Original research article

European Stroke Journal

2017, Vol. 2(1) 77–86
! European Stroke Organisation
Twelve-lead electrocardiogram 2016
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DOI: 10.1177/2396987316684706
ischaemic stroke journals.sagepub.com/home/eso

Jani Pirinen1,2,3, Jukka Putaala2, Karoliina Aarnio2, Aapo L Aro1,

Satu Mustanoja2, Juha Sinisalo1, Markku Kaste2,
Elena Haapaniemi2, Turgut Tatlisumak2,4 and Mika Lehto1

Abstract
Introduction: Ischaemic stroke at young age carries an increased risk for mortality in comparison to the general
population, but factors associated with mortality have been poorly studied. We studied the role of electrocardiogram
in mortality risk stratification in young stroke patients.
Patients and methods: The Helsinki Young Stroke Registry encompasses 1008 patients aged <50 years with ischaemic
stroke. We included 690 patients for this electrocardiogram substudy. Our endpoints were all-cause and cardiovascular
mortality. Cox regression models – adjusted for clinical and demographic characteristics – were used to identify the
electrocardiogram parameters associated with these endpoints.
Results: At a mean follow-up of 8.8 years, cumulative all-cause and cardiovascular mortality were 16.1 and 9.1%,
respectively. Factors associated with both endpoints included diabetes (type 1 for all-cause, type 2 for cardiovascular
mortality), heavy drinking, malignancy, as well as stroke severity and aetiology. Of the electrocardiogram parameters,
higher heart rate (hazard ratio 1.35 per 10/min, 95% confidence interval 1.21–1.49), a shorter P-wave (hazard ratio
0.78 per 10 ms decrement, 0.64–0.92) and longer QTc interval (1.09 per 10 ms, 1.03–1.16) were associated with
increased all-cause mortality. Only a higher heart rate (1.42 per 10/min, 1.24–1.60) was associated with death from
cardiovascular causes.
Conclusions: A higher heart rate during the subacute phase after stroke is associated with an elevated risk of all-cause
and cardiovascular mortality in young adults. A longer QTc interval is associated only with higher all-cause mortality.
P-wave characteristics and their possible association with mortality need further studies.

Keywords
Electrocardiogram, stroke, young stroke, prognosis, mortality
Date received: 22 September 2016; accepted: 27 November 2016

