Multipolar QRST isointegral maps and QT dispersion in old myocardial infarction

0231–424X/$ 20.00 © 2010 Akadémiai Kiadó, Budapest

Acta Physiologica Hungarica, Volume 97 (1), pp. 11–21 (2010)

DOI: 10.1556/APhysiol.97.2010.1.2

Multipolar QRST isointegral maps and QT dispersion in old myocardial infarction

I Mozos1, M Hancu1, N Jost2,3, A Cristescu1

1Department of Pathophysiology, University of Medicine and Pharmacy „Victor Babes”, Timisoara, Romania

2Division of Cardiovascular Pharmacology, Hungarian Academy of Sciences, Szeged and

3Department of Pharmacology & Pharmacotherapy, Faculty of Medicine, University of Szeged, Szeged, Hungary

Received: 3 June, 2009 Accepted after revision: 11 September, 2009

Chronic myocardial infarction (CMI) may create, due to structural heterogeneity, abnormal electrophysiological substrates which trigger reentrant life-threatening ventricular arrhythmias.

Methods: Electrical instability is assessed using body surface mapping (BSM) [multipolar isointegral QRST maps (mp IQRST)] and 12-lead ECG (QT dispersion: QTd: the difference between maximal and minimal QT interval). The aim was to find the relation between mp IQRST and QTd in CMI patients.

Results: 32 CMI patients, underwent 12-lead ECG and 64-lead BSM. 80% (25) of the patients had mp IQRST maps. QTd was larger in patients with mp than those with dipolar maps (dp): 170±20 ms in mp vs 94±19 ms in dp, respectively. The latter, mp IQRST was associated with a decrease of maximum and a stronger minimum.Conclusions: Multipolar IQRST is associated with a loss of maximum values and increased absolute values of the minimum in CMI patients. IQRST and QTd provide similar information in predicting postinfarction arrhythmia risk.

Keywords: myocardial infarction, body surface maps, ECG, QT dispersion

Chronic myocardial infarction (CMI) may create, due to structural heterogeneity, abnormal electrophysiological substrates which trigger reentrant life-threatening ventricular arrhythmias (18). The necrotic infarction area is replaced by fibrotic tissue, leading to repolarisation inhomogeneities, reentry and electrical instability. Electrical instability and arrhythmia risk are assessed using noninvasive methods like: body surface mapping (BSM) (multipolar isointegral QRST maps: mp IQRST) (5, 15) and 12-lead ECG (QT dispersion: QTd) (20).

BSM has multiple advantages compared to conventional electrocardiogram in providing diagnostic informations to detect electrical activity changes (8) and allows the most complete visualization of the heart activity mapped on the body surface. Many scientists used the isopotential analysis technique and maps generated in numerous moments of the cardiac cycle. This technique allows a detailed analysis of the sequential electrocardiographic changes, although the high amount of data makes this type of exploration difficult. This is the reason why the isointegral analysis technique was preferred, as a more effective and simple method.

Corresponding author: Ioana Mozos, MD, PhDDepartment of Pathophysiology University of Medicine and Pharmacy „Victor Babes”T. Vladimirescu Str. Nr 14, 300658 Timisoara, RomaniaPhone: +40745610004; Fax: +40256220484E-mail: [email protected]

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QTd is considered a marker of arrhythmia risk and of sudden death (11), a quantitative noninvasive method to determine myocardial repolarisation inhomogeneities (39), although there are several trials that deny the prognostic value of QTd (21).

It was the aim of the study to test whether changes in dispersion of ventricular depolarization and repolarisation were reflected simultaneously in IQRST maps and to find the relation between mp IQRST and QT dispersion in CMI patients.

Materials and Methods

Patients

32 CMI patients were included in the study. The investigations conform to the principles outlined in the Declaration of Helsinki (Cardiovascular Research 1997, 35, 2-4) and were approved by the Ethics Committee of the University. Written consent was obtained from every patient. The characteristics of the patients are described in Table I. The patients included in the study had all an myocardial infarction in the last 1–9 years, 16% (5 patients) with non-Q wave myocardial infarction. Considering myocardial infarction location, 18 patients (56%) had an anterior, 10 (31%) an inferior CMI and 4 (12.5%) multiple infarcts (anterior and inferior). The patients underwent BSM, using the electrocardiographic BSM device of the Functional Exploration Laboratory of the Pathophysiology Department, and 12-lead ECG.

