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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 5  |  Issue : 4  |  Page : 65-70

The diagnostic value of QT dispersion for acute coronary syndrome in patients with nondiagnostic initial electrocardiograms


1 Department of Intensive Care, New Najran General Hospital, Najran, Saudi Arabia
2 Department of Chest Diseases, Aswan university Faculty of Medicine, AI Azhar University, Cairo; Department of Cardiovascular Diseases, Assuit University, Asyut, Egypt

Date of Submission26-Feb-2021
Date of Acceptance23-Sep-2021
Date of Web Publication29-Nov-2021

Correspondence Address:
Sayed Abdelsabour Kinawy
New Najran General Hospital, Najran
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/sccj.sccj_6_21

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  Abstract 


Introduction: Chest pain is a frequent cause for admission to the emergency department (ED). It can be a sign of various conditions, from a minor disorder to a life-threatening disease such as acute myocardial infarction (AMI). Despite the availability of modern-day tools for the diagnosis of AMI, about 5% of patients with AMI are missed in the ED, with subsequent associated morbidity and mortality. QT dispersion as a marker for arrhythmic potential being a marker of in-homogeneity of ventricular repolarization. The QT dispersion is increased in myocardial ischemia. Aims: This study we hypothesized that QTD could accurately identify patients with the acute coronary syndrome (ACS) who presented with chest pain and nondiagnostic initial electrocardiograms (ECGs). Subjects and Methods: The study population included (50) patients (37 males, 13 females) and (10) chronic stable ischemic patients as a control group, they were all in sinus rhythm on admission. All the studied patients were subjected to: History taking; complete physical examination was performed to rule out any other medical problems, standard 12-lead ECG, cardiac markers, echocardiographic examination. QT interval was calculated. The difference between the maximum and minimum QT intervals, occurring in any of the 12 leads, was measured as QTD. A corrected QT interval (QTc) of >440 ms is defined as abnormal, and the difference between QTc max and QTc min was calculated as QTcD. QT dispersion ≤40 ms was considered normal. Results: In the present study, we found that 26 patients (52%) have prolonged QTD (mean 78.800 ms, standard deviation [SD] ±49.555) and 44 patients (88%) have prolonged cQTD (mean 83.322 ms, SD ± 48.491) For patients who were admitted to the ED with chest pain and nondiagnostic initial ECG but later diagnosed as having ACS. Furthermore, we found that only 6 (12%) of patients have a significant prolongation QTD than normal in initial nondiagnostic ECG with elevated cardiac biomarkers (creatine kinase myocardial band at 0 h 48, mean creatine kinase myocardial band (CK MP) at 12 h was 145.833 ± SD 52.660, creatine phosphokinase (CPK) at 0 h: 635.33, mean CPK at 12 h 2448.66 ± SD 538.744). It has been suggested that the initial QTD level has a low predictive power for new cardiac events but that QTD can be more helpful for low-risk patients. Conclusion: Hence, in this study, we found that QTD and QTcD values are higher for ACS patients than for patients without ACS with nondiagnostic initial ECG.

Keywords: Acute coronary syndrome, chest pain, emergency department, nondiagnostic electrocardiogram, QT dispersion


How to cite this article:
Kinawy SA, Assalahi AA, Balharith FH, Badawy OO. The diagnostic value of QT dispersion for acute coronary syndrome in patients with nondiagnostic initial electrocardiograms. Saudi Crit Care J 2021;5:65-70

How to cite this URL:
Kinawy SA, Assalahi AA, Balharith FH, Badawy OO. The diagnostic value of QT dispersion for acute coronary syndrome in patients with nondiagnostic initial electrocardiograms. Saudi Crit Care J [serial online] 2021 [cited 2022 Jan 17];5:65-70. Available from: https://www.sccj-sa.org/text.asp?2021/5/4/65/331516




  Introduction Top


Acute coronary syndrome (ACS) encompasses a spectrum of coronary artery diseases, including unstable angina, ST-elevation myocardial infarction (STEMI; often referred to as “Q-wave myocardial infarction” and non-STEMI (NSTEMI); often referred to as “non–Q-wave myocardial infarction”).

