Abstract: Background. Acute ST-elevation myocardial infarction (STEMI) is associated with significant arrhythmia and cardiac arrest. QT prolongation can occur in the setting of ischemia or acute STEMI as a risk factor for arrhythmia. The goal of this study was to investigate corrected QT interval (QTc), QT dispersion (QTd), and T-wave peak to end (TPE) times in this patient population and evaluate the effect of primary percutaneous coronary intervention (PCI) in STEMI patients on these indices. Methods. This study was a clinical trial, whereby eligible patients presenting with acute STEMI who were appropriate candidates for primary PCI were enrolled. QTc, QTd, and TPE indices were calculated before and after the procedure. Results. Eighty patients (60 male, 20 female) with a mean age of 58.8 years were evaluated. We found significant reduction in QTd after PCI (mean, 5.8 ms before PCI vs 3.6 ms after PCI; P<.001) and significant reduction in TPE after PCI (mean, 9.7 ms before PCI vs 7 ms after PCI; P<.001). QTc did not show significant changes before or after PCI (44.9 vs 43.7; P=.057). Conclusion. Our study showed that primary PCI was effective in reducing the degree of arrhythmogenic indices such as QTd and TPE. Our findings suggest that ischemia-induced QTd and TPE are important arrhythmogenic parameters responding to successful primary PCI and may be used as markers for successful reperfusion.
J INVASIVE CARDIOL 2013;25(5):232-234
Key words: coronary artery disease, QT, QT prolongation, QT dispersion, arrhythmia, primary PCI, TPE percutaneous coronary intervention, PTCA, stenting, acute myocardial infarction, acute coronary syndrome
The QT interval reflects the duration of ventricular electrical activity determined by the phases of depolarization and repolarization.1 It was proposed that the different electrocardiographic (ECG) leads magnify the ECG signal of different myocardial regions; consequently, QT dispersion (QTd), the maximum variation in the QT interval in 12-lead ECG, reflects inhomogeneity of ventricular repolarization and spatial dispersion of ventricular recovery time.2 Clinical and experimental studies have shown a clear relationship between dispersion and other repolarization indices,3,4 suggesting that QTd can show spatial projection in various ECG leads.5
The significance of QTd partially persists even with the use of 6 precordial leads instead of 12 leads, as well as with other lead combinations.2 QTd has been shown to correlate with increased arrhythmic vulnerability in various types of cardiac diseases, such as coronary artery disease,6 long QT syndrome,7 and congestive heart failure.8 It is also considered a predictor of ischemic cardiac events and sudden cardiac death.9,10 In addition, corrected QTd before percutaneous coronary intervention (PCI) has been associated with an increased risk of major adverse cardiac event (MACE) and mortality after successful PCI in acute ST-elevation myocardial infarction (STEMI).
Some researchers have shown an increase of QTd in STEMI patients.11 Interestingly, QTd variability has been reported to be associated with myocardial viability in the setting of acute STEMI12 and successful thrombolytic therapy has resulted in the reduction of QTd.13
A T-wave on surface ECG is a representative of voltage gradient between subendocardial and subepicardial region. In addition to QTd, some studies used T-wave peak to end (TPE) to evaluate repolarization inhomogeneity, where the peak of the T-wave coincides with the end of epicardial repolarization while the end of the T-wave indicates the end of repolarization of the whole ventricular myocardium.14,15 The goal of this study was to investigate corrected QT interval (QTc), QTd, and TPE in this patient population and evaluate the effect of primary percutaneous coronary intervention (PCI) in STEMI patients on these indices.
The patients enrolled were initially selected from those with clinical history and symptoms suggestive of a first episode of acute STEMI who had presented within 12 hours after the onset of symptoms. In all cases, acute STEMI was documented based on ECG and later confirmed by invasive coronary angiography. Ultimately, only patients who underwent successful PCI with TIMI flow grade 3 post PCI with a door-to-balloon time of <90 minutes were included.
