Carbon monoxide poisoning increases T(peak)–T(end) dispersion and QT(c) dispersion

OBJECTIVE: Carbon monoxide (CO) poisoning leads to cardiac dysrhythmia. Increased heterogeneity in ventricular repolarisation on electrocardiogram (ECG) shows an increased risk of arrhythmia. A number of parameters are used to evaluate ventricular repolarisation heterogeneity on ECG. The aim of our study is to investigate the effect of acute CO poisoning on indirect parameters of ventricular repolarisation on ECG. METHODS: Sixty-seven patients were included in this case–control study. Thirty patients with acute CO poisoning were assigned to group 1 (19 females, mean age: 30.8 ± 11.3 years). A control group was formed with patients without known cardiac disease (group 2, n = 37; 25 females, mean age: 26.0 ± 5.2 years). Twelve-lead ECG and serum electrolyte levels were recorded in all patients. Also, carboxyhaemoglobin (COHb) levels were recorded in group 1. T(peak)–T(end) (T(p)T(e)) interval, T(p)T(e) dispersion, T(p)T(e)/QT ratio, QT interval and QT(d) durations were measured as parameters of ventricular repolarisation. Corrected QT (QT(c)) and QT(c) dispersion (QT(cd)) intervals were determined with the Bazett’s formula. RESULTS: The mean COHb level in group 1 was 27.6 ± 7.4% and mean duration of CO exposure was 163.5 ± 110.9 min. No statistically significant difference was found in age, gender, serum electrolytes or blood pressure levels between the groups. QRS, QT, QT(c), T(p)T(e) interval and T(p)T(e)/QT ratio were similar between the groups (p > 0.05). QTcd (65.7 ± 64.4 vs 42.1 ± 14.2 ms, p = 0.003) and T(p)T(e) dispersion (40.5 ± 14.8 vs 33.2 ± 4.9 ms, p = 0.006) were significantly longer in group 1 than group 2. COHb level was moderately correlated with TpTe dispersion (r = 0.29; p = 0.01). CONCLUSION: To our knowledge, this is the first study to investigate T(p)T(e) interval and dispersion in CO poisoning. Our results showed that T(p)T(e) dispersion and QTc dispersion increased after CO poisoning.