International Journal of Cardiology 323 (2021) 118–123

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International Journal of Cardiology

journal homepage: www.elsevier.com/locate/ijcard

QTc interval in survivors of out of hospital cardiac arrest☆

A. Anilkumar a,⁎,1, E.J. Moore a,1, A.J. Gall a, E. Sammut a,b, P. Barman a
a
Bristol Heart Institute, University Hospitals Bristol NHS Foundation Trust, UK
b
University of Bristol, Bristol, UK

a r t i c l e i n f o a b s t r a c t

Article history: Background: QTc interval (QTc) prolongation is seen on the post-arrest electrocardiogram (ECG) of many out of
Received 27 May 2020 hospital cardiac arrest (OHCA) survivors. It remains unclear whether this is a transient phenomenon or a mani-
Received in revised form 23 July 2020 festation of an underlying arrhythmic substrate.
Accepted 26 August 2020 This observational study assessed the trend of QTc in an unselected group of patients presenting with OHCA. We
Available online 29 August 2020
sought to identify any relationship between QTc, gender and aetiology of arrest. We observed whether targeted
temperature management (TTM) is associated with malignant arrhythmia.
Keywords:
Out of hospital cardiac arrest
Method: We analysed 60 patients presenting with OHCA to the Bristol Heart Institute during a 20-month period.
QTc interval We measured QTc on admission and assessed for persistence, development and resolution of prolongation at up
Arrhythmia to 5 time points post-OHCA. Aetiology of arrest was divided into coronary, non-coronary or primary arrhythmic
Acute coronary syndrome (ACS) to investigate for patterns in QTc behaviour.
Results: 81.7% (49/60) of arrests were attributed to an acute coronary event. 55% (33/60) had QTc prolongation on
admission, of which 79% resolved. There were no significant differences in QTc behaviour by aetiology.
One patient presenting with a normal QTc, developed prolongation during admission and received a
genetic diagnosis of Long QT Syndrome. TTM was employed in 57/60, with no increased incidence of malignant
arrhythmia.
Conclusions: Prolonged QTc on admission does not imply a primary arrhythmic aetiology and resolves in the ma-
jority pre-discharge. However, an initial normal QTc post-OHCA does not preclude a diagnosis of Long QT syn-
drome, highlighting the importance of thorough investigations in these patients. TTM appears safe from a
cardiac perspective.
© 2020 Elsevier B.V. All rights reserved.

1. Introduction Given the high prevalence of myocardial ischaemia as a cause for

In the UK, there are approximately 60,000 out of hospital cardiac ar-
rests (OHCA) each year, Resuscitation is attempted by Emergency Med-
ical Services in 28,000 of these cases with only 8.6% patients surviving to
hospital discharge [1,2]. Around two thirds of cases of OHCA are attrib-
uted to a coronary cause, whether mediated by an acute coronary syn-
drome (ACS) or ischaemic scar [1,3,4]. However, 2% of patients show
no structural cardiac abnormality on autopsy [5], rising to 40% in pa-
tients aged ≤35 years [6] indicating the potential of a primary arrhyth-
mic cause for OHCA in this patient cohort. A previous study from our
unit has demonstrated that in a cohort of 217 cases admitted with an
OHCA, 10.1% were felt to have sustained a cardiac arrest due to a non-
coronary cause [7].
☆ All authors take responsibility for all aspects of the reliability and freedom from bias of
the data presented and their discussed interpretation
⁎ Corresponding author.
E-mail address: a.anilkumar@doctors.org.uk (A. Anilkumar).
1
Joint first authors.
OHCA, many centres have adopted the practice of immediate transfer
for angiography. The Bristol Heart Institute (BHI) is a tertiary centre
which serves a population of 5.29 million in the South West of England.
In this region, all survivors of OHCA without a clear non-cardiac cause
are transferred to the BHI for urgent angiography [8] and potential an-
gioplasty as per our care pathway. If intubated, patients are then trans-
ferred to intensive care, where iatrogenic lowering of body temperature
(targeted temperature management (TTM)) is generally employed for
its favourable effects on neurological recovery [9–11].
Post cardiac arrest, the appearance of a prolonged QTc interval on
the surface electrocardiogram (ECG) has been described [12,13]. It is un-
clear whether this is a transient phenomenon, or a manifestation of an
underlying arrhythmic substrate such as Long QT syndrome (LQTS).
Furthermore, QTc interval prolongation has been described in associa-
tion with TTM, although previous studies have not linked this with in-
creased incidence of malignant arrhythmias [12–16].
In this observational study, we sought to clarify the incidence of QTc
interval prolongation post-OHCA, the behaviour of QTc interval during
admission and persistence at discharge. Specifically, we aimed to