Exclusion criteria were: bundle branch block, atrial fibrillation or flutter at the moment of investigation and electrolyte imbalances. Diagnostic electric criteria for CMI were defined according to those of the Joint European Society of Cardiology and the American College of Cardiology Committee for the Redefinition of Myocardial Infarction (35).

There were no significant differences between the patients with multipolar and dipolar maps considering: age, sex, medication, associated diseases, associated cardiovascular risk factors.

The control group was described in two previous articles (25, 28).

Table I Characteristics of the 32 chronic myocardial infarction investigated patients (mean±SEM)

• Age: 63±3 years • Sex: 26 men and 6 women• MI survival: 1–9 years• MI location: 18 (56%): anterior; 10 (31%): inferior; 4 (12.5%): anterior and inferior• Non-Q wave MI: 5 (16%)• Ejection fraction: 48±3%: only 2 patients (6%) with an EF<30%; 17 (53%) patients had an EF≥50%• Heart rate: 79±4 b/min • Associated cardiovascular risk factors: diabetes mellitus: 10 (31%) , obesity: 12 (37.5%),

hypertension: 6 (18.75%), smoking: 4 (12.5%)• Associated diseases: heart failure: 8 (25%) (NYHA II: 4; NYHA III:4), left ventricular aneurism: 2 (6.25%),

chronic bronchitis: 4 (12.5%), chronic kidney disease 11 (34%)• Arrhythmia history: atrial fibrillation: 2 (6.25%), premature ventricular contractions: 5 (16%),

non-sustained ventricular arrhythmias: 3 (9%)• Medication: angiotensin conversion enzyme inhibitors: 16 (50%), calcium blockers: 4 (12.5%),

nitrates: 28 (87.5%), beta-blockers: 22 (68.75%), digitalis: 4 (12.5%), class III antiarrhythmics: 8 (25%).

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Isointegral maps and QT dispersion in myocardial infarction

Body surface mapping:

The 64 electrodes vest was applied to each patient, and a reference electrode on each arm. The ECG signal recording electrodes were placed around the thorax on 7 rows and 13 columns, as an incorporated network in the 64 electrodes vest. The rows were placed at a fixed distance of 5 cm. 9 columns were placed in the antero-lateral part of the thorax between the right mid-axillary line and the left mid-axillary line, and 4 columns explored the posterior part of the thorax, on the mid-scapular and paravertebral lines (24).

The ECG signals from the 64 thorax leads were recorded, using the Wilson’s central terminal as a reference point, they were amplified using adjustable amplifiers (gain between 500–4500), they were multiplexed with a sampling rate of 5 ms and digitally converted with a 10 bits resolution. The data were processed using a Pentium computer with a 400 Mhz frequency, 36 MB RAM memory, coloured monitor and printer. The maps were displayed in a rectangular format, which corresponds to the surface of the thorax, as a section on the right mid-axillary line. The minimal increment between successive contour levels was 0.075 mV and this increment was automatically increased by the computer in the case of higher potential gradients, preventing the superposition of the contour lines.

Isointegral maps provide a distribution of the sum of potentials over a specified time interval. QRST isointegral maps represent the QRST areas for each lead, from the start of the QRS complex through the end of the T wave. The start of the Q wave and the end of the T wave were marked using a cursor. The Lepeschkin method was used to assess the end of the T wave (19).

The time integral of the QRST intervals was calculated. The integral values for each extrapolated lead were stored in a matrix used to trace the isointegral contour lines through linear interpolation. Isointegral maps were then analyzed to assess the number of extreme positive values (maxima) and extreme negative values (minima) (Fig. 1) and the amplitude for minimum and maximum. Only the highest maximum and minimum absolute values were considered in the case of mp (Fig. 2).

QT dispersion

12-lead ECG was assessed using a Siemens-Megacart electrocardiograph at a paper speed of 25 mm/sec.

The 12-lead ECGs and isointegral maps were examined by two independent observers, who weren’t informed about the clinical data. QTd and QTdc (heart rate corrected QTd, using the Bazett formula (3): QTc = QT/√ RR, where QTc is the heart rate corrected QT interval and RR, the R-R distance), were calculated according to a technique which was previously described (26).

