why did qt dispersion die?

Cardiac Electrophysiology Review 2002;6:295–301©C 2002 Kluwer Academic Publishers. Manufactured in The Netherlands.

Why Did QT Dispersion Die?Pentti M. RautaharjuEPICARE Center, Wake Forest University School of Medicine,Winston-Salem, North Carolina, USA

Abstract. Background: Considerable controversy ex-ists about the meaning of QT dispersion (QTD). Theworking hypothesis of the present paper was that thenecessary although not sufficient condition for the va-lidity of QTD concept is the association of QTD withnondipolar voltage (NDPV) in T waves of the 12-leadECG.

Methods and Results: ECGs of 4890 subjects, 966with coronary heart disease (CHD) and 3844 consideredCHD-free were processed using computer programs formeasurement of the ratio of the first two eigenvalues(E2/E1), nondipolar voltage (NDPV), terminal T wavedirection and ECG estimate of left ventricular mass(LVM). The mean NDPV in T wave was 11 µV (SD 3.9),with 6 µV (SD 1.3) in terminal 40 ms. NDPV alone ex-plained only 6% and NDPV, E2/E1 and LVM combined13% of QTD variance. There was a modest increase inthe fraction of subjects with QTD >60 ms among subjectswith NDPV in terminal T > 7 µV compared to those withNDPV ≤ 7 µV (15% vs. 10%). A more profound increasewas associated with terminal T wave direction deviat-ing from normal (37% vs. 12% among those with nor-mal direction), reflecting dipolar rather than nondipo-lar components.

Conclusions: The association between QTD andNDPV is weak, and QTD is unlikely to represent anymeaningful myocardial repolarization event in the in-terval domain. It seems more logical to use direct mea-surement of NDPV as a potential marker of localizeddispersion and heterogeneity of ventricular repolariza-tion for evaluation of the risk of adverse cardiac events.

Key Words. QT, QT dispersion, cardiovascular, electro-cardiography

Background and the Present State

QT dispersion (QTD) was introduced in 1990 bya British group of scientists [1]. One year follow-ing the introduction of QTD, the group reportedresults from a clinical trial demonstrating reduc-tion in QTD by sotalol [2]. This finding aroused theinterest in the QTD concept among clinical inves-tigators and electrocardiographers and the pub-lication activity increased steadily, showing char-acteristics of an epidemic with a relatively longincubation period. A similar proliferation of com-munications was seen in scientific meetings ofprofessional societies such as the annual sci-entific sessions of the American Heart Associa-tion and the American College of Cardiology. Themost recent MEDLARS literature search lists 488communications with QTD in the subject head-

ings. The interest in QTD is still very much alive,and in the decade since its introduction it becamethe most fashionable topic in the realm of QT in-vestigations since the long period of domination ofQT and QT rate adjustment studies after Bazettpublished his formula in 1920. Therefore, the titlethat was suggested for the present paper is ratherprovocative and challenging. It is provocative withits connotation that QTD is dead. It is challengingin demanding proof that the concept is indeed in-valid. The present paper will first summarize thearguments presented for and against the QTD con-cept, followed by presentation of some new datarelevant to this intriguing controversy.

Arguments for and against the validityof QT dispersion conceptMost of the QTD publications have enthusiasti-cally supported the concept. There is a definitepublication bias—reviewers and editors of profes-sional journals as well as investigators in generaltend to have the attitude that negative results donot warrant particularly serious consideration. Inthe majority of the reports, the support presentedcomes from circumstantial, indirect evidence as-sociating QTD with excess risk of adverse eventsin a large variety of conditions summarized in anextensive monograph by Malik and Batchvarov [3]and in other review articles [4–6].

General arguments presented previouslyagainst the validity of the QTD concept aresummarized in Table 1. The main argumentpresented against the concept is that morphologicT waveform variations associated with dipolarcomponents of repolarization can produce large

The author thanks Mr. James Warren, M.Sc. for his con-tributions to the development of the ECG MorphologyProgram, and Mr. Charles Campbell, B.Sc. and Mrs.Zhu-Ming Zhang, M.D., for their contributions to var-ious ECG processing and data analysis tasks.