Patients with history of previous myocardial infarction, atrial fibrillation, left bundle branch block, QRS >12 ms, or difficult to determine end of T-wave were excluded from the study. Informed consent was obtained from each patient involved in this study. The study was approved by institutional review committee.
Analysis of QT interval. All standard 12-lead ECGs were recorded at 25 mm/s speed and 10 mm/mv gain. The QT data obtained at admission and 24 hours after primary PCI were manually measured with a ruler. QT interval was measured from the beginning of QRS to the end of the T-wave. The end of the T-wave was defined as the point of return to the isoelectric line. In cases where the T-wave was interrupted by a U-wave, the end of the T-wave was defined as the nadir between the T- and U-waves. In instances where the T-wave could not be reliably determined due to extremely low voltage (<.1 mv), measurement of QT interval was not established and consequently these leads were excluded from analysis. In order to exclude the effects of heart rate (HR) on the QT interval, the QT interval was corrected according to the Bazett formula (QTc = QT/square root of RR interval). QTd was defined as the difference between the maximum and minimum QT intervals. TPE was measured with a ruler from the peak of the T-wave to its end. The criteria to determine the endpoint of the T-wave were similar to the aforementioned criteria considered for QT measurement. Statistical analysis of data was performed with SPSS 16 software. Differences in mean values before and after PCI were compared using paired T-tests and P-values <.05 were considered statistically significant.
The study population consisted of 80 patients (60 male, 20 female) diagnosed with acute STEMI who underwent successful primary PCI. Baseline characteristics of our patients are summarized in Figure 1. After coronary angiography, the left anterior descending (LAD) coronary artery was found to be the most common culprit vessel (42 patients; 60%), whereas the left circumflex (LCX) coronary artery and right coronary artery (RCA) were equally affected (18 patients each; 20%). Coronary artery stenosis distribution is summarized in Table 1. After PCI, ejection fraction (EF) was >50% in 12 patients, between 35%-50% in 38 patients, and <35% in 30 patients. We found significant reduction in QTd after PCI (mean, 5.8 ms before PCI vs 3.6 ms after PCI; P<.001) and significant reduction in TPE after PCI (mean, 9.7 ms before PCI vs 7 ms after PCI; P<.001). QTc did not show any significant changes before or after PCI (44.9 ms vs 43.7 ms, respectively; P=.057). Table 2 shows the mean ± standard deviation (SD) of these indices. There was no significant correlation between QTd and TPE before PCI (r=-0.1) or after PCI (r=.2). Among our total population of 80 patients, fifty-two patients (65%) demonstrated a decrease in QTd post PCI, while 2 cases (2.5%) showed an increase with no difference observed in the 26 remaining patients (32.5%).
QTd has an upper normal limit of 50 ms and is longer in patients with previous myocardial infarction than in normal subjects. Some studies have shown that even transient balloon inflation during angioplasty has an impact on action potential and repolarization duration.16,17 Increased QTd reflects inhomogeneous ventricular repolarization, which may predispose to significant ventricular arrhythmias. Effective management of acute myocardial infarction may reduce QTd after successful reperfusion using thrombolysis as well as revascularization with angioplasty or coronary bypass surgery.18-20 Therefore, a significant decrease in QTd may be used as an electrocardiographic marker of successful reperfusion.21 In one study, reduction in QTd was stronger in primary PCI patients in comparison to thrombolysis, suggestive of higher myocardial reperfusion rate and salvage with primary PCI in comparison to thrombolysis. The LAD was the most common culprit vessel in our study, whereas the RCA has been the most common culprit vessel (49%) in previous studies.16,22 We did not use corrected QTd by HR since another clinical and experimental study has failed to find correlation between HR and dispersion of ventricular recovery times measured with QTd.2 In concordance with other studies, our results revealed that rapid and complete reperfusion with primary PCI reduces arrhythmic vulnerability based on analysis of QTd and TPE.15,22,23 QTd is time dependent and continues to improve days after successful PCI24 and is an independent risk factor for MACE and dysarrhythmias.25,26 Furthermore, QTd changes can also occur in the setting of elective PCI, including successful PCI of chronic total occlusions suggesting that chronic ischemia also affects QTd.27,28 QTd measured before PCI also has been found to have direct prognostic value on outcome.29 Even very late successful PCI in the setting of myocardial infarction has shown to improve QTd.30 Our study did not show any significant differences in regard to QTc before or after PCI. The reason for this finding is most likely related to the timing of ECG obtained after the reperfusion. It is known that QT is prolonged during ischemia.31 However, the timing of normalization of QT after reperfusion is not immediate and usually occurs 5 days post reperfusion.31 The reason for this time delay is not known, but it explains why our study did not show any difference in the QTc before or after PCI since our ECGs were done in the first 24 hours after successful PCI and not after 5 days. Based on our findings, QTd and TPE appear to be markers of successful reperfusion. However, our study is limited by the small number of patients enrolled and larger trials are needed to correlate our findings with long-term outcomes.