https://doi.org/10.1016/j.ijcard.2020.08.090
0167-5273/© 2020 Elsevier B.V. All rights reserved.
A. Anilkumar, E.J. Moore, A.J. Gall et al. International Journal of Cardiology 323 (2021) 118–123

identify any pattern between QTc behaviour and aetiology of arrest with
the hypothesis that the incidence of QTc prolongation on admission post
OHCA and subsequent behaviour may relate to aetiology of cardiac ar-
rest. Specifically, we were interested in the QTc on and after admission
in those with a primary arrhythmic cause of arrest and we hypothesised
that there may be a more prolonged QTc which persisted in these
patients.
We also sought to evaluate QTc alongside the use of TTM and inves-
tigate whether the use of TTM appears to be associated with the devel-
opment of further malignant arrhythmia.
2. Methods
A retrospective review of electronic and paper case notes was per-
formed of survivors of OHCA who were admitted to the BHI between
March 2014 and November 2015.
Inclusion criteria included patients who sustained OHCA requiring
intubation pre-hospital or on arrival to hospital. All patients included
underwent immediate coronary angiography on arrival, and had a min-
imum of an ECG at the point of admission (“time-zero”) and at least one
further ECG over the course of admission (in order to assess trend in QTc
interval).
Baseline demographics were recorded for each patient, including
age, gender and comorbidities, blood test results and angiogram
findings.
ECGs recorded throughout the admission for each patient were
reviewed and grouped into time ‘zero’ –at time of admission,
‘24–48 h’, ‘3–5 days’, ‘6–10 days’ after admission and ‘pre-discharge’ if
beyond this time point. For each patient, ECGs for each time interval
were analysed, and the manually determined QTc documented. The
QT interval was measured by two clinicians - a ruler was used to mea-
sure the start of the QRS complex to the point where the steepest gradi-
ent of the downslope of the T wave crossed the isoelectric line, in lead
V5 or V6. The R-R interval was measured in the same lead and the QTc
was calculated using Bazett's formula. A prolonged QTc was defined as
≥460 ms for males and ≥ 470 ms for females.
Follow up and further investigations were recorded by review of
electronic case notes. At the BHI, patients suffering from non-coronary
cardiac arrests have a transthoracic echocardiogram (TTE), a cardiac
MRI and then potentially specific investigations such as Ajmaline or ge-
netic testing based on individual case details. Patients then go on to re-
ceive an ICD before discharge unless a reversible cause is identified. In
those who received an implantable defibrillator device, we reviewed
device interrogation routine follow up data to investigate for subse-
quent aborted arrhythmic sudden cardiac death.
Statistical analyses were performed via Excel, Graphpad Prism, and
IBM SPSS.
3. Results
patients died as a result of a hypoxic brain injury, one (6.25%) due to car-
diogenic shock and one (6.25%) due to septic shock secondary to aspira-
tion pneumonia. Details on baseline demographics of the study cohort
are included in Table 1.
30-day mortality data was available for 59 patients, with 42/59
(71.2%) patients being alive at this time-point. At 6 months post-
OHCA, 40/59 patients (66.7%) were still alive.
3.2. Cardiac arrest
The majority of cardiac arrests (56/60, 93.3%) were witnessed in the
pre-hospital setting. The predominant initial rhythm was ventricular
tachycardia (VT) or ventricular fibrillation (VF) (57/60 patients,
95.0%). Time taken to achieve ROSC ranged from 1 to 79 min, with a
mean downtime of 24.5 min. On presentation to our centre, the majority
of patients were found to be acidotic on initial blood gas, with 3/60
(5.0%) patients having a pH <7.0 (median (SEM) pH 7.2 ± 0.02, range
6.80–7.43). There was a significant difference in pH of the 16 patients
who died (median (SEM) 7.17 ± 0.045), range 6.80–7.38) when com-
pared to that of the survivors (median (SEM) 7.23 ± 0.018, range
6.80–7.43), p = 0.046.
39/60 (65.0%) patients had a lactate >3.0 mmol/L (4.9 ± 0.45 mmol/L,
range 1.2–16.0 mmol/L) and in 4/60 (6.7%) it was >10.0 mmol/L.
Initial electrolytes revealed hypokalaemia in 13 (21.7%) patients and
hyperkalaemia in 4 patients (6.7%) (K+ 3.85 ± 0.11 mmol/L, range
2.6–5.9). Hypomagnesaemia and hypocalcaemia were identified in 9
(15.0%) and 18 (30.0%) patients respectively (Mg2+ 0.84 ±
0.04 mmol/L, range 0.56–2.22, Ca2+ 2.22 ± 0.01 mmol/L, range
1.89–2.48). On univariate linear regression, QTc interval was not associ-
ated with electrolyte (Mg2+, K+, Ca2+) imbalances, lactate or pH
level. See Table 2 for further details.
3.3. QTc interval
Of the 60 individuals, 33 (55%, 28/51 males and 5/9 females) had a
prolonged QTc on admission (time zero). Seven of the 33 (21%) had a
persistent QTc prolongation at discharge. 13/60 (22%) patients had a
normal QTc interval at time zero but developed QTc prolongation during
their admission. This resolved in 11/13 (85%).
In total therefore, 46/60 (77%) demonstrating documented QTc pro-
longation at some stage post-OHCA.
Fig. 1 and Table 3 show detailed results on behaviour of the QTc in-
terval over the course of admission according to aetiology of arrest
and gender.

