literature on measurement of QT interval in patients of right bundle branch block, fascicular blocks, nonspecific intraventricular conduction defects, and paced rhythm.
(B) Correction for Heart Rate
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With increasing heart rate, repolarization shortens so that myocardium is excitable when the next impulse comes. QT interval, therefore, shortens with increasing heart rate. Therefore, exact significance of QT interval can be judged only after correcting it for heart rate. QTc interval is called "QTc."
(a) Formulae for correction
(i) Current understanding
Several formulae have been proposed for correction of QT interval.[8],[21]
Bazett's formula[22] is most commonly used.[2] It is as follows:
R-R is the preceding R-R interval. QT is measured in milliseconds and RR is measured in seconds. It works best between heart rate of 60–100 beats/min. It may give erroneous results at both slower (overcorrection) and faster heart rates (undercorrection).[8]
Linear Framingham method for correction of QT interval is as follows:
QTC = QT + 0.154 (1-RR)
It may give more uniform rate correction over wider range of heart rates.[15]
Fridericia formula for QT interval correction is as follows:[23]
QTc = QT/(R-R)0.33
This formula fails at high heart rates.[24]
Another formula suggested for rate correction is as follows:
QTc = QT + 1.75 (HR-60).[1]
HR is heart rate. Intervals are measured in milliseconds. It has been shown to be relatively insensitive to heart rate.[21]
(ii) Limitations
All formulae have some or other shortcoming.[8] For a given ECG, there can be significant difference in the results of various formulae. Therefore, the formula used for correction should be mentioned in the report.[2] Bazett's formula is easy to use and gives reasonably working information in most of the patients with normal heart rates. Most of the studies on QT interval have used this formula. It is most commonly used.[8]
(b) Heart rate-QT interval nomogram
(i) Current understanding
One heart rate-QT interval nomogram has been described for stratification of risk of torsades de pointes in drug-induced QT prolongation.[25] QT interval is measured manually and then plotted against the heart rate on the QT nomogram. Nomogram takes heart rate rather than R-R interval. Higher is the QT– heart rate pair above the nomogram, greater is the risk of drug-induced torsades de pointes.[4]
(ii) Limitations
The nomogram does not correct the QT interval for heart rate. It only gives some impression about risk of torsades de pointes of a given QT interval and heart rate. It is important to remember that several other factors contribute to the risk of drug-induced torsades de pointes at a given QT interval. Further, there is substantial intersubject variability in the relation between heart rate and QT interval[26]
Nomogram has been validated only for evaluation of drug-induced QT prolongation. It has not been validated in other causes of QT prolongation. The relationship between QT interval, heart rate, and risk is uncertain at rapid heart rate. Therefore, an interrupted nomogram line has been used for heart rates above 104/min.[21] Therefore, nomogram cannot be used reliably at fast heart rate.
Thus, no formula or nomogram provides an ideal rate correction for a given subject in a particular clinical setting.[3] This is especially true when assessing the minor changes of QT interval induced by drugs.[27]
(c) Correction in irregular rhythm
(i) Current understanding
It is not possible to measure correct QT interval in irregular rhythm, for example, in sinus arrhythmia, atrial fibrillation, or frequent ectopic beats. QT interval may be prolonged in ectopic and postectopic beat. Although it is not the correct QT, such phenomena may suggest increased risk of arrhythmias in patients with long QT.[8]
(ii) Limitations
Musat et al.[28] correlated QT interval correction methods during atrial fibrillation and sinus rhythm. They observed that Fridericia method most closely approximates the QTc interval during atrial fibrillation to QTc during sinus rhythm. Patients were being treated with dofetilide. They studied the last ECG in atrial fibrillation to the first ECG in sinus rhythm. Therefore, their observation cannot be extrapolated to a routine case of atrial fibrillation.
