Original ContributionA new marker for myocardial injury in carbon monoxide poisoning: T peak–T end
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.
Section snippets
Study population
The study included patients older than 17 years who presented to the our hospital with CO poisoning between 2011 and 2012 and a healthy control group. The study protocol was approved by the hospital ethics committee, and informed consent was obtained from patients who were conscious, the relatives of unconscious patients, and control subjects.
Study protocol
Medical history was obtained from conscious patients and the relatives of unconscious patients, and all home medications were recorded. Demographic data
Results
Ninety-four patients with CO poisoning (median age, 35.5 [24] years; male, 47.9%) and 40 controls (median age, 35.5 [19] years; male, 47.5%) were included in this study. The demographic and ECG findings of the study participants are presented in Table 1. The Tp-e, Tp-e dispersion, and Tp-e/QT ratio in the patient group at admission were significantly higher than those in the control group (Tp-e: 89.5 ± 13.2 milliseconds vs 68.5 ± 5.0 milliseconds, P < .001; Tp-e dispersion: 27.0 [17.0]
Discussion
The present study demonstrates that transmyocardial repolarization parameters (noninvasive ECG indicators of ventricular arrhythmia) were longer in patients with CO poisoning than in control subjects and that Tp-e correlated with myocardial injury.
Carbon monoxide poisoning can lead to permanent tissue damage, including damage to the brain and heart, which are especially vulnerable to hypoxia [13]. Lippi et al [14] stated that CO leads to cardiotoxicity because it increases ischemia and has a
Conclusion
Identifying cardiotoxicity in patients with CO poisoning can be difficult, especially in asymptomatic patients. In the present study, the novel transmyocardial repolarization parameters Tp-e, Tp-e dispersion, and the Tp-e/QT ratio were longer in the patients with CO poisoning than in controls subjects. Moreover, a prolonged Tp-e interval was a marker of myocardial injury. Based on these findings, ECG—a simple, inexpensive, and noninvasive technique—can be used to help determine the risk of
References (34)
- et al.
Electrocardiographic changes in carbon monoxide poisoning
Am J Cardiol
(1963) - et al.
Tpeak-Tend and Tpeak-Tend dispersion as risk factors for ventricular tachycardia/ventricular fibrillation in patients with the Brugada syndrome
J Am Coll Cardiol
(2006) - et al.
The QT and Tp-e intervals in left and right chest leads: comparison between patients with systemic and pulmonary hypertension
J Electrocardiol
(2005) - et al.
Cardiovascular manifestations of moderate to severe carbon monoxide poisoning
J Am Coll Cardiol
(2005) - et al.
T(p-e)/QT ratio as an index of arrhythmogenesis
J Electrocardiol
(2008) - et al.
Pathophysiology, clinics, diagnosis and treatment of heart involvement in carbon monoxide poisoning
Clin Biochem
(2012) - et al.
Carbon monoxide intoxication: an updated review
J Neurol Sci
(2007) - et al.
Cellular basis for QT dispersion
J Electrocardiol
(1998) - et al.
Left ventricular hypertrophy amplifies the QT, and Tp-e intervals and the Tp-e/QT ratio of left chest ECG
J Biomed Res
(2010) - et al.
Carbon monoxide cardiotoxicity
J Toxicol Clin Toxicol
(2001)
Silent myocardial infarction caused by acute carbon monoxide poisoning
G Ital Cardiol
Effects of exposure to low concentrations of carbon monoxide on exercise performance and myocardial perfusion in young healthy men
Occup Environ Med
The evaluation of myocardial damage in 83 young adults with carbon monoxide poisoning in the East Anatolia region in Turkey
Hum Exp Toxicol
Immediate and late electrocardiographic changes in the course of acute carbon monoxide poisoning
Lille Med
Electrocardiographic changes in acute carbon monoxide poisoning
Minerva Med
Comparative reproducibility of QT, QT peak, and T peak–T end intervals and dispersion in normal subjects, patients with myocardial infarction, and patients with hypertrophic cardiomyopathy
Pacing Clin electrophysiol
Reversible increases in QT dispersion and P wave dispersion during carbon monoxide intoxication
Hong Kong J Emerg Med
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