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.
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.