3.1. Demographics Table 1

Cohort population demographics.

In total, from 217 patients with OHCA during the study period, the Demographics n
final study cohort consisted of 60 patients (males 51/60 (85%), mean Age (years) (mean, range) 63.1 (21–86)
age 63.1 years (range 21–86 years)). 44/60 patients (73.3%) had at Male 51 85%
least one documented co-morbidity, of which the most common were
Comorbidities
hypertension (50%), dyslipidaemia (35%) and pre-existing ischaemic Hypertension 30 50%
heart disease (30%). The mean number of ECGs available per patient Diabetes 12 20%
for analysis was 3.0 (range 2–5). IHD 18 30%
The majority (57/60 patients, 95.0%) of patients underwent TTM to CKD (stage 3–5) 5 8%
Smoker 10 17%
32–34 °C for 24 h, as per trust protocol. There was no further incidence
Dyslipidaemia 21 35%
of cardiac arrest leading to a resuscitation attempt within the patients History of atrial arrhythmia 4 7%
studied during admission or the follow up period. Heart failure 4 7%
All 60 survived to discharge from ITU, with 44/60 (73.3%) patients Previous MI 17 28%
surviving to discharge from hospital. The mean length of stay was Previous PCI 7 12%
Previous CABG 5 8%
24.8 days (range 4–381 days). Of the 16 patients who died, 14 (87.5%)

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A. Anilkumar, E.J. Moore, A.J. Gall et al. International Journal of Cardiology 323 (2021) 118–123

Table 2 3.4. Cause of arrest

Cardiac arrest variables.

Number Proportion (%) 3.4.1. Coronary-related

Electrolytes
31/60 (51.7%) patients (26/51 (51.0%) male) arrested secondary to
Potassium (mmol/L) an acute coronary syndrome (ACS) and were subsequently
>5.0 7 11.7 revascularised. Mortality in this subgroup was 29.0% (9/31). Of the 31
3.5–4.9 32 53.3 patients in the ACS subgroup, 15 (48.4%) had a prolonged QTc interval
<3.5 13 21.7
on admission. Of the 22/31 patients who survived to discharge, two
Unknown 8 13.3
Magnesium (mmol/L) (8.7%) had a persistent prolonged QTc. The reduction in QTc from ad-
>1.0 12 20.0 mission to pre discharge was significant in men (p = 0.011), but not
<0.7 9 15.0 in women (p = 0.617). None of the ACS patients went on to receive
Unknown 6 10.0 an implantable cardioverter defibrillator.
Calcium (mmol/L)
>2.6 0 0.0
18/60 (30.0%) had coronary artery disease with no culprit lesion iden-
<2.2 18 30.0 tified (non-culprit CAD), 100% male, age 43–83 years. These patients were
Unknown 2 3.3 found to have coronary disease at angiography which was not felt to be
Lactate (mmol/L) causing an acute coronary syndrome by the consultant operator. Mortal-
≥10 5 8.3
ity in this subgroup was 22.2% (4/18). Of the 18 patients in the non-culprit
3.0–9.9 35 58.3
0–2.9 15 25.0 CAD subgroup, 12 (66.7%) had a prolonged QTc interval on admission. Of
Unknown 5 8.3 the 14/18 patients who survived to discharge, four (28.6%) had a persis-
pH tent prolonged QTc. The reduction in QTc from admission to pre-
≤7.00 3 5.0 discharge was significant within this group (p = 0.019, all male).
7.01–7.34 44 73.3
Of the 14 patients with non-culprit CAD surviving to discharge,
7.35–7.45 8 13.3
Unknown 5 8.3 12/14 (85.7%) were discharged with an ICD with the remaining two