Address correspondence to: Pentti M. Rautaharju, M.D., Ph.D.,Suite 505, Piedmont Plaza Two, 2000 West First Street,Winston-Salem, NC 27104, USA.E-mail: [email protected]

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296 Rautaharju CEPR 2002; Vol. 6, No. 3

Table 1. Arguments against the QT dispersion concept and against equating conceptually QT dispersion withdispersion of ventricular repolarization

Arguments Against QTD Concept Comments

1. Measured QTD determined primarily by dipolarcomponents and do not represent dispersion ofventricular repolarization

The range of QTD in leads generated from strictlydipolar components is of the same order ofmagnitude than in the original 12-leads

2. Interlead differences in measured QT largelydetermined by T wave “loop” morphology and bythe projection of terminal T wave vector onindividual leads

Long QT values obtained when terminal T vector is indirection along the axis of the lead vector in a givenlead and short when near 90◦ angle.

3. Abnormal T wave morphology has a stronginfluence on QTD

Abnormal strictly dipolar morphology patterns cancause large interlead differences in QT. Theserepresent variability in amplitude/time domainrather than any physiologically meaningfulintervals related to repolarization events

4. Overall technical variability of QTD measurementis so large that no feasible threshold can beestablished to separate normal from abnormalQTD. Short- and long-range variability alsoreduces repeatability

General current consensus is that QTD values inexcess of 100 ms can be considered abnormal. Suchlarge variations are commonly occurring withgrossly abnormal T wave morphology

5. Variations in lead vector strength, T wave amplitudeand noise level cause additional QTD variation

Most Toffset detection algorithms use fixed thresholdsso that T wave amplitude variations from projectionof strictly dipolar components may cause largevariations in QTD

6. Presence of non-dipolar components in body surfaceECG during repolarization has not beendemonstrated

Their presence is a necessary condition for detection ofthe end of localized ventricular repolarization andlocalized dispersion from QT measurements

variations in QTD (Argument 1 in Table 1).Lee et al. [7] reported that QTD in 12-lead ECGgenerated by transformation from a strictlydipolar source was 53 (SD 49) ms and it was notsignificantly different from QTD in the original12-lead ECG (49 (23) ms)). Argument 2 relatesto the fact that T wave loop morphology (“flat” Tvector loop) is an important determinant of QTD[8]. A similar T wave morphology descriptor isT wave “complexity” expressed as the ratio ofthe second and the first eigenvalues (E2/E1) [9].Abnormal T wave morphology certainly increasesQTD. However, dipolar components alone leave alarge part of QTD variability unexplained as willbe shown later.

Argument 3 in Table 1 relates to methodologi-cal problems in determination of QTD. The overalltechnical variability, procedural differences andother factors induce so large indeterminacy in es-timation of QTD that it has not been possible to es-tablish a definition for abnormal QTD as pointedout by Malik et al. [3]. In contrast, Macfarlaneet al. have concluded that the upper normal limitof 50 ms is “highly specific” [10]. It is conceivablethat with improved methodology QTD measure-ment may become more meaningful if the conceptotherwise can be proven valid. The fact that onlytwo of the six limb leads have independent signalcomponents implies that only one pair of QT differ-ences can be a valid measure of QTD [11]. Lead-to-

lead variations of the measured QT in limb leadsare due to projection differences, variations in leadstrength when a constant threshold value is cho-sen for defining the end of the T wave and a varietyof other factors [12].

The controversy about the meaning of QTDprompted publication of an editorial in 2000 inEuropean Heart Journal titled: “QT dispersion:time for an obituary?” by Malik [13] who con-cluded: “Despite the serious difficulties with theconcept and despite the fact that a clear publica-tion bias exists towards positive findings, the hugenumber of studies showing some meaningful re-sults with QT dispersion measurements cannot bedismissed lightly.”

In summary, while the arguments against thevalidity of QTD have considerably weakened thepractical utility of QTD, they have not proven thatthe concept is invalid, and the voluminous publi-cations supporting the concept QTD have failedto produce evidence fulfilling the necessary andeven less the sufficient condition for the validityof the concept. The crucial necessary although notsufficient condition for the validity of QTD con-cept is that nondipolar components in body surfaceECG exist during ventricular repolarization andthat these in turn are of sufficient magnitude tohave a significant association with QTD. Withoutsuch evidence, the whole QTD concept has beendenounced by some as “fallacy” [14].