(C) Normal Value of Qtc
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(i) Current understanding
Previously, normal upper limit of QTc was considered as 460 ms for women and 450 ms for male.[2] Subsequently, valves of 470 ms for male and 480 ms for female were suggested as limits of normality.[29] Later, values of 440–450 ms in men and 440–470 ms in women were considered as borderline.[27] Recent European guidelines for the management of patients with ventricular arrhythmias and prevention of sudden cardiac death have, however, suggested that QTc normally ranges between 360 ms and 480 ms.[30]
(ii) Limitations
QTc interval is affected by age, sex, sympathetic tone, posture, meals, heart rate, and diurnal pattern.[31],[32],[33] Therefore, minor fluctuations should not be given undue importance and a rigid cut of value is not justified. A tip that helps identify normal QT interval on visual ECG examination is that it is less than half of the preceding R-R interval.[13] QTc >500 ms predisposes to torsades de pointes.[3],[27],[31]
(D) Qt Dispersion
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(i) Current understanding
Onset of QRS and end of T wave do not occur simultaneously in every lead. QT interval, therefore, varies from lead to lead. This variation in QT interval is known as dispersion of QT interval (QTD). Initially, it was considered as an indicator of arrhythmogenicity.[34],[35]
(ii) Limitations
Subsequent studies did not confirm initial impression of relation with arrhythmogenicities
Reported normal values vary widely (10–71 ms)[36]
Main cause of QT dispersion is, in fact, the unreliable localization of the end of T wave[37]
Depending on QRS vector, initial part of QRS may be isoelectric in some leads. This results in incorporation of q wave in the P-R segment.[14] It also contributes to QTD
QT dispersion is sensitive to age, time of day, season of year, and even body position[38]
QTD per se does not represent underlying heterogeneity in repolarization and does not itself confer increased cardiovascular risk[37]
It has not been found to be a clinically useful parameter[24] and is no longer used.[39]
(E) Significance of Variations in Qt Interval
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(1) Prolonged QT
Initially, prolonged QT interval per se was considered to be a very important risk factor for cardiac arrhythmias and sudden death. Over the past two decades, there has been significant advancement in our understanding of significance of prolonged QT interval. Following conclusions can be drawn from the literature.
(a) Congenital or familial prolongation of QT
(i) Current understanding
Congenital prolongation of QT interval is caused by mutation in ion channels (potassium, calcium, or sodium). More than 15 mutations have been identified.[13] Hereditary long QT syndromes (Jervell Lange–Nielson syndrome, Romano–Ward syndrome, Andersen–Tawil syndrome, and Timothy syndrome) are associated with high risk of cardiac events.[40] Other mutations in long QT susceptibility genes may or may not manifest QT prolongation on a resting 12-lead surface ECG[41],[42] and are mostly without consequence.[41]
(ii) Controversies
Triggers such as exertion, swimming, emotion, auditory stimuli, and postpartum period can rarely increase electrical instability of heart resulting in potentially life-threatening arrhythmias.[41],[43] In these cases, a normal QT interval does not exclude the risk
Some gene suggestive electrocardiographic findings have been suggested.[44] LQT1 is frequently associated with broad-based T wave. LQT2 is usually associated with low amplitude, notched, or biphasic T wave. Long isoelectric ST segment followed by a narrow-based T wave is common in LQT3. However, exceptions to these relative gene-specific T wave patterns exist.[41] These T wave patterns can only raise suspicion of type of long QT syndrome from among the three common types in the absence of genetic testing (primarily due to cost issues). These T wave changes can give clue to propensity for syncopal attacks due to torsades de pointes in patients with long QT syndrome.[45] Significance of these T wave patterns in general population is also not clear
T wave alternans is defined as beat-to-beat change in amplitude or polarity of the T wave. It may be present at rest or may appear during emotional or physical stress or with drug-induced QT prolongation.[12] It has been observed as a precursor to torsades de pointes in some cases.[46] Independent significance of this finding in persons without other risk factors is not clear
It has been suggested that in patients with strong clinical suspicion, abnormal QT interval may be unmasked by sudden standing[47],[48] or during recovery from exercise stress test.[49],[50] However, there is no documentation that these findings correlate with risk of future cardiovascular events. Intravenous pharmacologic provocation testing (e.g. with epinephrine) can unmask inappropriate prolongation of the QTc interval. However, there is risk of induction of arrhythmias. It is also not clear if epinephrine-induced QT prolongation correlates with risk of arrhythmias in day-to-day life. As for today, the risk in such mutations with normal QTc interval in resting ECG can be evaluated confidently only be genetic study and not by the QT interval alone.[13],[27],[51] However, genetic testing is limited by cost and is recommended only when there is strong clinical index of suspicion
Many patients with unexplained congenital prolongation of QT interval never experience torsades de pointes.[17] Reason is not clear. At present, there is no method to find which patients of congenitally prolonged QT interval are immune to life-threatening arrhythmias.