The term “acute coronary syndrome” is useful because the initial presentation and early management of unstable angina, STEMI, and NSTEMI frequently are similar.

QT dispersion represents the spatial heterogeneity of ventricular repolarization, which is defined as the dispersion of repolarization duration in simultaneously recorded leads.

QT dispersion is the difference between the maximum and minimum QT interval occurring at any of the electrocardiographic leads. The underlying rationale is that the QT dispersion is likely to reflect heterogeneities in the recovery of excitability, a factor known to increase the propensity for ventricular fibrillation.

QT dispersion has been proposed as a noninvasive measurement of the degree of in homogeneity in myocardial repolarization. From a practical point of view, grossly prolonged QT dispersion, perhaps 100 ms or greater, must be interpreted simply as a sign of abnormal course of the repolarization.

QT dispersion is increased after myocardial infarction and levels are higher in patient with ventricular fibrillation than those who did not develop ventricular fibrillation. The changes in QT dispersion are dynamic and may reflect the changing pattern of underlying ventricular recovery of ventricular excitability, which is profoundly disturbed in the earliest phase of acute infarction. The QT dispersion might be a useful marker of cardiovascular morbidity and mortality.

The QTc dispersion, like signal averaging, can predict postmyocardial infarction ventricular tachycardia. This has a clinical implication and it shed new light on the mechanism of postmyocardial infarction arrhythmogenesis.

The difference between the maximum and the minimum QT intervals to measure the QT dispersion found that increased QT dispersion may identify the patient who have a high likelihood of having cardiac morbidity and mortality. Conversely, decrease QT dispersion appears to identify patients who have a very low probability of having cardiac morbidity and mortality that is why the measurement of the QT dispersion may improve the cost-effectiveness of electrophysiology testing in patients with ACS.

QT dispersion is of significant predictive value for the prognosis of acute myocardial infarction (AMI). The QT dispersion in the surface electrocardiogram (ECG) in patient with AMI prone to ventricular fibrillation may allow early identification of high-risk patients soon after hospital admission.

The QT dispersion seems to be a powerful predictor of ventricular electrical instability as it can identify potential re-entry circuits for ventricular tachyarrhythmias.[1]


  Subjects and Methods Top


The study population included 50 patients with typical retrosternal anginal pain and without diagnostic initial ECG findings indicating ACS on emergency room presentation. In addition, ten patients with chronic stable angina were recruited as a control group, who were age- and sex-matched with the study group.

Approved from ethical committee, IRB registration number with KACST, KSA: H-11-N-081.

Exclusion criteria

The following patients were excluded from the study:

  1. ECG with diagnostic features for ACS (S-T segment elevation, S-T segment depression, inverted T-wave)
  2. Unclear to measurement QT interval in at least seven ECG leads
  3. Ventricular bigeminay
  4. Atrial fibrillation
  5. Pacemaker rhythm
  6. Current drug use affecting QT interval: Antihistamines antibiotics (clarithromycin), antineoplastic (tamoxifen), antiarrhythmic (sotalol, amiodarone)
  7. Patients known to have ischemic heart disease
  8. Advanced renal disease
  9. Significant valvular disease
  10. Cardiomyopathy.


Diagnosis of acute coronary syndrome

All study patients were examined and treated according to the usual practice.

Diagnosis of acute coronary syndrome was based on

  • Typical clinical features (typical retrosternal chest pain relieved by sublingual nitrate)
  • Diagnostic ECG criteria for IHD during follow-up ((S-T segment elevation, S-T segment depression, inverted T-wave)
  • Serum markers were evaluated for indications of cardiac damage: Specifically, initial cardiac troponin-T, creatine kinase myocardial band (CK-MB), and total (CPK) were measured initially and repeated after the 6th h. If the result was positive, samples were taken at 12-h intervals also.


All the studied patients were subjected to

History taking

Thorough history was taken from each patient with special highlighting on the following:

  1. Chest pain analysis as regard nature, radiation, duration
  2. The presence of risk factors for ischemic heart disease


  3. Such as smoking, hypertension, diabetes mellitus, hyperlipidemia, and a positive family history for ischemic heart disease.