Introduction
Ischaemic stroke (IS) is known to decrease survival in
young adults.1,2 In this patient population, vascular dis-
eases are the most common cause of excess mortality,
while known factors increasing the risk for death
include more severe stroke, increasing age, higher
CRP levels, malignancy, heart failure, myocardial
infarction, heavy drinking, type 1 diabetes (T1D), dif-
ferent stroke aetiologies, recurrent stroke, leukoaraiosis
and accumulation of multiple risk factors.1,3–8
Since many electrocardiogram (ECG) findings are
related to increased mortality in the general population,
we hypothesised that ECG could be useful in assessing
the risk of mortality in young patients with IS.
1
Department of Cardiology, Heart and Lung Center, Helsinki University
Hospital, Helsinki, Finland
2
Clinical Neurosciences, Neurology, University of Helsinki and
Department of Neurology, Helsinki University Hospital, Helsinki,
Finland
3
Department of Clinical Physiology and Nuclear Medicine, HUS Medical
Imaging Center, Helsinki University Hospital and University of Helsinki,
Helsinki, Finland
4
Department of Neurology, Institute of Neuroscience and Physiology,
Sahlgrenska Academy, University of Gothenburg and Sahlgrenska
University Hospital, Gothenburg, Sweden
Corresponding author:
Jani Pirinen, Department of Cardiology, Heart and Lung Center, Helsinki
University Hospital, Haartmaninkatu 4, FIN-00029 Helsinki, Finland.
Email: jani.pirinen@helsinki.fi
78
Such findings in the general population have included
intraventricular conduction delay (IVCD), left ven-
tricular hypertrophy (LVH), T-wave inversions,
P-terminal force (PTF), atrial fibrillation (AF), a wide
QRS-T angle and bundle branch blocks (BBBs).9–16 In
older stroke populations, pathological Q-waves, AF
and a higher heart rate have been found as markers
of higher mortality.17–20 In contrast, a large study on
young stroke patients observed no association with AF
and increased mortality.21
To our knowledge, risk factors for cardiovascular
death after stroke in young adults have not been sys-
tematically studied and the value of ECG findings asso-
ciated with increased mortality has neither been
studied. In this study, we assessed the risk factors for
cardiovascular death in particular, and whether ECG
abnormalities are associated with long-term risk of
death after stroke in young adults.
Patients and methods
Study population
The relevant authorities approved the study, and it was
carried out at the Departments of Neurology and
Cardiology, Helsinki University Hospital. This retro-
spective study investigated data from the Helsinki
Young Stroke Registry, with 1008 consecutive patients
with first-ever IS aged 15–49 years and admitted to our
hospital between 1994 and 2007.22
Patients were examined according to a standard
protocol, involving a 12-lead ECG on admission and,
in most cases, also during the stay at the hospital.22 To
exclude changes related to the acute phase of stroke and
obtaining an ECG close to baseline, we analysed ECGs
taken 1–14 days after the onset of stroke symptoms and
at least one day after admission.23
Risk factors
We included in our analyses the following demographic
factors: age and sex, and the following comorbidities:
obesity, hypertension, smoking, dyslipidaemia, known
AF, cardiovascular disease, T1D, type 2 diabetes (T2D)
mellitus, malignancy and heavy drinking. Definitions of
the comorbidities are described in detail in the online-
only supplement (Table e1). Stroke characteristics
analysed were NIH Stroke Scale (NIHSS) score on
admission, stroke aetiology according to Trial of Org
10172 in Acute Stroke Treatment classification (with
modifications to better adapt the classification for
young patients; Supplementary Table e3), lesion size
(ordinal scale ranging from 1 to 4) and lesion multipli-
city (one or more lesions).24 A lesion was defined as
small when it was measured as <1.5 cm. A medium
European Stroke Journal 2(1)
size lesion was defined as a lesion of a cortical superficial
branch of the anterior, middle or posterior cerebral
artery. A large anterior lesion involved the complete ter-
ritory of the anterior or middle cerebral artery and a
large posterior lesion involved the complete territory of
the posterior cerebral artery with border zone territories.
Follow-up data
We obtained data on deaths and causes of death from
Statistics Finland. The reliability of this register is
described elsewhere.25 Follow-up data were obtained
until 31 December 2011.
Definition of endpoints
The primary endpoint was death from any cause. Our
secondary endpoint was death from cardiovascular dis-
ease, defined as any of the three primary reasons
(underlying cause of death, intermediate cause of
death or immediate cause of death) being a diagnosis
from 390 to 459 in ICD-9 or from category I in ICD-10.
Death due to index stroke was counted as both primary
and secondary endpoint regardless of time from stroke
onset.
ECG analysis
JPi, blinded to clinical data at time of analysis, analysed
the ECGs. In uncertain cases he consulted two senior
cardiologists (ML and AA) for consensus.
We considered the continuous ECG parameters
heart rate, P-wave duration, P-wave axis, PR interval,
QRS complex duration, QRS frontal axis, T-wave fron-
tal axis, corrected QT interval and QRS-T angle. The
dichotomised ECG parameters we considered were
IVCD, first-degree AV block, P-wave duration
<80 ms, PTF, LVH, pathological Q-waves, J-waves
(early repolarisation pattern), T-wave inversions,
BBBs, prolonged QTc, rhythm, QRS duration
>110 ms and frontal QRS-T angle >110 . Detailed def-
initions of ECG characteristics used in this registry are
previously published.23
Statistical analysis
We used the Cox proportional hazards model to inves-
tigate the factors associated with the endpoints. First,
we performed a univariate analysis and determined
which of the demographic factors, predefined risk fac-
tors and index stroke characteristics fell below signifi-
cance level of P < 0.10. For both endpoints, a unique
set of covariates was thus created for the multivariate
analysis. Second, we tested all of the significant param-
eters in multivariate models, one model for each
Pirinen et al. 79