(b) Acquired prolongation of QT
Several acquired conditions are known to cause QT prolongation. Risk of serious arrhythmias is, however, variable.
(i) Heart failure, myocardial diseases, or coronary artery disease
Controversy
Top
Risk of serious cardiovascular events in patients with cardiac disease depends on severity of underlying disease, magnitude of left ventricular dysfunction, electrolyte imbalance, presence of high degree or complete atrioventricular block, presence of bradycardia or pauses,[3] frequent ventricular premature beats with compensatory pause,[3] sustained ventricular tachycardia, and instability of repolarization and genetic susceptibility,[52] rather than on QT interval prolongation alone.[53] It is, therefore, not clear as to which patients with cardiac disease and prolonged QT interval will benefit from prophylaxis against life-threatening arrhythmias.
(ii) Electrolyte imbalance
Hypokalemia, hypomagnesemia, and hypocalcemia prolong QT interval.
Controversy
Top
The risk correlates with magnitude of electrolyte imbalance, disturbance of other electrolytes, and concomitant cardiac status in addition to magnitude of QT interval prolongation.
(iii) Drug-induced QT prolongation
There is a long list of drugs that prolong QT interval. Common drugs include quinidine, piscarnomed, disopyramide, flecainide, sotalol, ibutilide, and cisapride. However, several other factors control occurrence of fatal arrhythmias.
Controversies
In patients with drug-induced prolongation of QT interval, conclusions about the risk of torsades de pointes based solely on prolongation of QTc interval may turn out to be highly flawed.[27] Risk is dependent on several factors as follows:
Magnitude of QT prolongation[53]
Patients who develop drug-induced torsades de pointes usually have QTc interval >500 ms[3],[54] or there is more than 60–70 ms increase from baseline value.[29] However, only a small subset of these patients develop torsades de pointes.[55] Other factors contribute to the risk of torsades de pointes.[55]
Drug responsible for QT prolongation
List of drugs that can prolong QT interval is extensive.[56] However, there is no documentation of torsades de pointes in most of the case reports.[4] Some drugs rarely produce arrhythmias although they prolong QT interval, for example, amiodarone, dronedarone, ranolazine, lithium, terfenadine, astemizole, antibiotics, and antipsychotics.[4],[52],[55] For some drugs as dofetilide, the risk of torsades de pointes is much higher.[57]
Dose, route, and rate of administration, drug metabolism, and excretion[55]
Risk of sotalol-induced torsades de pointes is dose dependent.[58] Risk of torsades de pointes with haloperidol is usual after intravenous injection.[59]
Concomitant use of other drugs prolonging QT[51]
Concomitant electrolyte imbalance, for example, hypokalemia, hypocalcemia, and hypomagnesemia[52],[55]
Underlying cardiac status, for example, heart failure, myocardial infarction, and active ischemia
Genetic predisposition: Genetically determined reduced repolarization reserve[60] or rate of drugs metabolism or excretion[61]
Subclinical mutations in congenital LQTS genes[60],[62],[63]
Renal and/or hepatic failure in patients being treated with drugs requiring renal elimination (e.g. sotalol)[55] or hepatic metabolism (e.g. methadone).[55]
In the absence of other factors, drug-induced QT prolongation alone rarely produces torsades de pointes and subsequent sudden death.[41]
(iv) QT prolongation associated with intracerebral or subarachnoid hemorrhage and myxedema
QT prolongation in these conditions is usually not associated with increased risk of cardiac arrhythmias.[64] Reason is not clear.