Statistics

Statistical analysis was performed using the Student t-test (results were considered significant when P was found to be less than 0.05), the Bravais-Pearson linear correlation coefficient (r) and the relative risk (RR).

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Fig. 1. Isointegral QRST dipolar map of a healthy person. The left and right margins of the map indicate the right midaxillary line. The upper/lower border corresponded to the neck/waist. The time integrals

of the QRST intervals were calculated. The interval of integration was determined by two cross-cursors, as shown under the map. The integral values for each extrapolated lead were stored in a matrix used to trace the isointegral

contour lines through linear interpolation. The site of maximum is indicated by + with the numerical value in mV.ms. Maximum (+153 mV.ms) may be observed in the mammary region. The right minimum is on the back, in the right-upper region and its value is about –65mV.ms. Dotted fields represent negative time integral values.

Positive values are indicated by solid contour lines. The zero potential line is identified by a heavier trace

Fig. 2. QRST isointegral map with multiple maxima (5) and minima (6) in a chronic myocardial infarction patient, reflecting the regional heterogeneity of the repolarisation process and arrhythmia vulnerability. The highest maximum was: +137 mV.ms) (in the mammary region) and the highest minimum:

–44 mV.ms (in the left axila)

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Results

80% of the patients (25 patients) had mp IQRST maps (40%-13 with multiple maxima, 13%-4 with multiple minima and 27%-8 with multiple minima and maxima) and only 20% dipolar maps (dp). Maxima were 115±12 mV.ms (mean±SEM) and minima 80±7 mV.ms. QTd were: 159±20 ms and QTdc: 33±4 ms (mean±SEM). QTd and QTdc were significantly prolonged (p<0.05) compared to the values obtained in 30 age-matched healthy controls (QTd: 49±3 ms; QTdc: 10±1 ms). The control group was described in papers previously published (25, 28).

There were significant higher values and higher medians for QTd (137 ms for patients with mp, and 97 ms for those with dp) and QTdc (30 ms and 19 ms) in patients with mp compared to those with dipolar IQRST (Table II). The appearance of mp IQRST was associated with a decrease of maximum (median value: 95 mV.ms compared to 103 mV.ms in patients with dipolar maps) and a stronger minimum (-53 mV.ms compared to -43mV.ms in dipolar maps) (Table III).

The maximum inversely correlated with QTd and QTdc (Table IV, Fig. 3), considering the Bravais-Pearson linear correlation coefficient r.

There were no significant differences for isointegral QRST maxima, minima, QTd and QTdc considering myocardial infarction location (anterior and inferior) (Table V).

Both multipolar maps and QTd>100ms were significantly associated with ventricular arrhythmias (premature ventricular contractions and non-sustained ventricular arrhythmias). The relative risk (RR) was 1.96 for multipolar maps and 1.28 for QTd>100ms.

Table II QT dispersion (QTd) and heart rate corrected QT dispersion (QTdc) in patients with multipolar and dipolar isointegral QRST maps

Parameter Multipolar maps(ms)

Dipolar maps(ms)

p

QTd 170±20137

94±1997

0.0275

QTdc 36±330

23±519

0.0208

In each row values represent mean±SEM (upper) and the median values (below).

Table III Maximum (Max) and minimum (Min) in multipolar (mp) and dipolar (dp) maps

Parameter Mean±SEM(mV.ms)

Median values(mV.ms)

p

Max mpdp

115±13102±3

95103

0.04877

Min mpdp

–81±8–41±1

–53–43

0.0419

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Table IV The correlation between maximum, minimum, QTd (QT dispersion) and QTdc (heart rate corrected QT dispersion); r = the Bravais–Pearson linear correlation coefficient

Correlation between: rQTd, maximum –0.53QTdc, maximum –0.56QTd, minimum –0.33QTdc, minimum –0.30

Fig. 3. The correlation between QTdc (heart rate corrected QT dispersion in ms) and QRST isointegral maxima (Max) (in mV.ms); r=–0.56. r is the Bravais–Pearson linear correlation coefficient

Table V Isointegral QRST maxima (Max), minima (Min), QTd (QT dispersion) and QTdc (heart rate corrected QT dispersion) in patients with anterior and inferior old myocardial infarction