Our study showed that primary PCI was effective in reducing the degree of arrhythmogenic indices such as QTd and TPE. Our findings suggest that ischemia-induced QTd and TPE are important arrhythmogenic parameters responding to successful primary PCI and may be used as markers for successful reperfusion.
- Antzelevitch C, Shimizu W, Yan GX, Sicouri S. Cellular basis for QT dispersion. J Electrocardiol. 1998;30(Suppl):168-715.
- Malik M, Batchvarov VN. Measurement, interpretation and clinical potential of QT dispersion. J Am Coll Cardiol. 2000;15;36(6):1749-1766.
- Zabel M, Portnoy S, Franz MR. Electrocardiographic indexes of dispersion of ventricular repolarization. An isolated heart validation study. J Am Coll Cardiol. 1995;25(3):746-752.
- Hilton H. Does QT dispersion reflect dispersion of ventricular recovery? Circulation. 1992;86(Suppl):392.
- Coumel P, Maison-Blanche P, Badilini F. Dispersion of ventricular repolarization, reality? Illusion? Significance? Circulation. 1998;97(25):2491-2493.
- Zareba W, Moss AC, le Cessie S. Dispersion of ventricular repolarization and arrhythmic cardiac death in coronary artery disease. Am J Cardiol. 1994;74(6):550-553.
- Day CP, McComb JM, Campbell RW. QT dispersion: an indication of arrhythmia risk in patients with long QT intervals. Br Heart J. 1990;63(6):342-344.
- Barr CS, Naas A, Freeman M, Lang CC, Struthers AD. QT dispersion and sudden unexpected death in chronic heart failure. Lancet. 1994;343(8893):327-329.
- Higham PD, Furniss SS, Campbell RW. QT dispersion and components of the QT interval in ischemia and infarction. Br Heart J. 1995;73(1):32-36.
- Yi G, Elliott P, McKenna WJ, et al. QT dispersion and risk factors for sudden cardiac death in patients with cardiomyopathies. Am J Cardiol. 1998;82(12):1514-1519.
- Ueda H, HayashiT, Tsumura K. QT dispersion and prognosis after coronary stent placement in acute MI. Clin Cardiol. 2007;30(5):229-233.
- Gabrielli F, Balzotti L, Bandiera A. QT dispersion variability and myocardial viability in acute myocardial infarction. Int J Cardiol. 1997;61(1):61-67.
- Moreno FL, Villanueva T, Karagounis LA, Anderson JL. Reduction in QT interval dispersion by successful thrombolytic therapy in acute myocardial infarction. TEAM-2 study Investigators. Circulation. 1994;90(1):94-100.
- Yan GX, Lankipalli RS, Burke JF, Musco S, Kowey PR. Ventricular repolarization components on the electrocardiogram, cellular basis and clinical significance. J Am Coll Cardiol. 2003;42(3):401-409.
- Antzelevitch C. Heterogenity and cardiac arrhythmia: an overview. Heart Rhythm. 2007;4(7):964-972.
- Libby P, Bonow R, Mann D, Zipes D. Braunwald’s Heart Disease. A Textbook of Cardiovascular Medicine. Eighth edition. Saunders Elsevier, 2008: p. 1289.