endpoint. The ECG parameters were then added – one Table 1. Causes of 111 deaths during the follow-up.
at a time, in order to avoid overcorrection – into these
N (%)
models, creating an adjusted model for each ECG par-
a
ameter. To correct for the performed multiple partly Underlying cause of death cardiovascular 55 (50)
correlated ECG parameters, we applied a principal Coronary artery disease or myocardial infarction 17 (15)
component analysis of all ECG parameters to define Index stroke 13 (12)
the amount of underlying uncorrelated components. New ischaemic or haemorrhagic stroke 15 (14)
The resulted number of components needed to explain Cardiomyopathy 7 (6)
95% of the overall variability in ECG parameters was
Thrombophlebitis of lower extremities 1 (1)
8, which we used as a correction factor in Bonferroni
Endocarditis 1 (1)
correction. P < 0.05 was considered statistically signifi-
cant. Kaplan–Meier survival plots were finally created Aortic valve stenosis 1 (1)
to graphically demonstrate the major findings. We per- Underlying cause of death other 56 (50)
formed all analyses on SPSS 22.0 for Windows (SPSS than cardiovascular
Inc., IBM, Armonk, USA). Malignancy 24 (22)
Alcoholic liver disease 3 (3)
Alcoholic pancreatitis 3 (3)
Results Infection 3 (3)
A total of 690 patients fulfilled our inclusion criteria Accident, suicide or poisoning 8 (7)
and were included in the present study. Of the original Complications of type 1 diabetes 8 (7)
1008 patients, four patients were excluded due to false Systemic lupus erythematosus 2 (2)
primary diagnosis (stroke mimic), 48 due to unknown Muscle diseases 2 (2)
exact stroke date, 25 were treated only as outpatients Chronic obstructive pulmonary disease 2 (2)
and 241 had no ECG of good quality obtained during
Duodenal ulcer 1 (1)
the required time window. Thirty-three patients (4.6%)
a
received thrombolysis. Brain imaging was performed by In addition to these, eight other patients had a cardiovascular intermedi-
either CT or MRI on all patients: CT was performed on ate or immediate of death, hence 63 patients in the cardiovascular cause
of death group.
662 patients (95.9%) and MRI on 452 patients (65.5%).
On 424 patients (61.4%), both imaging modalities were
used. Compared with the excluded patients, the
included patients had higher NIHSS score, longer cor- drinking, malignancy, stroke aetiology, NIHSS score
rected QT interval, wider QRS-T angle, more cardio- and lesion size. Factors associated with cardiovascular
vascular disease and a different distribution of stroke death were age, hypertension, cardiovascular disease at
aetiology (Supplementary Table e3). Mean follow-up baseline, T2D, AF, heavy drinking, malignancy, stroke
of the study cohort was 8.8 years (interquartile range aetiology, NIHSS score and lesion size (data not
6.3–12.1). Supplementary Table e2 shows baseline shown). The multivariate analyses on demographic
comorbidities and medication data. and clinical factors were constructed including these
parameters (Tables 2 and 3). Factors associated with
all-cause mortality in the multivariate analysis were
Mortality age, T1D, heavy drinking, malignancy, NIHSS score,
Of our patients 111 (16.1%) died during follow-up of lesion size and stroke aetiology. Factors associated with
whom 63 (9.1%) died due to cardiovascular causes. cardiovascular mortality in the multivariate analysis
Fifteen patients died during the first 30 days after the were cardiovascular disease at baseline, T2D, heavy
index stroke. The most frequent primary causes of drinking, malignancy, NIHSS score, lesion size and
death were recurrent stroke, malignancy and coronary stroke aetiology.
artery disease. The most common cardiovascular causes
of death were coronary artery disease, index stroke and
recurrent stroke (Table 1).
ECG findings associated with long-term mortality
In the Bonferroni-corrected multivariate analysis, heart
Association between demographic and clinical factors rate, QTc interval and P-wave duration were associated
with death from any cause (Table 4). Only heart rate
and long-term mortality
was statistically significantly related to cardiovascular
In the univariate analyses, factors associated with all- death (Table 5). Kaplan–Meier survival plots of heart
cause mortality were age, hypertension, smoking, car- rate tertiles are presented for all-cause mortality and
diovascular disease at baseline, AF, T1D, heavy cardiovascular mortality (Figures 1 and 4).
80 European Stroke Journal 2(1)

Table 2. Risk factors for death from any cause. Multivariate analysis with Cox regression of different
parameters and their hazard ratio: demographics, comorbidities and index stroke characteristics, only those
significant in univariable analysis included.

HR (95% CI) P-value

Age, per year 1.04 (1.01–1.08) 0.019

Hypertension 1.29 (0.84–1.99) 0.242
Smoking 1.07 (0.69–1.65) 0.768
Cardiovascular disease 1.04 (0.59–1.81) 0.896
Known atrial fibrillation 1.17 (0.47–2.88) 0.740
Type 1 diabetes 3.11 (1.55–6.22) 0.001
Heavy drinking 2.88 (1.83–4.53) <0.001
Malignancy 7.62 (3.42–17.00) <0.001
NIHSS on admission, per point 1.06 (1.03–1.10) <0.001
Lesion size (reference: small)a
Medium 1.11 (0.63–1.95) 0.720
Large posterior 1.57 (0.76–3.24) 0.228
Large anterior 2.27 (1.26–4.08) 0.006
Aetiology (modified TOAST, reference: ICAD)
Large artery atherosclerosis 7.46 (2.14–26.07) 0.002
Cardioembolism, low-risk source 4.60 (1.12–18.92) 0.035
Other rare causes 9.25 (2.55–33.47) <0.001
Undetermined 6.11 (1.80–20.79) 0.004
Vertebral artery dissection 5.21 (0.97–28.02) 0.055
Cardioembolism, high-risk source 11.47 (3.07–42.88) <0.001
Small vessel disease 7.65 (1.96–29.87) 0.003
ICAD: Internal carotid artery dissection; NIHSS: National Institutes of Health Stroke Scale; TOAST: Trial of Org 10172 in
Acute Stroke Treatment.
a
See methods for definitions.