CEPR 2002; Vol. 6, No. 3 Why Did QT Dispersion Die? 297

The publication by Malik in 2000 was the firstpaper documenting that significant amounts ofnondipolar components indeed exist in the T waveof the standard 12-lead ECGs of normal subjectsand of patients with hypertrophic and dilated car-diomyopathy and survivors of acute myocardialinfarction [15]. However, QTD did not correlatesignificantly with nondipolar components exceptfor borderline correlation in patients with hyper-trophic cardiomyopathy (p = 0.03), and the au-thor concluded that QTD is unrelated to nondipo-lar components of the T wave.

The Objective of the Present Study

The present communication will address thequestion of the determinants of QTD includingnondipolar components in normal subjects andsubjects with coronary heard disease (CHD). Theprimary objective was to determine the magni-tude of nondipolar components (square root of to-tal dipolar energy or nondipolar voltage, (NDPV))in the T wave of the standard 12-lead ECG and toevaluate if the association of QTD with nondipolarcomponents is sufficiently strong to fulfill the nec-essary condition for the validity of QTD concept.

Study groupsECG data of 4,890 subjects (60% females, 40%males) from community-based populations wereselected from the files of the EPICARE Center, acentral ECG laboratory for population studies andclinical trials. An older adult group was selectedfor the study (64 years and older) in order to ob-tain an adequately large subgroup of subjects withclinical evidence of coronary heart disease (CHD).ECGs with QRS duration ≥ 120 ms and those withan electronic pacemaker, atrial fibrillation or flut-ter were excluded from the study. The CHD groupof 966 subjects was selected on the basis of con-firmed history of myocardial infarction or anginapectoris or invasive cardiac procedures related tocoronary artery disease. The remaining 3844 sub-jects of the study group were considered CHD-free.Silent MI by ECG alone was not used as an exclu-sion criterion. From the total group of 4890 sub-jects, a subgroup of 4810 was used for some moredetailed analyses with a more complete set of ECGdata related to quantitative morphologic T waveanalysis, including evaluation of the terminal Twave.

ECG methodologyECGs were recorded in resting supine state follow-ing strictly standardized procedures for ECG ac-quisition, including electrode placement [16]. AllECGs received at the EPICARE Center were in-spected visually to detect technical errors, miss-ing leads and inadequate quality, and such records

were rejected from ECG data files. The 12SLECG Program (GE Medical Systems Information,Milwaukee, Wisconsin) was used for ECGmeasurement. The ECG Morphology Program(Novaheart Inc., Winston-Salem, NC) was usedfor quantitative vector analysis of repolarizationwaveform patterns. The program has modules forextraction of dipolar components and distributionsin 12 preferential spatial directions of the ST-Tsubinterval vectors in a rhombododecahedron ref-erence frame [17,18]. In addition, the QT Guardprogram of the GE Medical Systems Informationwas used for QTD measurement. ECG estimatesof left ventricular mass were determined usinggender- and race-specific algorithms of the NOVA-CODE program [19].

Data analysisDifferences in QTD distributions were firstexamined in subgroups stratified according tothe CHD status, the ratio of the eigenvalues ofthe first two principal components (E2/E1) and themagnitude of the nondipolar components inthe T waves of the standard 12-lead ECG. The sig-nificance of the differences between group meanswas performed using the t-test. Multiple regres-sion models were used to evaluate the associationof various variables of interest with QTD. In subse-quent analyses, stratification was performed intodichotomized categories according to the magni-tude of the nondipolar components and spatial dis-tribution of the terminal T wave in a window from(Toffset −40 ms) to Toffset. A ratio test for performedto evaluate the significance of the differences inthe proportion of QTD exceeding 60 ms in variousstratified subgroups. All analyses were performedusing Microsoft Excel Version 5.0 (Microsoft Cor-poration, Seattle, Wa) and SAS/STAT Version 8.0(SAS Institute, Inc., Cary, NC).