Fig. 1. Line graph showing change in QTc during admission according to aetiology and gender.

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A. Anilkumar, E.J. Moore, A.J. Gall et al. International Journal of Cardiology 323 (2021) 118–123

Table 3
Median QTc interval values for each subgroup.

Subgroup Timepoint QTc admission

to discharge
Time-zero (ms) 24–48 h (ms) 3–5 days (ms) 6–10 days (ms) Pre-discharge (ms)

ACS All 458 ± 9.8 448 ± 12.7 426 ± 11.8 413 ± 18.6 400 ± 17.5 ⁎0.049
Male 457 ± 8.8 438 ± 14.5 428 ± 13.1 393 ± 17.6 397 ± 15.8 ⁎0.011
Female 515 ± 34.4 503 ± 22.3 424 ± 30.4 498 462 ± 35.8 0.617
Non-culprit CAD All 480 ± 19.5 464 ± 25.1 443 ± 12.3 507 ± 27.8 416 ± 14.9 ⁎0.019
Male 480 ± 19.5 464 ± 25.1 443 ± 12.3 507 ± 27.8 416 ± 14.9 ⁎0.019
Female – – – – – –
Non-coronary All 503 ± 21.6 500 ± 16.0 459 ± 26.4 466 ± 25.4 418 ± 23.5 0.178
Male 511 ± 24.8 No data 491 ± 31.5 433 ± 17.0 389 ± 16.8 ⁎0.011
Female 432 ± 35.1 500 ± 16.0 427 ± 32.4 484 ± 36.4 475 ± 41.0 0.482
⁎ Denotes p significance ≤ 0.05.

patients being transferred to another hospital with a recommendation
for ICD insertion locally. 11/12 (91.7%) received a dual chamber ICD
and 1/12 (8.3%) received a cardiac resynchronisation defibrillator
(CRT-D). There was no device therapy in the 11 patients who received
a dual chamber ICD at a mean follow-up of 43.4 months. The patient
who received a CRT-D received one episode of therapy consisting anti-
tachycardia pacing for ventricular tachycardia followed by shock ther-
apy for ventricular fibrillation.
continued to improve afterwards in the majority of patients with a cor-
onary aetiology. In contrast, the median QTc interval prolonged during
TTM before improving to less than pre-TTM duration after cessation of
TTM in the majority of patients in the non-coronary subgroup. This
was however not associated with any increased incidence of malignant
arrhythmia.
4. Discussion