Table 3. Risk factors for death from cardiovascular cause. Multivariate analysis with Cox regression of different
parameters and their hazard ratio: demographics, comorbidities and index stroke characteristics, only those
significant in univariate analysis included.

HR (95% CI) P-value

Age, per year 1.01 (0.97–1.057) 0.573

Hypertension 1.22 (0.68–2.19) 0.504
Cardiovascular disease 2.11 (1.02–4.34) 0.043
Known atrial fibrillation 2.02 (0.69–5.91) 0.198
Type 2 diabetes 3.19 (1.43–7.10) 0.004
Heavy drinking 2.33 (1.27–4.27) 0.006
Malignancy 5.72 (1.78–18.34) 0.003
NIHSS on admission, per point 1.08 (1.04–1.12) <0.001
Lesion size (reference: small)a
Medium 1.18 (0.50–2.78) 0.702
Large posterior 3.97 (1.53–10.31) 0.005
Large anterior 3.58 (1.57–8.21) 0.003
Aetiology (modified TOAST, reference: ICAD)
Large artery atherosclerosis 6.74 (1.40–32.34) 0.017
(continued)
Pirinen et al. 81

Table 3. Continued.

HR (95% CI) P-value

Cardioembolism, low-risk source 4.69 (0.83–26.36) 0.081

Other rare causes 6.21 (1.17–32.97) 0.032
Undetermined 4.53 (0.97–21.04) 0.054
Vertebral artery dissection 4.45 (0.55–35.80) 0.161
Cardioembolism, high-risk source 7.66 (1.47–40.03) 0.016
Small vessel disease 12.50 (2.22–70.33) 0.004
ICAD: Internal carotid artery dissection; NIHSS: National Institutes of Health Stroke Scale; TOAST: Trial of Org 10172 in Acute
Stroke Treatment.
a
See methods for definitions.

Table 4. ECG parameters’ relation to death from any cause. Multivariate analysis with Cox regression, adjusted for age,
hypertension, smoking, type 1 diabetes, cardiovascular disease, known AF (except for rhythm), malignancy, heavy
drinking, stroke aetiology, NIHSS and lesion size.

Continuous ECG parameters HR (95% CI) Uncorrected P Corrected P

a
Heart rate , per 10/min 1.35 (1.21–1.50) <0.001 <0.001
P-wave duration, per 10 ms 0.79 (0.65–0.93) 0.004 0.033
P-wave axis, per 10 0.95 (0.87–1.04) 0.293 1
PR interval, per 10 ms 0.99 (0.90–1.07) 0.778 1
QRS duration, per 10 ms 0.97 (0.84–1.11) 0.711 1
QRS axis, per 10 1.02 (0.96–1.08) 0.477 1
Corrected QT interval, per 10 ms 1.09 (1.03–1.16) 0.006 0.047
T-wave axis, per 10 1.04 (1.00–1.07) 0.050 0.398
QRS-T angle, per 10 1.00 (0.95–1.05) 0.970 1
Dichotomous ECG parameters
Rhythm (AF versus sinus rhythm) 1.77 (0.69–4.50) 0.234 1
P-terminal force 1.99 (0.93–4.28) 0.076 0.609
LVH (Sokolow-Lyon) 0.92 (0.55–1.53) 0.749 1
LVH (Cornell voltage) 1.38 (0.73–2.60) 0.323 1
LVH (Cornell voltage duration) 1.73 (1.03–2.89) 0.038 0.302
Intraventricular conduction delay 0.60 (0.22–1.66) 0.325 1
T-wave inversion 0.78 (0.46–1.34) 0.368 1
Pathological Q-wave 0.96 (0.45–2.07) 0.925 1
J-wave 1.14 (0.62–2.11) 0.633 1
P-wave duration <80 ms versus >80 ms 4.04 (1.85–8.81) <0.001 0.004
Prolonged corrected QT interval 1.31 (0.78–2.18) 0.304 1
First-degree atrioventricular block 1.26 (0.54–2.92) 0.594 1
Bundle branch block 1.13 (0.40–3.21) 0.814 1
Broad QRS >110 ms 0.80 (0.38–1.68) 0.549 1
QRS-T angle >110 0.93 (0.49–1.77) 0.829 1
AF: atrial fibrillation; ECG: electrocardiogram; LVH: left ventricular hypertrophy; NIHSS: National Institutes of Health Stroke Scale.
a
Only considered for patients in sinus rhythm.