Parameter Anterior myocardial infarction Inferior myocardial infarction pMax (Mean±SEM) 94±7 mV.ms 86±6 mV.ms 0.372Min (Mean±SEM) 80±10 mV.ms 48±1 mV.ms 0.277QTd (Mean±SEM) 159±19 ms 145±15 ms 0.66QTdc (Mean±SEM) 33±3 ms 29±3 ms 0.567

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Discussion

The spatial features of the body-surface potential distributions during both the depolarization and the repolarisation of ventricular myocardium are likely to reflect an anatomic and electrophysiological substrate for sustained ventricular arrhythmias. Such disparities can be assessed from body surface distributions of electrocardiography QRST integrals (14). Isointegral QRST maps represent the distribution of the Wilson „ventricular gradient” and reflect ventricular repolarisation inhomogeinities, due to the amplitude and duration differences of the action potential.

QRST integral maps of healthy subjects show a stable overall pattern along the time coordinate (17). Isointegral QRST maps (9) have, in normal persons, only two extremes: a maximum and a minimum (figure 1), a dipolar character. Negative values are recorded in thorax areas corresponding to myocardial regions with longer repolarisation, and positive values in cardiac regions with shorter repolarisation. A QRST isointegral extreme was defined as a circumscribed peak in the smooth and graduated potential distribution (1). A more general definition of map extrema was given for isopotential maps (16): maximum (the highest potential) in an area where the current flows towards the body surface and minimum (the lowest potential) in an area where the current flows into the heart. On isointegral maps, the extreme will represent the prevailing direction of current spread during the analysed time interval.

A complex, multipolar QRST map, with more maxima and minima reflects the regional heterogeneity of the repolarisation process and arrhythmia vulnerability (12).

Myocardial infarction and subsequent ventricular remodeling creates a substrate with altered electrophysilogic properties, which is very arrhythmogenic (5), modifies local repolarisation properties, and nondipolar isointegral QRST maps may appear. The number of extrema in the QRST isointegral map offers the possibility for arrhythmia evaluation (22) because those ventricular repolarisation inhomogeinities, facilitate the appearance of reentry circuits, leading to ventricular tachyarrhythmias.

BSM was previously used to assess repolarisation changes which appear in CMI patients. When slow conduction velocities were assigned, BSM showed multiple extrema on the isointegral maps (30). Potential amplitude is reduced by 50% in the presence of an infarction in the underlying myocardium. At 48 ms after the stimulation, the formation of a large region of negative potentials over the infarcted left ventricle, as a result of the underlying electrically inactive necrotic tissue, is described (5). Our study managed to correlate this potential loss with QTd and QTdc. The absolute values of maxima and minima were also higher in healthy controls compared to patients with ischemic heart disease, showing the hypopolarisation in the ischemic tissue (38).

QRST integral distribution on the epicardium is well preserved in that observed on the body surface during the evolution of localized ventricular ischemia and changes in myocardial repolarisation dispersion resulting from localized ischemia can be identified with high-resolution torso ECG mapping (29). Those facts were demonstrated comparing ventricular epicardial and body surface QRST integral changes in left anterior descendent coronary artery ligated pigs.

Gardner et al (12) compared isointegral QRST maps of 97 normal subjects, 16 patients resuscitated from ventricular fibrillation or sustained ventricular tachycardia and 27 patients 6 to 12 months after myocardial infarction but without clinically significant arrhythmia. A score was assigned to each map, based on the number of extrema; each maximum or minimum

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scored one point, with the exception of simultaneously occurring anterior and posterior minima on the right shoulder (frequently occurring in normal subjects), which scored together only one point. They found the highest score in patients with repetitive ventricular arrhythmia, possibly reflecting dispersion of underlying properties of ventricular recovery.

Kozmann et al (17) assessed experimentally noninvasive spatio-temporal depolarization and repolarisation dynamics, using long BSM records (from 64 chest positions), taken on healthy subjects and arrhythmia patients. The dynamics of repolarisation disparity were characterized by the QRST integral map non-dipolarity index (NDI), analyzed both in the time and frequency domain. Results revealed that repolarisation changes are causally preceded by perturbations in the depolarization process and NDI increases immediately after a single premature stimulus, though in arrhythmia patients significant NDI peaks may occur without premature stimuli as well.