  4. History of intake of drugs affecting QT interval.


Complete physical examination was performed to rule out any other medical problems

General examination: General condition, pulse, blood pressure, respiratory rate, temperature, neck vein, edema of both lower limbs, chest auscultation for evidence of pulmonary venous congestion.

Local examination: Auscultation for heart sounds, additional sounds, and murmurs.

A standard 12-lead electrocardiogram with a paper speed of 25 mm/s, 10 mm/mv was assessed for

  1. Diagnostic ECG criteria for ischemic heart disease (IHD) during follow-up (S-T segment elevation, S-T segment depression, inverted T-wave)
  2. Measurement of QT, QTc, and QTc dispersion.


QT interval was measured from the onset of the QRS complex to the point of return of the T wave to the isoelectric line. Three sequential complexes were measured, and the mean value was used for QT interval calculation. The QT intervals were measured in the initial ECG obtained on presentation. The ECGs were included only if the QT interval could be measured on at least eight out of 12 leads. The QT dispersion was calculated as the difference between the longest and shortest QT intervals in all measured leads.[2]

For the patients with biphasic T waves, the intersection point of down stroking maximum T wave curve and the line tangential to the isoelectric line was accepted as the endpoint. If there was a U wave, the lowest point between the two waves was accepted as the endpoint of the T wave.[3] QTc max and QTc min were determined with the Bazett formula (QTc = QT/√RR). A corrected QT interval (QTc) of >440 ms was defined as abnormal. The difference between QTc max and QTc min was calculated as QTc dispersion, QTcD ≤40 ms was considered normal.[4] The QTcD were compared for cases versus the control group

Myocardial markers

Serum CK-MB, total CPK level. Troponin I levels were measured, Normal levels were (0–25 mg/dL for CK-MB), (24–171 mg/dL for CPK), and (0–0.10 ng/mL for Troponin I).

Determination of myocardial necrosis:

  1. Serial increase in plasma CK-MB level (more than 25% increase between two measurements)
  2. CK-MB to total CK levels is more than 5%
  3. Within the first 12 h, Troponin I value exceeded 0.1 ng/mL.


Echocardiographic study

Echocardiographic examination (HP machine, probe 2.5 M. Hrz) was performed on all patients to omit patients with any of the exclusion criteria and to assess left ventricular systolic (LV) function and segmental wall motion abnormalities (SWMA). Standard echocardiography, including Doppler studies, was performed. The LV dimensions (end systolic and end diastolic) ESD and EDD, respectively, were calculated. Changes in LV volume and ejection fraction (EF) were assessed by Simpson's equation using the apical 4-chamber and 2-chamber views.


  Results Top


Statistical analysis

Data were collected, revised, verified, and then edited on a personal computer. It was then statistically analyzed using SPSS version 12 (SPSS, Chicago) under Windows (Microsoft, Inc., Redmond, WA). The following tests were used:

  1. X = Mean
  2. Standard deviation (SD)
  3. Paired t-test
  4. T-test for independent sample means
  5. x2 = Chi-square test
  6. r = Pearson correlation coefficient
  7. Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and accuracy.


The study population included (60) patients who were divided into two groups;

  • Group (1) included 50 patients with typical retrosternal chest pain and without diagnostic initial ECG findings indicating ACS on ER presentation
  • Group (2) included 10 patients with chronic stable angina as a control group.


They were age- and sex-matched with the patients' group. They were identified by the history of recurrent typical chest pain with other echocardiographic evidence of IHD.

The baseline demographic, electrocardiographic, echocardiography, and laboratory characteristics of the studied population are demonstrated in the following tables, with electrocardiographic, echocardiographic evidence of coronary artery disease.

In the present study, we found that 26 patients (52%) have prolonged QTD (mean 78.800 ms, SD ± 49.555) and 44 patients (88%) have prolonged cQTD (mean 83.322 ms, SD ± 48.491) For patients who were admitted to the emergency department (ED) with chest pain and nondiagnostic initial ECG but later diagnosed as having ACS by clinical criteria (typical retrosternal chest pain relieved by sublingual nitrate), ECG criteria for IHD during follow-up ((S-T segment elevation, S-T segment depression, inverted T wave) and follow-up increase myocardial markers, the gold slandered was longer than 40.0 ms.

