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Letters to the Editor

Is the Evaluation Sufficient? Interpretation on the Cardiac Inhomogeneity Without Considering the Transmural Dispersion

Omer Yiginer, MD1;  Abdullah Haholu, MD2;  Mehmet Tezcan, MD3;  Namik Ozmen, MD1

Keywords
March 2015

Dear Editor:

We have read the article, “Corrected QT-Interval and Dispersion After Revascularization by Percutaneous Coronary Intervention and Coronary Artery Bypass Graft Surgery in Chronic Ischemia” by Mirbolouk, et al with great interest.1 In this study, they investigated the effects of revascularization on cardiac repolarization parameters of QT interval (QTI), corrected QT interval (QTc), QT dispersion (QTd), and corrected QT dispersion (QTcd). The authors concluded that both of the revascularization procedures reduced the QTc and QTcd and thereby improved electrical instability of ischemic myocardium.

Inhomogeneity in the duration of cardiac action potential causes the electrical instability leading to arrhythmias. This situation can be demonstrated in the electrophysiologic laboratory via monophasic action potential mapping.2 Meanwhile, QTd is the most frequently used non-invasive method to reveal electrical heterogeneity of the myocardium. However, there are varying results in studies related to QTI due to the technical limitations in the QTI measurement.3 QTI can be measured both manually and automatically. It is well known that the reproducibility of QTI measurements is low both in manual and automatic measurements.2,3 In addition, in manual measurements, inter- and intraobserver variability of QTd is very high.3 In this study, the measurements have been performed by one cardiologist using a ruler without transferring the data to the digital platform. Also, electrocardiographic (ECG) recordings were done with a paper speed of 25 mm/msec and amplitude of 10 mm/mV. In order to obtain more accurate data in manual measurements, it is recommended that the measurements be performed by at least two cardiologists using a digital platform.2,3 The accuracy of the measurements could also be increased by recording the ECG tracings with the paper speed of 50 mm/msec and amplitude of 20 mm/mV. Determination of the end of the T-wave is one of the technical issues of the QTI measurement.4 Tangential, differential threshold, and visual methods may be used to determine the end of the T-wave.4 Despite all efforts, the end of the T-wave cannot be determined in some leads. As the number of the leads in which QTI cannot be measured increases, accuracy of the QTd decreases. In order to overcome this limitation, different methods (standard deviation of the QTI, relative QTd, adjusted QTd) have been developed by some investigators instead of QTd.3

In order to quantify the inhomogeneity of the myocardium, in addition to QTd, transmural dispersion of repolarization (TDR) was introduced in the beginning of the 2000s.5 Isolated cells from different layers of the myocardium exhibited that the myocardium comprises three distinct myocyte types – namely, endocardial, epicardial, and midmyocardial M-cells.6 Despite the fact that these myocytes are morphologically similar, they exhibit different electrophysiological characteristics. Midmyocardial M-cells typically have the longest action potential duration. Furthermore, when  myocardium is exposed to the conditions prolonging repolarization phase such as agents or bradycardia, action potential duration of the M-cells is more prolonged than the other cell types.6 This electrical heterogeneity seems to be caused by varying responses of the distinct cell types in the different myocardial layers. ECG may reflect these discrepancies. While repolarization phase of the epicardial region ends at the peak of the T-wave, repolarization phase of the M-cells continues until the end of the T-wave.6 Therefore, the time between the peak and end of the T-wave is termed the “Tp-e interval,” as an index of TDR. Tp-e/QT ratio has also been used as an index of TDR. The role of TDR in the prediction of life-threatening arrhythmic events has been demonstrated in the Brugada, short QT, and long QT syndromes.6 Previously, we showed that TDR was increased in patients with obstructive sleep apnea and chronic arsenic exposure via drinking water.7,8 It has been demonstrated that TDR is also increased in the course of ST-elevation myocardial infarction.6 Tasolar et al have also shown that the TDR decreases as the collateral circulation increases in stable coronary artery disease.9 However, there is no study investigating the effects of revascularization procedures on the TDR. The stenosis in the epicardial coronary arteries primarily leads to ischemia beginning from the endocardial region toward the epicardium. The repolarization phase of myocytes in the midmyocardial and endocardial layers is more affected by ischemia than the epicardial layer. Therefore, chronic ischemia may augment TDR, and alleviating ischemia via revascularization procedures may decrease the TDR. 

In conclusion, it seems that adding the transmural dispersion data to the study would completely reveal the effects of revascularization procedures on electrical heterogeneity of myocardium in every respect.

References

  1. Mirbolouk F, Arami S, Salari A, et al. Corrected QT-interval and dispersion after revascularization by percutaneous coronary intervention and coronary artery bypass graft surgery in chronic ischemia. J Invasive Cardiol. 2014;26(9):444-450.
  2. Statters DJ, Malik M, Ward DE, Camm AJ. QT dispersion: problems of methodology and clinical significance. J Cardiovasc Electrophysiol. 1994;5(8):672-685.
  3. Malik M, Batchvarov VN. Measurement, interpretation and clinical potential of QT dispersion. J Am Coll Cardiol. 2000;36(6):1749-1766.
  4. Kasamaki Y, Ozawa Y, Ohta M, et al. Automated versus manual measurement of the QT interval and corrected QT interval. Ann Noninvasive Electrocardiol. 2011;16(2):156-164.
  5. Antzelevitch C. Tpeak-Tend interval as an index of transmural dispersion of repolarization. Eur J Clin Invest. 2001;31(7):555-557.
  6. Gupta P, Patel C, Patel H, et al. T(p-e)/QT ratio as an index of arrhythmogenesis. J Electrocardiol. 2008;41(6):567-574. 
  7. Kilicaslan F, Tokatli A, Ozdag F, et al. Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio are prolonged in patients with moderate and severe obstructive sleep apnea. Pacing Clin Electrophysiol. 2012;35(8):966-972.
  8. Yildiz A, Karaca M, Biceroglu S, et al. Effect of chronic arsenic exposure from drinking waters on the QT interval and transmural dispersion of repolarization. J Int Med Res. 2008;36(3):471-478.
  9. Taşolar H, Ballı M, Cetin M, Otlu YO, Altun B, Bayramoğlu A. Effects of the coronary collateral circulation on the Tp-e interval and Tp-e/QT ratio in patients with stable coronary artery disease. Ann Noninvasive Electrocardiol. 2015;20(1):53-61. Epub 2014 Jun 16. 

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