CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 3, May/June 2014
108
AFRICA
hypotension, dysrhythmia, ischaemia, infarction, and, in some
cases, cardiac arrest.
15,16
Previous studies reported that episodes
of atrial fibrillation, premature ventricular beats and sinus
tachycardia developed in patients with acute CO poisoning.
6,7
QT and QT
c
show ventricular repolarisation on ECG. A
prolonged QT interval indicates impaired myocardial
refractoriness. ProlongedQTandQT
c
intervals can cause a number
of arrhythmias, including torsades de pointes, polymorphic
ventricular tachycardia and ventricular fibrillation.
17,18
A number
of studies have investigated the effect of acute CO poisoning on
QT and QT
c
intervals. These studies found that QT
c
but not QT
interval was prolonged in CO-poisoned patients compared to
control subjects.
4,19
In our study, however, we found that neither
QT nor QT
c
intervals was prolonged after CO poisoning.
QT and QT
c
dispersion represent physiological variability
of regional ventricular repolarisation. Increased QT and QT
c
dispersions are related to heterogeneity of regional ventricular
repolarisation and are accepted as the markers of arrhythmias.
17,20
Data concerning the effect of acute CO poisoning on QT and
QT
c
dispersion is limited. However, it has been reported that CO
poisoning increased QT and QT
c
dispersion.
4,19
We found that the
durations of QT
cd
were significantly prolonged in adult patients
with acute CO poisoning.
T
p
T
e
interval is used as an index of transmural dispersion
of ventricular repolarisation.
10
T
p
T
e
dispersion, T
p
T
e
/QT ratio
and T
p
T
e
/QT
c
ratio are also used as an electrocardiographic
index of ventricular arrhythmogenesis.
12,21
Sicouri
et al.
found a
relationship between ventricular arrhythmia and prolonged T
p
T
e
interval.
22
Previous studies have demonstrated that prolongation of
T
p
T
e
duration is associated with increased mortality in Brugada
syndrome, long QT syndromes, hypertrophic cardiomyopathy,
and in patients undergoing primary percutaneous coronary
intervention for myocardial infarction.
11
In our study, T
p
T
e
interval,
T
p
T
e
/QT ratio and T
p
T
e
/QT
c
ratio did not change significantly
after CO poisoning. However, we did find a correlation between
T
p
T
e
dispersion and COHb levels.
In our study we found that only QT
c
dispersion and T
p
T
e
dispersion increased in patients with CO poisoning.We concluded
that these two parameters are more valuable among the ECG
parameters to demonstrate risk of ventricular arrhythmia in
patients with CO poisoning.
The limitation of this study was the relatively small number of
patients with CO poisoning. Therefore, a follow-up investigation
with a larger sample size is warranted.
Conclusion
Our results showed that T
peak
–T
end
dispersion and QT
c
dispersion
increased after CO poisoning. We believe that CO poisoning
impaired the homogeneity of ventricular repolarisation and may
have caused increased T
peak
–T
end
dispersion and QT
c
dispersion.
Further studies are needed to evaluate the importance of
electrocardiographic parameters in CO poisoning.
References
1.
Gandini C, Castoldi AF, Candura SM, Priori S, Locatelli C, Butera R,
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3.
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2012 Jun 5. doi: 10.1111/j.1540-8159.2012.03439.x.
Table 3. Correlations between electrocardiographic
measurements and COHb levels.
R
p*
QT interval (ms)
–0.12
0.52
QT
c
interval (ms)
–0.11
0.53
QT
d
interval (ms)
0.07
0.68
QT
cd
interval (ms)
0.18
0.33
T
p
T
e
time (ms)
0.19
0.33
T
p
T
e
dispersion (ms)
0.39
0.03
*
T
p
T
e
/QT time (ms)
0.08
0.66
T
p
T
e
/QT
c
(ms)
0.17
0.35
T
p
T
e
/QT
d
(ms)
0.06
0.71
T
p
T
e
/QT
cd
(ms)
0.07
0.69
100
80
60
40
20
10.00
20.00
30.00
40.00
COHb, %
T
peak
-T
end
dispersion
R
2
linear
=
0.039
Fig. 1.
A moderately significant positive relationship between
T
p
T
e
dispersion and COHb levels.