(2) Short QT interval
Definition
Current understanding
Short QT interval is considered as a risk factor for cardiac arrhythmias and sudden death. Normal lower limit is suggested as 390 ms.[2]
Controversies
Some authorities feel that QT interval <320 ms should be considered as "short."[41] It is considered realistic to prevent overdiagnosis and excessive investigations.[41],[65] However, the definition of a lower limit of QTc in short QT interval syndrome and its association with serious cardiac arrhythmias is less clear.[50] QT interval <300 ms may not be associated with serious cardiac arrhythmias.[66] It is possible that very short QTc (200–260 ms) may be associated with an increased cardiac risk.[51] Markers other than QTc interval are needed to identify patients at risk.[51]
(a) Congenital or familial short QT syndrome
Current understanding
It is due to mutation in some specific ion channels. Several specific genotypes have been identified.[67] There is no structural heart disease. It has been observed that congenital short QT interval may be associated with increased risk of paroxysmal atrial fibrillation, syncope, or cardiac arrest.[68] Episodes occur most often during periods of rest or sleep.[41]
Controversy
Some ECG findings have been suggested to be associated with congenital short QT syndrome. These include no or short ST segment and tall peaked T waves.[41] Recent studies have, however, shown that there are no diagnostic electrocardiographic findings[64] and risk is related to genetic mutation.[51],[69]
(b) In general population
Short QT interval is rare and is not associated with increased cardiac risk.[65],[66],[70]
(c) Early repolarization
It may be associated with short QT interval.[71] Some patients with early repolarization syndrome (J wave syndromes) may be associated with increased risk of arrhythmias.[72] However, increased risk is not related to shortening of QT interval.[71],[73]
(d) Hypercalcemia, hypermagnesemia, and acidosis
These can shorten QT interval. Risk is related to magnitude of abnormality and severity of underlying disease rather than to shortening of QT interval.
(e) Digitalis
Magnitude of shortening of QT interval in digitalis overdose has no relation to digitalis-induced arrhythmias which depend on concomitant electrolyte imbalance and underlying cardiac status.
(f) Other drugs
Clinical significance of QT shortening induced by other drugs is still under evaluation.[74]
(F) Subanalysis of Qt Interval
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Failure of QTc to reliably predict the risk of arrhythmias[75] has resulted in evaluation of other electrocardiographic parameters to evaluate repolarization heterogeneity.[25] Following parameters have been evaluated.
(1) J point to peak of T wave
(a) Current understanding
Normally, it is around 200 ms.[10] In the presence of prolonged QT interval, it can exceed 300 ms. In setting of short QT interval, it can be as short as 100 ms. It is less sensitive to changes in posture and respiration-related changes in T wave morphology.[76] It is affected by heart rate.
(b) Controversies
It has not been evaluated in detail in normal population and patients at high risk of cardiac arrhythmias. It is not clear if this parameter alone has any independent significance over other electrocardiographic parameters.
(2) Interval from peak of T wave to its end
(a) Current understanding
Most typically lead V5 is used for this measurement.[77] Difficulties can arise in measurement particularly with low T wave amplitude or when T waves are notched or biphasic.[17] It is less sensitive to changes in posture and respiration-related changes in T wave morphology.[76] Control subjects have been shown to have a value of <90 ms.[78],[79] Some authors feel that this interval provides some measure of repolarization heterogeneity independently associated with sudden cardiac death.[37],[80],[81] It has been suggested that the peak of T wave to its end (Tp-Te) interval may serve as an index of total dispersion of repolarization (transmural, apicobasal, and global). This interval has been used in predicting arrhythmias and sudden cardiac death in some cardiac channelopathies.[82],[83] Tp-Te >100 ms has been shown to predict malignant ventricular arrhythmias within 24 h of ST-segment elevation myocardial infarction.[84]
(b) Controversies
Genesis of arrhythmias and sudden death in the setting of acute coronary syndrome is also dependent on several other factors, for example, electrolyte imbalance, extent of infarction, left and right ventricular functions, extent of underlying coronary artery disease, and persistence of ischemia. Further, all patients with prolonged Tp-Te interval do not develop malignant arrhythmias. Therefore, it is difficult to determine additional independent prognostic significance of this interval in patients with acute coronary syndrome
This interval has also been found to be prolonged in conditions such as coronary ectasia,[78] nondipper blood pressure pattern in patients with metabolic syndrome,[79] and patients with coronary slow flow.[85] These conditions are not known to be associated with high risk of malignant arrhythmias and sudden death
Arrhythmogenic risk of this parameter has not been evaluated in context of various drug, other conditions predisposing to arrhythmias, and patients without cardiovascular disease or risk factors.
