A new marker for myocardial injury in carbon monoxide poisoning: T peak–T end

Abstract

Objectives

Carbon monoxide (CO) poisoning frequently affects repolarization, resulting in abnormal electrocardiography findings. The goal of this study was to examine the effect of CO poisoning on the novel transmyocardial repolarization parameters T peak–T end (Tp-e), Tp-e dispersion, and Tp-e/QT and the relationship of these parameters to myocardial injury (MI).

Methods

This prospective study included 94 patients with CO poisoning and 40 healthy controls. Participants received an electrocardiography and had their blood drawn at admission and 6 and 24 hours after admission. The QT, Tp-e, Tp-e dispersion, and the Tp-e/QT ratio were calculated. Myocardial injury was determined based on an elevation in troponin any time during the first 24 hours. The patients were divided into 2 subgroups: those with and without MI.

Results

T peak–T end, Tp-e dispersion, and the Tp-e/QT ratio were higher at admission than after 6 and 24 hours of hospitalization and were higher than the control group (P < .001). There was a correlation between the carboxyhemoglobin level at admission and Tp-e and Tp-e dispersion (P < .001). The MI subgroup (n = 14) had a higher Tp-e at admission than did the non-MI subgroup (n = 80) (96 [11] milliseconds vs 87 [12] milliseconds, P = .03). There were no any significant differences in the Tp-e dispersion or the Tp-e/QT ratio between the 2 MI subgroups. Receiver operating characteristic analysis showed that a Tp-e cutoff value for MI of 91.5 milliseconds had a sensitivity of 72.7% and a specificity of 67.2%.

Conclusion

Transmyocardial repolarization parameters indicative of arrhythmia were prolonged in patients with CO poisoning. T peak–T end was associated with MI.

Introduction

Carbon monoxide (CO) causes cardiotoxicity via electrical, functional, and morphologic changes in the heart [1]. Cardiotoxicity due to CO poisoning may be silent [2]. In patients with prominent neurologic findings and respiratory symptoms, cardiotoxicity may be misdiagnosed. It has been shown that the morbidity and mortality rates secondary to cardiotoxicity can be lowered with appropriate treatment [3], [4]. Nonspecific repolarization changes and arrhythmias are seen on electrocardiography (ECG) in patients with CO poisoning. Sudden death due to CO poisoning is thought to occur because of arrhythmias originating in the ventricles [5], [6], [7]. The T wave is an ECG finding indicative of ventricular repolarization. It was recently reported that transmyocardial repolarization parameters, which include the T peak–T end interval (time from the peak to the end of the T wave [Tp-e]), Tp-e dispersion, and the Tp-e/QT ratio, are associated with an increased risk of cardiac arrhythmias [8], [9], [10]. The goals of the present study were to examine the effects of CO exposure on transmyocardial repolarization parameters and to determine if there is a relationship between these parameters and myocardial injury.