3.4.2. Non-coronary cohort
9/60 (15.0%) patients had normal/near normal coronary arteries on
coronary angiography post OHCA (5/9 (55.6%) males (21–76 years)
and 4/9 (44.4%) females (28–74 years)). Mortality in this subgroup
was 11.1% (1/9). 8/9 (88.9%) patients survived to discharge from
hospital.
The final diagnosis within the non-coronary cohort was variable:
Patient 1 received a diagnosis of Wolff-Parkinson-White syndrome
and underwent an accessory pathway ablation. Patient 2 had a loop re-
corder implanted in-situ at the time of arrest, which demonstrated slow
atrial fibrillation degenerating into ventricular fibrillation deemed to be
the aetiology for cardiac arrest and went onto receive a pacemaker. Pa-
tient 3 went onto receive a diagnosis of hypertrophic cardiomyopathy.
Patient 4 received an ICD before discharge, but was not investigated lo-
cally. Patient 5 had a negative ajmaline test and was diagnosed with
early repolarisation syndrome. Patient 6 had a family history of sudden
cardiac death but did not receive a formal diagnosis - this patient re-
ceived an ICD and has subsequently received successful device therapy.
Patient 7 received a genetic diagnosis of long QT syndrome, with KCNH2
mutation. Patient 8 received a diagnosis of idiopathic VF and underwent
a VF ablation, before going onto receive an ICD.
On admission, 5/9 patients (55.6%) had a prolonged QTc interval,
with this resolving in all five of these patients at discharge. Overall the
reduction seen in QTc was not significant (p = 0.178) however when
analysed by gender, it was significant in men (p = 0.011) but not in
women (p = 0.482). Of the four patients with a normal QTc on admis-
sion, 2/4 (50%) developed a prolonged QTc interval during their admis-
sion which persisted at the point of discharge. One of these two patients
went onto receive a diagnosis of Long QT Syndrome (patient 7).
6/8 patients (75%) within this cohort had an ICD inserted. 4/6 pa-
tients have been followed up locally, with a mean follow-up of
46.9 months. Only 1 patient (25%) has received successful device ther-
apy for ventricular fibrillation (patient 6).
There was no significant difference in QTc at time zero (p = 0.151)
or pre discharge (p = 0.721) between the three groups (ACS, non-
culprit CAD and non-coronary) as determined by one-way ANOVA.
3.5. QTc and TTM
57/60 (95%) received targeted temperature management for 24 h
after admission. Median (SEM) QTc interval improved during TTM and
In this observational study we provide a descriptive account of the
admission and behaviour of QTc interval in a non-selected group of pa-
tients presenting with OHCA.
Our data demonstrates that a prolonged QTc interval was present in
more than half of our study population at time of admission. However,
our data shows that the QTc interval resolves to within the normal
range in the majority.
More detailed analysis by one-way ANOVA shows no significant dif-
ference between QTc on admission or pre-discharge, between the sub-
groups, according to aetiology of cardiac arrest. There was a trend
towards a less prolonged mean QTc during admission in those with an
acute coronary cause. Those presenting with a non-culprit coronary
cause more frequently had a prolonged QTc at discharge though only
the patient with impaired ventricular function requiring CRT in this sub-
group went on to receive appropriate device therapy- a condition which
in itself promotes ventricular arrhythmia.
The probability of QTc prolongation at discharge was not related
to admission blood tests. Patients with blood abnormalities known
to prolong the QT interval (hypokalaemia, hypocalcaemia,
hypomagnesaemia) were not at an increased risk of QTc interval prolon-
gation on admission (Table 2) in this patient cohort.
Current literature suggests pH is an independent factor associated
with survival to discharge [17], this supports our finding of a significant
difference in pH between patients who survived and those who died.
The literature with reference to QTc interval post-OHCA is limited
and variable. Weitz and colleagues [12] observed a median QTc interval
of 470 ms in their series of twenty patients admitted after OCHA. How-
ever, Storm et al. [16] quote a normal median QTc interval of 440-
460 ms post-OHCA but prior to TTM in their study of 34 patients.
Almost all (95%) of patients within our cohort underwent therapeu-
tic hypothermia (TTM), in keeping with the current Resuscitation Coun-
cil guidelines [9]. Therapeutic hypothermia has been shown to be
neuroprotective and improve mortality after OHCA, but is also associ-
ated with a prolonged QTc interval in a population already at increased
risk of life-threatening arrhythmia [11,13–15]. Previous studies have
recognised QTc interval prolongation during TTM, with no increased
risk of malignant arrhythmia [12,16]. Given almost all patients included
in this study underwent TTM, it was not possible to explore the effects of
TTM on QTc however the absence of malignant arrhythmia while in ITU
is a reassurance. There was some difference noted in response of QTc
whilst on TTM between patients according to subgroup however a

