CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 3, May/June 2014
106
AFRICA
Carbon monoxide poisoning increases T
peak
–T
end
dispersion and QT
c
dispersion
Murat Eroglu, Omer Uz, Zafer Isilak, Murat Yalcin, Ali Osman Yildirim, Ejder Kardesoglu
Abstract
Objective:
Carbon monoxide (CO) poisoning leads to cardiac
dysrhythmia. Increased heterogeneity in ventricular repolari-
sation 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 electro-
lyte levels were recorded in all patients. Also, carboxyhae-
moglobin (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). QT
cd
(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 T
p
T
e
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 QT
c
dispersion
increased after CO poisoning.
Keywods:
carbon monoxide, electrocardiogram, dysrhythmia,
ventricular repolarisation
Submitted 20/7/12, accepted 24/2/14
Cardiovasc J Afr
2014;
25
: 106–109
DOI: 10.5830/CVJA-2014-012
Carbon monoxide (CO) poisoning may cause myocardial
toxicity and life-threating cardiac arrhythmias.
1-3
Acute coronary
syndrome, myocardial injury, myocardial dysfunction, cardiac
arrest and various types of arrhythmias have been reported
in patients with acute CO poisoning.
4
CO binds myocardial
myoglobin and reduces myocardial oxygen reserve.
5
Previous
studies reported that episodes of atrial fibrillation, premature
ventricular beats and sinusal tachycardia may be seen in patients
with acute CO poisoning.
6,7
Recent studies also suggested that
risk of atrial and ventricular arrhythmia is increased in CO
poisoning, due to prolonged QT
c
and QT
c
dispersion.
2,3,8
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.
9
T
peak
–T
end
(T
p
T
e
) 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.
10
T
p
T
e
/QT
ratio and T
p
T
e
/QT
c
ratio were used in previous studies as an
electrocardiographic index in the evaluation of risk of ventricular
arrhythmia.
11,12
The effect of acute CO poisoning on QT intervals was
investigated in a number of studies.
2,3,8
However, to the best of our
knowledge, T
p
T
e
interval, T
p
T
e
dispersion, T
p
T
e
/QT ratio and T
p
T
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.
Methods
The ethics committee of Gulhane Military Medical Academy
Haydarpasa Teaching Hospital approved the study protocol.
The control group was composed of 37 healthy medical staff
or volunteers aged from 20 to 40 years (mean 26.0; SD
=
5.2),
comprising 25 women and 12 men. Patients who were treated
with normobaric oxygen for CO poisoning at the Emergency
Department of Gulhane Military Medical Academy between
1 October 2005 and 31 May 2006 comprised the study group.
Diagnosis of CO poisoning was made based on medical history
and a COHb level
>
5% (10% in smokers).
Patients excluded from the study were those with coronary
artery disease or other known heart disease, such as valvular
Department of Emergency Medicine, Haydarpasa Teaching
Hospital, Gulhane Military Medical Academy, Istanbul, Turkey
Murat Eroglu, MD,
Ali Osman Yildirim, MD
Department of Cardiology, Haydarpasa Teaching Hospital,
Gulhane Military Medical Academy, Istanbul, Turkey
Omer Uz, MD
Zafer Isilak, MD
Murat Yalcin, MD
Ejder Kardesoglu, MD
