Carbon monoxide poisoning increases Tpeak–Tenddispersion and QTc dispersion

摘要

Carbon monoxide (CO) poisoning may cause myocardial toxicity and life-threating cardiac arrhythmias.- Acute coronary syndrome, myocardial injury, myocardial dysfunction, cardiac arrest and various types of arrhythmias have been reported in patients with acute CO poisoning. CO binds myocardial myoglobin and reduces myocardial oxygen reserve. Previous studies reported that episodes of atrial fibrillation, premature ventricular beats and sinusal tachycardia may be seen in patients with acute CO poisoning., Recent studies also suggested that risk of atrial and ventricular arrhythmia is increased in CO poisoning, due to prolonged QTc and QTc dispersion.,,Ventricular repolarisation can be evaluated by measuring QT interval, corrected QT interval, and QT dispersion. Among these parameters, QT dispersion represents the heterogeneity of ventricular repolarisation and was clearly shown to be associated with ventricular arrhythmia. Tpeak–Tend (TpTe) interval is defined as the interval between the peak point and endpoint of the T wave on surface electrocardiography and is a novel index of transmural dispersion of ventricular repolarisation. TpTe/QT ratio and TpTe/QTc ratio were used in previous studies as an electrocardiographic index in the evaluation of risk of ventricular arrhythmia.,The effect of acute CO poisoning on QT intervals was investigated in a number of studies.,, However, to the best of our knowledge, TpTe interval, TpTe dispersion, TpT_e/QT ratio and T_pT_e/QT_c ratio have not been investigated sufficiently in patients with CO poisoning. In this study, we aimed to investigate the effect of acute CO poisoning on electrocardiographic parameters, which indirectly show ventricular repolarisation heterogeneity. We also investigated the relationship between carboxyhaemoglobin (COHb) levels and these parameters.