Results

Mean values with standard deviations for vari-ables of key interest concerning QTD are listedin Table 2. The range of QTD values was wide inboth study groups, with the mean value in totalstudy group 34 ms (23.5 ms). QTD exceeded 75 msin 5% of the subjects and 95 ms in 2%. QTD was7 ms wider in the CHD group than in the CHD-free group (p ≤ 0.001) and also the eigenvalue ra-tio E2/E1 differed significantly between the twogroups, 14% (13.9) in the CHD-free and 19% (16.5)in the CHD group (p < 0.01). The question ofkey interest in the present context is the mag-nitude of nondipolar components in the standard12-lead ECG in relation to QTD. The NDPV was11 µV (14.8), exceeding 18 µV in 5% of the sub-jects. Thus, there are nondipolar components of


Table 2. Mean values (SD) of total and precordial QT dispersion, nondipolar voltage and eigenvalue ratio insubjects with coronary heart disease (CHD) and in CHD-free subjects

No-CHD CHD Group All(n = 3844) (n = 960) (n = 4890)Mean (SD) Mean (SD) Mean (SD)

Heart rate (cpm) 65 (10.5) 63 (11.1) 65 (10.6)QRS (ms) 88 (10.0) 92 (11.3)*** 89 (10.4)QTrr (ms)† 420 (16.8) 423 (20.0)*** 420 (17.5)QTD‡, total (ms) 33 (22.0) 40 (27.6)*** 34 (23.5)QTD, precordial (ms) 26 (20.5) 30 (24.3)* 26 (21.5)NDPV& (µV) 11 (3.6) 12 (4.9)** 11 (3.9)Eigenvalue Ratio (E2/E1) (%) 14 (13.9) 19 (16.5)** 15 (14.8)Fraction (%) with QTD > 60 ms 9.5 16.3*** 10.9Fraction (%) with NDPV > 15 µV 11.7 19.7*** 14.3Fraction (%) with QTD > 60 ms 2.4 6.3*** 3.2

and NDPV > 15 µV

*p < 0.05, **p < 0.01, ***p < 0001 for one-tailed test for difference between group means or ratios.†QT adjusted to ventricular rate by linear function of RR.‡QT dispersion.&NDPV = nondipolar voltage.

Table 3. Contingency table for the longest and the shortest QT in chest leads*

Lead with Longest QTTotal

V1 V2 V3 V4 V5 V6 (%)

Lead with V1 — 424 740 694 371 196 2425 (50.4)Shortest QT V2 255 — 408 482 252 93 1490 (40.0)

V3 46 60 — 52 17 46 221 (4.6)V4 15 87 34 — 31 9 176 (36.6)V5 18 100 42 16 — 7 183 (3.8)V6 22 131 98 48 16 — 315 (6.5)Total 356 802 1322 1292 686 351 4810(%) (7.4) (16.7) (27.5) (26.9) (14.3) (7.3) (100)

*Omitted were 80 ECGs with measured QTD = 0 for technical reasons.Bold-faced figures indicate lead pairs with the longest and shortest QT in two adjacent leads in 1303 of the subjects (27.1%).

sufficient magnitude that could conceivably havea significant influence on QTD. The mean NDPVvalues differed by 1 µV between the CHD-free andthe CHD groups (p < 0.01). Although the meangroup difference is negligible, the possibility thatthe group difference will become more pronouncedat the higher range of QTD and NDP values hasto be considered. Table 2 lists also the fraction ofsubjects with QTD exceeding 60 ms and NDPV ex-ceeding 10 µV and their combination. Ratio testsindicated that both fractions were significantlylarger in the CHD group than in the CHD-freegroup, as was the fraction with subjects exceedingboth thresholds (p < 0.001 for all).

Are QT intervals really dispersed?The origin of the word dispersion is dispersere,to scatter, implying separation and moving apartin different directions without order or regular-

ity. The question is whether QT distribution istruly dispersed or is there some measure of reg-ularity in the distribution among adjacent ECGleads. The rationale behind this question is theconsideration that irregularity or dispersion of thefunctional refractory period or repolarization timeat localized level over relatively short distancesenhances propensity for triggered activity andre-entry. Such localized myocardial dispersionshould produce QTD in adjacent ECG leads pro-vided that nondipolar components are present insufficient magnitude in body surface ECGs.

Joint distribution of the chest leads with thelongest and the shortest QT are shown in Table 3.Limb leads were omitted from this table becausethe lead vectors of the limb and chest leads arespatially in different planes in image space so thatdipolar projection differences can be expected tobe larger between these two sets of leads. A closeexamination of Table 3 revealed that the longest


Table 4. Correlations between variables of key interestin relation to determinants of QTD

(E2/E1)QTD NDPV Ratio

QTD — 0.25 0.27NDPV* 0.25 — 0.11(E2/E1) Ratio† 0.25 0.11 —ECG LV Mass 0.12 −0.06 0.11QRS Interval 0.01 −0.06 0.14

*NDPV = nondipolar voltage in T wave.†E2/E1 = ratio of the first two principal components.

and the shortest QT often resided between two ad-jacent chest leads, for instance between V1 andV2 in 675 (14%) and overall between two adjacentleads in 1303 subjects (27%).