Large randomized controlled trials with long-term follow-up are needed to find if this parameter alone has any independent clinical significance.
(3) Interval from peak of T wave to its end/QT ratio
(a) Current understanding
Normal range of this ratio is very wide (0.15–0.25).[86] It remains relatively constant between the heart rate from 60 to 100 beats/min.[87] Higher ratio (>0.30) has been linked to increased risk of arrhythmias in patients with long QT syndrome, Brugada syndrome, short QT syndrome, and acute myocardial infarction.[84],[86],[87],[88]
(b) Controversies
This interval has also been found to be prolonged in conditions such as coronary ectasia,[78] nondipper blood pressure pattern in patients with metabolic syndrome,[79] and patients with coronary slow flow.[85] These conditions are not known to be associated with risk of malignant arrhythmias and sudden death.
Arrhythmogenic risk of this parameter has not been evaluated in context of various drug, other conditions predisposing to malignant arrhythmias, and patients without cardiovascular disease or risk factors.
Large randomized controlled trials with long-term follow-up in "normal" population and in patients with other conditions known to prolong QT interval or associated with risk of malignant arrhythmias and sudden death are needed to find actual independent significance of this parameter.
(4) Status of various components of QT interval
(a) Current understanding
Different etiological factors affect different components of QT interval. Flecainide causes broadening of QRS.[64] Tricyclic antidepressants also produce QRS widening without lengthening of J-T interval.[4] Long QT3 syndrome is associated with long ST segment and late-onset T wave.[44] Sotalol produces broad T wave with increased Tp-Te interval.[37] ST elevation myocardial infarction also prolongs Tp-Te interval.[80],[86] In hypokalemia, it is the Q-U interval that is prolonged.
(b) Queries
There is no literature regarding following issues:
Duration of different components of QT interval in normal population
Effect of age, gender, ethnic group, posture, and diurnal variation on
various components of QT interval
Effect of heart rate on various components of QT interval and method to correct them for given heart rate
Abnormality of which channel affects which part of the QT interval?
What is the clinical significance of prolongation of different components in normal population and in patients known to have high risk of arrhythmias and sudden death?
Correlation of arrhythmogenic risk of various drugs and other factors to various parts of QT interval
Will the management differ depending on prolongation of different components of QT interval?
Well-designed prospective studies with long-term follow-up are needed to answer these queries.
Controversies regarding QT interval are summarized in [Table 1].
Table 1: Controversies/limitations regarding QT interval
Click here to view
(H) Conclusion
Top
Manual measurement of QT interval is associated with interindividual variability. Automated measurement and heart rate correction by ECG machine can give working information unless the ECG is abnormal. There is no consensus regarding measurement of QT interval if T wave is bifid or fuses with U orPwave, QRS is broad or rhythm is irregular
There can be significant difference in the results of various formulae recommended for correction of QT interval for heart rate. Therefore, the formula used for rate correction should be mentioned in the report for proper follow-up of patient. Bazzett's formula is easy to use and gives reasonably working information in most of the patients
Normal QTc interval has a wide range – 360–480 ms. QTc is also affected by sympathetic tone, posture, meals, and diurnal pattern. Therefore, undue significance should not be given to minor changes
QT dispersion alone does not correlate with risk of arrhythmias
Hereditary long QT syndromes are associated with increased risk of arrhythmias and sudden death. Other genetic mutations are mostly without consequences. In acquired prolonged QT interval, risk depends more on genetic predisposition, underlying cardiac status, and electrolyte or metabolic disturbances. All drugs prolonging QTc interval do not carry similar risk
Hereditary short QT syndromes carry some risk of paroxysmal atrial fibrillation, syncope, or cardiac arrest. Most of the other cases do not have any risk
Independent significance of various parts of QT interval is not clear.
Financial support and sponsorship
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Conflicts of interest
There are no conflicts of interest.
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