- Macfarlane PW, McLaughlin SC, Rodger JC. Influence of lead selection and population on automated measurement of QT dispersion. Circulation. 1998;98(20):2160-2167.
- Kelly RF, Parillo JE, Hollenberg SM. Effect of coronary angioplasty on QT dispersion. Am Heart J. 1997;134(3):399-405.
- Kosar F, Nisanoglu V, Aksoy Y, Colak C, Erdil N, Battaloglu. B. Effects of coronary revascularization and concomitant aneurysmectomy on QT interval duration and dispersion. J Electrocardiol. 2006;39(2):194-198.
- Gulcan O, Sezgin AT, Demircan S, Atalay H, Turkoz R. Effect of coronary artery bypass grafting and aneurysmectomy on QT dispersion in moderate or severe left ventricular dysfunction. Am Heart J. 2005;149(5):917-920.
- Nikiforos S, Hatzisavvas J, Pavlides G, et al. QT-interval dispersion in acute myocardial infarction is only shortened by thrombolysis in myocardial infarction grade 2/3 reperfusion. Clin Cardiol. 2003;26(6):291-295.
- Opthof T, Coronel R, Wilms-Schopman FJ, et al. Dispersion of repolarization in canine ventricle and the electrocardiographic T wave: Tp-e interval does not reflect transmural dispersion. Heart Rhythm. 2007;4(3):341-348.
- Bonnemeier H, Wiegand UK, Giannitsis E, et al. Temporal repolarization inhomogeneity and reperfusion arrhythmias in patients undergoing successful primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction: impact of admission troponin T. Am Heart J. 2003;145(3):484-492.
- Bilen E, Yasar AS, Bilge M, et al. Effect of primary percutaneous coronary intervention on myocardial repolarization. J Cardiovasc Med (Hagerstown). 2011;12(11):795-799.
- Pan KL, Hsu JT, Chang ST, Chung CM, Chen MC. Prognostic value of QT dispersion change following primary percutaneous coronary intervention in acute ST elevation myocardial infarction. Int Heart J. 2011;52(4):207-211.
- Okishige K, Kanda S, Shimura T, et al. Clinical study of the electrophysiological effects of ischemic post-conditioning in patients with acute myocardial infarctions. J Cardiol. 2011;58(2):137-142.
- Monshizadeh E, Arefi H, Moghadam M, Hassanijirdehi M. QT dispersion before and after coronary artery angioplasty: a case study from Iran. Ann Cardiol Angeiol (Paris). 2012;61(1):27-31.
- Goodhart DM, Hubacek J, Anderson TJ, et al; TOSCA Investigators. Effect of percutaneous coronary intervention of non acute total coronary artery occlusions on QT dispersion. Am Heart J. 2006;151(2):529.e1-529.e6.
- Ueda H, Hayashi T, Tsumura K, et al. QT dispersion and prognosis after coronary stent placement in acute myocardial infarction. Clin Cardiol. 2007;30(5):229-233.
- Pristipino C, Granatelli A, Capasso M, et al. Effects of reperfusion obtained two to six months after acute myocardial infarction on myocardial electrical stabilization in patients with an occluded infarct-related coronary artery. Am J Cardiol. 15;96(6):769-772.
- Endoh Y, Kasanuki H, Ohnishi S, Shibata N, Hosoda S. Influence of early coronary reperfusion on QT interval dispersion after acute myocardial infarction. Pacing Clin Electrophysiol. 1997;20(6):1646-1653.
From the 1Shahid Beheshti University of Medical Sciences. Cardiovascular Research Center, Tehran, Iran, 2CareMore, Tucson, Arizona, and 3University of Arizona, Tucson, Arizona.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted November 21, 2012, provisional acceptance given January 2, 2013, final version accepted February 25, 2013.
Address for correspondence: Mohammad Reza Movahed, MD, PhD, FACC, FSCAI, FACP, CareMore Regional Cardiology Director of Arizona, Professor of Medicine, University of Arizona, 7091 East Speedway Blvd, Tucson, AZ 85710. Email: email@example.com