Horacek (14) enrolled 102 ventricular tachycardia patients and 102 patients with remote myocardial infarction without history of ventricular arrhythmias, in his study. The patients underwent BSM, using 117 unipolar thoracic leads. QRST isointegral maps were reduced to 16 principal patterns (eigenvector maps) and the author examined how these patterns contributed to QRST-integral maps in each diagnostic group. He concluded that multiple body-surface electrocardiograms do contain valuable spatial information that identifies the presence of an arrhythmogenic substrate in the myocardium.

Martinka et al (22) used the vulnerability index, the spatial analogue of the ventricular gradient that expresses inhomogeneity of ventricular repolarisation, as a parameter evaluating the risk of arrhythmia development derived from isointegral maps.

De Ambroggi et al (9) used mean difference maps, obtained by subtracting the mean map of 35 healthy control subjects from that of arrhythmogenic right ventricular dysplasia patients (9 with episodes of sustained ventricular tachycardia and 13 without). To detect minor heterogeneities of ventricular repolarisation, the principal component analysis was applied to all recorded ST-T waves in each subject studied, which provides a better quantitative

assessment of the "complexity" of repolarisation than other ECG measurements widely used in clinical practice.

Some of the drugs could have influenced the results. 8 of the patients had been receiving class III antiarrythmic drugs, but the effect of amiodarone on QTd might be controversial. Amiodarone produces QT lengthening (10, 31, 34), but some authors found a decrease of QTd (7, 33), others an increase (36) and some considered that QTd was not modified (13, 23). Angiotensin conversion enzyme inhibitors (50%-16 of the patients was taking ACEI) and beta-blockers (68.75%-22 were patients was taking beta-blockers) decreased QTd (27). Other causes of QT interval elongation are: diabetes mellitus (40), advanced age, heart failure, hypertension, left ventricular hypertrophy and obesity (6, 32).

Heart failure is thought to be one of the main causes of electrical instability. Most of the patients included in our study had a preserved EF (EF was below 30% only in 2 patients and below 40% in 5 patients). Sudden cardiac death occurs most frequent in patients with an EF below 40% (41), and patients with heart failure with preserved ejection fraction (>50%) have a better prognosis. But there were some studies considering that the prognosis of patients with heart failure with preserved ejection fraction was similar or worse compared to that of patients with reduced ejection fraction (4, 37).

QT dispersion values and extreme maximum and minimum amplitude presented in this paper seem larger than some previously published data, but there is no standardisation.

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The Bazett formula (3) is still the simplest and the most practical solution for heart rate correction of QT interval duration, despite its limitations, and time has proven its usefulness in everyday clinical practice (2).

Our study reveals that multipolar IQRST is associated with a loss of maximum amplitude and a stronger minimum. Changes in dispersion of ventricular depolarization and repolarisation are reflected simultaneously in body surface IQRST maps and 12-lead ECG. The two methods provide similar information in predicting postinfarction arrhythmia risk. Identifying patients at risk of such abnormalities is useful in managing their condition.

This study has some potential limitations. One of them is the low number of patients; therefore the results need to be confirmed in larger groups. Besides that, only the value of the highest maximum and deepest minimum of the QRTS isoarea maps could be a assessed in multipolar maps. But these values are only a part of the information in cases with more maxima and minima. Most patients with a history of ventricular arrhythmias were taking antiarrhythmic drugs at the time of BSM recording, including drugs that affect repolarisation. Despite therapy, we found that both multipolar maps and QTd >100ms were significant associated with a history of ventricular arrhythmias.

If the results are confirmed in larger patients groups, QT dispersion, a very simple and inexpensive method, could replace BSM in predicting ventricular arrhythmia in patients with an old myocardial infarction. This information can be valuable in current clinical management of post-infarction patients and might support the selection of post-infarction patients at high risk of life threatening ventricular arrhythmias.

Acknowledgements

This work was supported by grants from the Hungarian Scientific Research Fund (OTKA F-67879), by the National Office for Research and Technology (Hungarian–Roumanian Bilateral project, RO-24/2007 and 55/2008), the Hungarian Academy of Sciences, and by the János Bolyai Research Scholarship (N. J.).

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Multipolar QRST isointegral maps and QT dispersion in old myocardial infarction

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