Determinants of QTDNDPV as a possible indicator of the dispersion ofventricular repolarization and E2/E1 ratio as anindex of morphologic T wave abnormalities in timedomain not directly related to any repolarizationintervals are of key interest in this context as pos-sible determinants of QTD. In addition, ECG es-timate of left ventricular mass (LVM) and QRSduration were also considered because anychanges in ventricular excitation may cause sec-ondary repolarization abnormalities. Correlationmatrix in Table 4 shows relatively modest andequal level of correlation between QT and NDPV(r = 0.25) and E2/E1 ratio (r = 0.27) and a lowercorrelation with LVM (r = 0.12). Multiple regres-sion models (not shown) with NDPV and E2/E1ratio entered as simultaneous covariates into re-gression on QTD produced R-square value 0.075.Entering LVM as the third covariate increasedR-square value to 0.13. Thus, there three pri-mary determinants of QTD combined explainedjust 13% of the total QTD variance, leaving 87% ofthe variance unexplained.

QTD in Relation to NDP Voltageand the Direction of the Terminal T Wave

Spatial distribution of the mean terminal T vectordetermined in a window from (Toffset − 40 ms) toToffset was determined in reference to 12 principalspatial directions in a duododecahedron referenceframe [17,18]. In the CHD-free group, the direc-tion of the terminal T wave vector was inferior-left-anterior, anterior-left or left in 95.5% of thesubjects, corresponding closely to the spatial dis-tribution of the normal mean T vector. The meanvalue of the NDP voltage in the terminal 40 mswindow was 6 µV (1.3) in the CHD-free group and

Table 5. Fraction (%) of subjects with QTD >60 ms insubgroups stratified by terminal T wave orientation,coronary heart disease status and nondipolar voltage

Subgroup No. QTD > 60 ms

Terminal T Direction

Normal (ILA, AL, L)* 4583 549 (12.0)Other (abnormal) 307 79 (36.7)‡

CHD† Status

CHD-free 3915 397 (9.4)CHD 975 159 (16.3)‡

Nondipolar voltage

≤7 µV 4214 429 (10.2)>7 µV 676 99 (14.6)‡

*ILA = inferior-left-anterior, AL = anterior-left, L = left in a12-directional duododecahedron reference frame.†CHD = Coronary heart disease.‡p < 0.001 for ratio test for group differences.

6 µV (1.5) in the CHD group. Thus, the amplitudeof the NDP components in the terminal T wavewere approximately one half of that in the totalT wave window.

The fraction of QTD values exceeding 60 ms wasthen evaluated in subgroups stratified by the di-rection of the terminal T wave (normal vs. abnor-mal), the CHD status, and the fraction of NDPvoltage in this terminal T window exceeding 7 µV

0

5

10

15

20

25

30

35

QTD > 60 ms (%)

No CHD; ILA, AL or L

No CHD; Other

CHD;ILA, AL or L

CHD;Other

CHD Status and Terminal T Direction

CHD Status

T Direction

p < 0.05

NS

NS

NS

Fig. 1. The fraction of QTD exceeding 60 ms insubjects with NDPV > 7 µV (filled columns) comparedto those with NDPV ≤ 7 µV (open columns) insubgroups stratified by CHD status and direction of theterminal T wave vector. Note the pronounced increasein the fraction of abnormal QTD with abnormalterminal T wave direction both in CHD-free and CHDgroups. In comparison, the fraction is significantlydifferent only in CHD-free subjects with normalterminal T wave direction.


(Table 5). Seven µV (approximately mean +1*SD)was chosen in order to obtain an adequate num-ber of subjects in various subgroups for statis-tical evaluation. The increase in the fraction ofQTD exceeding 60 ms with two-way stratifica-tion by the NDP voltage, terminal T wave direc-tion and CHD status was significant (p < 0.001)in all of these major subgroups. However, theincrements in the fraction of QTD > 60 were con-siderably larger with stratification by T wave ori-entation and also by CHD status than that bystratification by NDP voltage, and the ratio testfor NDPV subgroups was significant (p < 0.05)only in the CHD subgroup with normal terminalT wave direction (Figure 1).