In the present study, we found that only 6 (12%) of patients have a significant prolongation QTD than normal in initial nondiagnostic ECG with elevated cardiac biomarkers (CK-MB at 0 h 48, mean CK MP at 12 h was 145.833 ± SD 52.660, CPK at 0 h: 635.33, mean CPK at 12 h 2448.66 ± SD 538.744), It has been suggested that initial QTD level has low predictive power for new cardiac events, but that QTD can be more helpful for the low-risk patient.

Hence in this study, we found that QTD and QTcD values are higher for ACS patients than for patients without ACS with nondiagnostic initial ECG [Figure 1] and [Figure 2].
Figure 1: Nondiagnostic electrocardiogram of acute coronary syndrome with abnormal QT parameter. R-R: 840 ms, Shortest QT: 380 ms, Longest QT: 440 ms, QTD: 60 ms, QTcD: 65.50 ms

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Figure 2: Initial non diagnostic electrocardiogram of acute coronary syndrome with abnormal QT parameter. R-R: 800 ms, Shortest QT: 380 ms, Longest QT: 440 ms, QTD: 60 ms, QTcD: 67.11 ms

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[Table 1] shows there was a statistically significant difference between both groups as regards the shortest, longest Q-T, and cQ-T interval. (Mean cQ-T of Group I: 532.438 (mean cQ-T of Group II: 465.475).
Table 1: Difference between both groups as regards the shortest, longest Q-T, and cQ-T interval

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[Table 2] shows relation between different Q-T parameters and follow-up cardiac biomarker in the first 12 h on admission that revealed a significant increase of CPK at 12 h concomitant with a significant prolongation of Q-T dispersion.
Table 2: Relation between different Q-T parameters and follow-up cardiac biomarker in the first 12 h on admission

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[Table 3] show ROC curve between Group I and group II in QT dispersion: It shows the cut-off point of QT dispersion between Group I and Group II was >80 ms (QT dispersion >80 ms), sensitivity was 32.0%, and specificity was 100%, PPV 100.0, NPV 22.7, the accuracy was 0.554 [Figure 3].
Table 3: Receiver operator characteristic curve between patients and controls in QT dispersion

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Figure 3: Shows receiver operating characteristic curve between patients and controls in QT dispersion

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[Table 4] show ROC curve between Group I and Group II in cQT dispersion: This table shows cut-off point of cQT dispersion between Group I and Group II was >89 ms (QT dispersion >89 ms), sensitivity was 32.0%, and specificity was 100%, PPV 100.0, NPV 22.7, the accuracy was 0.553 [Figure 4].
Table 4: Receiver operator characteristic curve between patients and controls in cQT dispersion

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Figure 4: Shows receiver operating characteristic curve between patients and controls in cQT dispersion

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[Table 5] show ROC curve between Group I and Group II in cQT interval: This table shows cut-off point of cQT interval between Group I and Group II was >48.875 ms (QT dispersion >48.87 ms), sensitivity was 72.0%, and specificity was 80%, PPV 94.7, NPV 36.4, the accuracy was 0.792 [Figure 5].
Table 5: Receiver operator characteristic curve between patients and controls in cQT

Click here to view
Figure 5: Shows receiver operating characteristic curve between patients and controls in cQT interval

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Discussion

In the present study, we found that for patients with chest pain and non-diagnostic initial ECGs who were admitted to the ED, the QTD and cQTD means were different for the ACS patients confirmed by biomarkers rather than the control group. The QTD and QTcD values that were found to be useful in ACS diagnosis were ≥40 ms. These results were concordant with the observations.[5]

Hence, QTD may serve as a useful diagnostic and decision-making tool in patients with acute chest pain and nondiagnostic ECGs. These results were concordant with the observations.[6]

