Time Variance of Electrocardiographic Transmural Dispersion in Acute Myocardial Infarction

Jin-Sun Park,Joon-Han Shin,So-Yeon Choi,Sun-Mi Kim,Kyoung-Woo Seo,Myeong-Ho Yoon,Byoung-Joo Choi,Gyo-Seung Hwang,Seung-Jea Tahk

doi:10.18501/arrhythmia.2016.030

Jin-Sun Park, Joon-Han Shin + Show 7 more

Open Access

https://doi.org/10.18501/arrhythmia.2016.030

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Abstract

Background and Objectives The mechanism responsible for lethal ventricular arrhythmia (LVA) after acute myocardial infarction (AMI) remains unclear. Subjects and Methods The corrected QT interval (QTc) and interval from the peak to the end of the T wave (TpTe) were measured, which indicated myocardial transmural dispersion of repolarization (TDR) in 72 patients with AMI. TpTe was also expressed as a corrected value, [TpTe/QTe]x100% and TpTe/âRR. These parameters were obtained from all the 12-leads of electrocardiography after arrival at the hospital, just before and after percutaneous coronary intervention (PCI), and at 4, 24, and 48 hours and 5 days after PCI. Results Analyzing with repeated measures analysis of variance, the TpTe, [TpTe/QTe]x100% and TpTe/âRR after AMI showed significant changes in time variance. The patients were divided into LVA (17 patients, 24%) and non-LVA group (55 patients, 76%). The [TpTe/ QTe]Ã100% (V2: 25Â±7% vs. 22Â±5%, p=0.036) and TpTe/âRR (V2: 109 Â± 42 ms vs. 88 Â± 22 ms, p=0.05, V3: 108Â±39 ms vs. 91Â±27 ms, p=0.048) in V2 and V3 leads were prolonged in the LVA group after PCI. The [TpTe/QTe]Ã100% (28Â±9 % vs. 22Â±5%, p=0.025) and TpTe/âRR (129Â±53 ms vs. 99Â±41 ms, p=0.05) in V3 lead were prolonged in the LVA group 24 hours after PCI. Conclusion The mechanisms responsible for LVA after AMI may be associated with increased TDR, and PCI may have an important role in reducing LVA. Key words: Myocardial Infarction; Cardiac Arrhythmia

Highlights

Lethal ventricular arrhythmia (LVA), including ventricular tachycardia (VT) and ventricular fibrillation (VF), usually develops within 48 hours of acute myocardial infarction (AMI)
The mechanisms responsible for lethal ventricular arrhythmia (LVA) after AMI may be associated with increased transmural dispersion of repolarization (TDR), and percutaneous coronary intervention (PCI) may have an important role in reducing LVA
Regardless of LVA, the patients with AMI tended to exhibit increased TDR before revascularization. These results suggested that the increased TDR may be one of the mechanisms responsible for the development of LVA after AMI and the interval between the peak and end of the T wave might be a valuable method of arrhythmia risk stratification in patients with AMI

Summary

Introduction

Lethal ventricular arrhythmia (LVA), including ventricular tachycardia (VT) and ventricular fibrillation (VF), usually develops within 48 hours of acute myocardial infarction (AMI). The mechanism responsible for lethal ventricular arrhythmia (LVA) after acute myocardial infarction (AMI) remains unclear. TpTe was expressed as a corrected value, [TpTe/QTe]x100% and TpTe/√RR These parameters were obtained from all the 12-leads of electrocardiography after arrival at the hospital, just before and after percutaneous coronary intervention (PCI), and at 4, 24, and 48 hours and 5 days after PCI. The [TpTe/ QTe]×100% (V2: 25±7% vs 22±5%, p=0.036) and TpTe/√RR (V2: 109 ± 42 ms vs 88 ± 22 ms, p=0.05, V3: 108±39 ms vs 91±27 ms, p=0.048) in V2 and V3 leads were prolonged in the LVA group after PCI. The [TpTe/QTe]×100% (28±9 % vs 22±5%, p=0.025) and TpTe/√RR (129±53 ms vs 99±41 ms, p=0.05) in V3 lead were prolonged in the LVA group 24 hours after PCI. Conclusion: The mechanisms responsible for LVA after AMI may be associated with increased TDR, and PCI may have an important role in reducing LVA

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Conclusion