Discussion

The results from the present study confirm thefindings by Malik et al. [15], demonstrating thatnondipolar components exist in the T waves ofthe 12-lead ECG. The mean value of NDPV was11 µV (14.8), exceeding 18 µV in 5% of the subjects.Although these values are below visual resolu-tion limits and smaller than amplitude thresholdsused by many computer algorithms to define theend of the T wave, it is possible that the occurrenceof nondipolar components at critical time points incertain leads can influence QTD measurements.The proportion of QTD exceeding 60 ms wassignificantly higher (p < 0.001) among subjectswith NDPV exceeding 7 µV than among subjectsbelow this threshold, although in subgroup analy-ses that the proportion was significantly differentonly in the CHD-free subgroup with normal direc-tion of the terminal T wave (p < 0.05).

An interesting observation was that the longestand the shortest QT often resided between two ad-jacent chest leads in 27% of the subjects, one halfof them between V1 and V2. The finding of suchlocalized dispersion of QT values is difficult to rec-oncile if QTD were solely due to projection differ-ences from the dipolar components of the T wave.Frequent occurrence between V1 and V2 may bein part due to the relatively large spatial anglebetween the lead vectors of these two leads. QTDmeasurement problems, including overlapping Uand T waves may account, in part for the remain-ing “dispersion.”

The fraction of subjects with QTD exceeding60 ms was prominently associated with an abnor-mal terminal T wave spatial direction, thus con-firming the findings of Kors et al. [8] about theimportance of this T wave feature as a determi-nant of QTD. Abnormal terminal T wave directionand other morphologic T wave changes are in prin-ciple determined by T wave components of dipolarrather than nondipolar sources.

Overall, the correlations of QTD with NDPVand with other factor evaluated (E2/E1 and LVM)were low, and these three strongest determinantsof QTD combined in multiple regression modelsexplained only a small fraction (13%) of the totalQT variability. A prominent part of this residualQTD variability is likely to be due to morphologicvariations in T wave patterns (other than E2/E1ratio) associated with dipolar rather than nondipo-lar sources and with methodological problems as-sociated with QTD measurement. Morphologic Twave patterns are best evaluated in amplitude do-main and it is unlikely that lead-to-lead variationsat the measured endpoint of the T wave are asso-ciated with any local variations in the endpoint ofmyocardial repolarization. Morphologic variationsin T wave patterns such as those manifested in in-creased E2/E1 ratio and abnormal direction of theterminal T vectors are certainly associated withheterogeneity of ventricular repolarization. Theseaberrations are likely to reflect regional hetero-geneity (changes in transmural or apex-to-base ac-tion potential duration gradients). They may welltake place with relatively small changes in tempo-ral profiles of action potential duration with smallor no changes in temporal dispersion of the end ofventricular repolarization.

It also remains to be proven that the existenceof NDPV is significantly associated with definablerepolarization intervals or subintervals at myocar-dial level before the presence of NDPV can be ac-cepted as a necessary condition to validate theQT dispersion concept. Evidence for the sufficientcondition has to come from cardiac electrophysi-ological studies. Until such evidence emerges infuture studies, low level correlation existing be-tween NDPV and QTD leaves the validity of theQTD concept highly questionable.

It should be noted that correlation betweenregional dispersion of ventricular repolarizationand QTD in surface leads [20] does not neces-sarily validate QTD concept. Dispersion of ven-tricular repolarization may increase QTD due tomorphologic changes of dipolar origin rather thandue to nondipolar components. It is imperative todemonstrate the association of localized timing ofthe end of myocardial repolarization with the endof the T wave in specific localized ECG leads, withnondipolar components as the direct link betweenthese two factors as a sufficient condition for thevalidity of QTD concept. Until and unless suchevidence emerges, it is inappropriate to equateQTD with any meaningful myocardial repolariza-tion events in the interval domain.

In conclusion, the correlation between QTDand NDPV of the T wave is weak and there areprofound methodological difficulties in QTD mea-surement. Direct measurement of nondipolar com-ponents calculated easily by computer programs


rather than QTD should be a more logical choicefor evaluation as a potentially valuable althoughstill unproven marker of localized heterogeneity ofventricular repolarization.

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why did qt dispersion die?

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