Manual QTD measurement is criticized as being operator dependent.[7] It has been reported that automatic and manual QTD measurements differ, but in good-quality ECGs, the difference between the normal and abnormal groups can be determined.[8]

In the present study, we found that 26 patients (52%) have prolonged QTD (mean 78.800 ms, SD ± 49.555) and 44 patients (88%) have prolonged cQTD (mean 83.322 ms, SD ± 48.491) For patients who were admitted to the ED with chest pain and nondiagnostic initial ECG but later diagnosed with having ACS by clinical criteria (typical retrosternal chest pain relieved by sublingual nitrate), ECG criteria for IHD during follow-up (S-T segment elevation, S-T segment depression, inverted T wave) and follow-up increase myocardial markers, the gold slandered was longer than 40.0 ms, these results were concordant with the observations of.[9]

In the present study, we found that only 6 (12%) of patients have a significant prolongation QTD than normal in initial nondiagnostic ECG with elevated cardiac biomarkers (CK-MB at 0 h 48, mean CK MP at 12 h was 145.833 ± SD 52.660, CPK at 0 h: 635.33, mean CPK at 12 h 2448.66 ± SD 538.744), It has been suggested that initial QTD level has low predictive power for new cardiac events, but that QTD can be more helpful for the low-risk patient.

This study showed that the risk factors had a significant correlation with QTD value.

Diabetes

The relation between Q-T dispersion, cQ-T dispersion, cQ-T intervals and DM, there was a statistically significant difference between cQ-T dispersion and presence of DM, (mean cQ-T dispersion in DM patients: 104.173, SD: 56.067 and in nondiabetic patients, the mean cQ-T dispersion: 74.386, SD: 42.664), P = 0.045. While there is no statistically significant difference with Q-T dispersion, cQ-T intervals and DM (mean Q-T dispersion in DM patients: 97.333, SD: 60.882 and in nondiabetic patients the mean Q-T dispersion: 74.386, SD: 42.664), P = 0.083, 0.132 consecutively.

Hypertension, dyslipidemia

There was a statistically significant difference between (Q-T dispersion, cQ-T dispersion, cQ-T interval) and the presence of HTN, (mean Q-T dispersion in HTN patients 10.00, SD: 55.714 and in non-HTN patients mean Q-T dispersion 55.833, SD: 28.271. mean cQ-T dispersion in HTN patients: 103.600, SD: 54.316 and in non-HTN patients, the mean cQ-T dispersion: 61.354, SD: 28.882. mean cQ-T interval in HTN patients 551.640, SD: 69.593 and in non-HTN patients mean cQ-T interval 511.635, SD: 59.119. P value was: 0.001, 0.001, 0.034) consecutively.

These results were concordant with those reported by Funck-Brentano, et al. and Macfarlane[10],[11] they found that the QTD was significantly prolonged in hypertensive and diabetic patients.

The median QTD value has been determined to be (78 ms ± SD 49.555) in patients group this agreement with.[7] As with earlier reports, the present study showed that if QTD and QTcD are over 40 ms, the development of ACS is very probable despite the normal initial ECGs.

Furthermore, these results were concordant with the observations of[12] as they study 104 patients with the diagnosis of ACS without persistent ST elevation, QT dispersion was prolonged among patients with NSTEMI (55 ms).

This observation was recorded several years ago by Dorogazi and Childers[13] who found QT prolongation in 8 of 14 patients with non-ST elevation myocardial infarction and in 19 of 49 patients with ST-elevation myocardial infarction.

In the same direction, these results are concomitant with Higham et al.,[14] found that QT dispersion in 25 patients with unstable angina was significantly shorter than in those with myocardial infarction.

Echo finding (LVEDD, LVESD, fractional shortening, ejection fraction, and SWMAI)

Mean left ventricular end diastolic dimension (LVEDD) 52.8 mm ± SD: 6.507, left ventricular end systolic dimension (LVESD) 34.44 mm ± SD: 6.97 and mean fractional shortening (FS) 31.8% ± SD: 6.53 mean EF 61.600% ± SD: 6.501. In comparison controlled group LVEDD, LVESD, FS were 56.6 mm, 41.4 mm, and 26.9% consecutively.

