Carbon monoxide poisoning increases Tpeak-Tend dispersion and QTc dispersion : cardiovascular topic

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...

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Veröffentlicht in:Cardiovascular Journal Of Africa 2014-06, Vol.25 (3), p.106-109
Hauptverfasser: Eroglu, Murat, Uz, Omer, Yildirim, Ali Osman, Isilak, Zafer, Kardesoglu, Ejder, Yalcin, Murat
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Sprache:eng
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Zusammenfassung: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. Tpeak-Tend (TpTe) interval, TpTe dispersion, TpTe/QT ratio, QT interval and QTd durations were measured as parameters of ventricular repolarisation. Corrected QT (QTc) and QTc dispersion (QTcd) 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, QTc, TpTe interval and TpTe/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 TpTe 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 TpTe interval and dispersion in CO poisoning. Our results showed that TpTe dispersion and QTc dispersion increased after CO poisoning.
ISSN:1995-1892
1680-0745
DOI:10.5830/cvja-2014-012