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A. Anilkumar, E.J. Moore, A.J. Gall et al.
specific study would need to be conducted to draw conclusions regard-
ing this.
Of the nine individuals with a non-coronary cause, there was a var-
iable pattern in QTc trend during admission. Five patients had a
prolonged QTc interval at presentation however this resolved. Two pa-
tients had a normal QTc interval on admission developed a prolonged
QTc during admission which persisted to discharge. One of these pa-
tients going onto receive a genetic diagnosis of Long QT Syndrome
type 2 making the important point that a normal admission QTc interval
does not preclude a diagnosis of long QT syndrome. Numbers are too
small to make a definitive conclusion from this.
The UK national survival rate to discharge for patients admitted to
ICU in a comatose state following OHCA in 2016 was 40–50% [9]. Our
study showed a higher rate than the national average, with 73% surviv-
ing to hospital discharge. This may reflect our centre being a primary PCI
centre that treats a large volume of OHCA patients, combined with the
fact we exclusively included patients with OHCA of cardiac aetiology.
In keeping with current National Institute for Health and Care Excel-
lence (NICE) guidance [18], all patients with serious ventricular arrhyth-
mia without a treatable cause were offered an ICD. Interestingly, within
our cohort there were two patients who were identified as having treat-
able causes for their arrhythmias, treated with accessory pathway abla-
tion and dual chamber pacemaker.
4.1. Clinical implications
In this observational study, we demonstrate that despite more than
half of patients being shown to have a prolonged QTc interval post-
OHCA, this is seen to resolve in the vast majority. It is important to
note that most patients who suffer a cardiac arrest and have a prolonged
QTc interval on admission do not have a primary arrhythmic aetiology
to their arrest. Whilst QTc prolongation in post-OHCA in patients under-
going TTM is common, it does not in itself appear to be arrhythmogenic.
Thorough investigation is required in all patients presenting with OHCA
without a clear coronary culprit, as importantly, a normal QTc on admis-
sion does not preclude a diagnosis of Long QT. Serial ECGs should be
measured during admission to assess QTc behaviour.
4.2. Limitations
This was a retrospective study and therefore suffers some inherent
bias. We however studied consecutive unselected patients meeting in-
clusion criteria and our data are comparable to other studies in terms
of patient characteristics.
- Our study included relatively small numbers of patients. We appre-
ciate that to make substantial conclusions within subgroups of
aetiology of arrest and gender, we would need to have included a
larger number of patients overall but feel our data provides basis
for further larger studies. Additionally, we would like to draw atten-
tion to previous observational studies with larger cohorts including
approximately 100–300 cases using data spanning 4 years or longer
[19–21], which is comparable to our cohort with a study length of
only 20 months.
For full analysis of temporal behaviour of QTc interval post-OHCA,
serial ECGs at frequent, pre-specified time-points would be required.
While all patients within this cohort had an admission (“time-zero”)
ECG and at least one further ECG available to assess trend, many did
not have ECG data for all five time-points. This is attributable to the
continuous cardiac monitoring available on the intensive care and
coronary care units. Furthermore, future prospective study with par-
ticipants recruited over a longer time frame would be able to assess
the trend following discharge with better accuracy.
- Almost all patients included in the study underwent TTM as part of
routine post OHCA care. This means that we were unable to specifi-
cally assess the impact of TTM on QTc interval. However, it is
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International Journal of Cardiology 323 (2021) 118–123
reassuring that none of the patients sustained further in-hospital
cardiac arrhythmia or arrest, suggesting TTM is safe.
- The selection criteria for the study was limited to patients who were
admitted post OHCA, who required intubation and underwent im-
mediate coronary angiography and had at least two 12 lead ECGs
during admission. Though not an exclusion criteria, the vast majority
of patients had sustained arrest with shockable rhythms, and we
recognise that our findings may not be relevant for non-shockable
rhythms.
- Many patients demonstrated a degree of coronary artery disease
without presenting with an acute coronary syndrome. The results
within this group show a heterogenous QTc pattern - this may be
due to this cohort of patients representing a varied and heteroge-
nous group or may simply reflect the small numbers included. The
aim of this study was to explore the relevance of QTc in more general
terms relating to aetiology, specifically primary arrhythmic causes.
We recognise that larger numbers and more detailed assessment
of patients in this subgroup would be needed to draw conclusions.
- Many drugs given for OHCA such as amiodarone are known to affect
QTc interval. Unfortunately this data was not reliably available in
this study due to pre-hospital administration and could not be reli-
ably correlated with 12 lead ECG at this time.
4.3. Future research
Although this study suggests that the majority of patients show res-
olution of an acquired long QT post-OHCA, more comprehensive serial
ECG data, and larger numbers of patients in each subgroup would better
elucidate this. Given the impact of some drugs on QTc it would be inter-
esting to have been able to explore this in more detail.
5. Conclusions
Despite more than half of patients having a prolonged QTc interval
post-OHCA, this resolves in the vast majority. There is no distinct pat-
tern in QTc according to aetiology of arrest and most patients who suffer
a cardiac arrest and have a prolonged QTc interval on admission do not
have a primary arrhythmic aetiology to their arrest. Importantly, a nor-
mal QTc interval on the admission ECG does not preclude a diagnosis of
Long QT syndrome. Larger, prospective studies are warranted to draw
firm conclusions.
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