The present study found that (8) cases 16% have prolonged QTD with FS ≤25%, (18) cases 27% have prolonged QTD with different RWMA.

Mean SWMAI 1.201 SD ± 0.621 of patients group with a significant prolongation of Q-T Dispersion.

Hence, QT dispersion reflects not only the electrical but also the mechanical functions of the heart.


  Conclusion Top


The present study demonstrated that QTD and QTcD means were markedly greater for patients who had a final diagnosis of ACS. The QTD value that was found to be useful in predicting the likelihood of ACS was 40 ms. However, difficulty with operator measurements of QT-dispersion would limit its value as a diagnostic test.

Recommendation

  1. Based on the results of this study, we recommend that measurement of QTc and QTc dispersion on admission may help in the diagnosis of ACS, especially for patients with chest pain and nondiagnostic initial ECG
  2. Further studies are recommended to be done on a larger number of patients.


Financial support and sponsorship

From New Najran General Hospital Administration.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Libby P, Bonow RO, Mann DL, Zipes DP. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 8th edition, Ch; 49. 2007. p. 1197.  Back to cited text no. 1
    
2.
Bolton E. Disturbances of cardiac rhythm and conduction. In: Tintinalli JE, editor. Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004. p. 179-202.  Back to cited text no. 2
    
3.
Calder KK, Tomongin C, Mallon WK, Genna T, Bretsky P, Henderson SO. Manual measurement of QT dispersion in patients with acute myocardial infarction and nondiagnostic electrocardiograms. Acad Emerg Med 2002;9:851-4.  Back to cited text no. 3
    
4.
Sarubbi B, Esposito V, Ducceschi V, Meoli I, Grella E, Santangelo L, et al. Effect of blood gas derangement on QTc dispersion in severe chronic obstructive pulmonary disease: Evidence of an electropathy? Int J Cardiol 1997;58:287-92.  Back to cited text no. 4
    
5.
Murat P, Ilgin K, Yunsur C, Sedat Y and Erdogan I: the Mount Sinai Journal of Medicine 2006;73.  Back to cited text no. 5
    
6.
Calder KK, Tomongin C, Mallon WK, et al. Manual measurement of QTdispersion in patients with acute myocardial infarction and nondiagnostic electrocardiograms. Acad Emerg Med 2002;9:851-4.  Back to cited text no. 6
    
7.
Kesek M, Jernberg T, Lindahl B, Englund A. QT dispersion measured by an automatic continuous method early in patients admitted for chest pain. Int J Cardiol 2002;85:217-24.  Back to cited text no. 7
    
8.
Murray A, McLaughlin NB, Campbell RW. Measuring QT dispersion: Man versus machine. Heart 1997;77:539-42.  Back to cited text no. 8
    
9.
Shah CP, Thakur RK, Reisdorff EJ, Lane E, Aufderheide TP, Hayes OW. QT dispersion may be a useful adjunct for detection of myocardial infarction in the chest pain center. Am Heart J 1998;136:496-8.  Back to cited text no. 9
    
10.
Funck-Brentano C, Legrand M, Samain E, Marty: JAMA 1993; 269:1532.  Back to cited text no. 10
    
11.
Macfarlane PW. QT dispersion: Lack of discriminating power WOSCOP study group. Circulation 1998;98 Suppl I:I-81.  Back to cited text no. 11
    
12.
Rukshin V, Monakier D, Olshtain-Pops K, Balkin J, Tzivoni D. QT Interval in Patients with Unstable Angina and NoncQ Wave Myocardial Infarction. A.N.E. 2002;7:343-8.  Back to cited text no. 12
    
13.
Dorogazi RM, Childers T. Time related changes in QT interval in acute myocardial infarction: Possible relation to local hypocalcaemia. Am J Cardiol 1978;41:684-8.  Back to cited text no. 13
    
14.
Higham P, Bogun F, Kwok K, Harvey M, Furniss S, Gampbell R, et al. QT dispersion and components of the QT interval in ischaemia Am J Gardiol 1996;71:16.  Back to cited text no. 14
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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