P-wave duration and all-cause mortality

with P-waves shorter than 80 ms, eight of whom died
We further investigated the role of P-wave duration and during follow-up. These patients had very variable
all-cause mortality. We tested dichotomising P-wave causes of death, and only four of them died due to
duration at a threshold of 80 ms. There were 16 patients cardiovascular causes.
82 European Stroke Journal 2(1)

Table 5. ECG parameters’ relation to death from cardiovascular disease. Multivariate analysis with Cox regression,
adjusted for age, hypertension, type 2 diabetes, cardiovascular disease, known AF (except for rhythm), malignancy, heavy
drinking, stroke aetiology, NIHSS and lesion size.

Continuous ECG parameters HR (95% CI) Uncorrected P Corrected P

Heart ratea, per 10/min 1.39 (1.22–1.57) <0.001 <0.001

P-wave duration, per 10 ms 0.89 (0.70–1.08) 0.251 1
P-wave axis, per 10 0.93 (0.82–1.04) 0.204 1
PR interval, per 10 ms 1.01 (0.91–1.11) 0.864 1
QRS duration, per 10 ms 1.02 (0.86–1.17) 0.938 1
QRS axis, per 10 1.00 (0.93–1.07) 0.945 1
Corrected QT interval, per 10 ms 1.07 (0.98–1.17) 0.109 0.869
T-wave axis, per 10 1.03 (0.99–1.07) 0.191 1
QRS-T angle, per 10 1.02 (0.96–1.07) 0.610 1
Dichotomous ECG parameters
Rhythm (AF versus sinus rhythm) 2.90 (0.92–9.12) 0.069 0.552
P-terminal force 1.91 (0.74–4.94) 0.184 1
LVH (Sokolow-Lyon) 1.15 (0.61–2.17) 0.666 1
LVH (Cornell voltage) 1.84 (0.90–3.78) 0.096 0.765
LVH (Cornell voltage duration) 1.98 (1.05–3.75) 0.035 0.282
Intraventricular conduction delay 1.13 (0.38–3.35) 0.832 1
T-wave inversion 0.89 (0.44–1.77) 0.731 1
Pathological Q-wave 1.01 (0.40–2.54) 0.990 1
J-wave 1.55 (0.72–3.33) 0.259 1
P-wave duration <80 ms versus >80 ms 2.57 (0.87–7.60) 0.089 0.712
Prolonged corrected QT interval 1.29 (0.66–2.50) 0.456 1
First-degree atrioventricular block 1.38 (0.48–3.97) 0.545 1
Bundle branch block 1.42 (0.42–4.84) 0.570 1
Broad QRS >110 ms 1.27 (0.55–2.95) 0.575 1
QRS-T angle >110 1.08 (0.52–2.25) 0.837 1
AF: atrial fibrillation; ECG: electrocardiogram; LVH: left ventricular hypertrophy; NIHSS: National Institutes of Health Stroke Scale.
a
Only considered for patients in sinus rhythm.

Higher heart rate was recently found to be asso-

Discussion
To our knowledge, this study is the first to identify ECG
findings associated with all-cause and cardiovascular
mortality in young adults with IS. It is the first study
to reveal factors associated with cardiovascular mortal-
ity in young adults with an IS. A higher heart rate was
related to increased all-cause and cardiovascular mor-
talities in our patients. We also found an association
between a longer corrected QTc interval and all-cause
mortality (Figure 2). We found a strong association
between a short P-wave and all-cause mortality, how-
ever; due to the relatively small number of deaths and
heterogeneous causes in this group, this most likely rep-
resents a chance finding. The non-significant association
between P-wave duration tertiles and all-cause mortality
emphasises the finding of only the very short, <80 ms, P-
waves being significant in our study (Figure 3).
ciated with increase in in-hospital mortality in a large
population of older stroke patients.20 Although our
study analysed the ECG in the subacute phase and
not the acute phase, as in the study of Eldur et al.,
the results of both studies strongly suggest that heart
rate is associated with mortality both in the elderly and
also in the younger IS patients.
There are many hypotheses on why a higher heart
rate is associated with higher mortality, observed in
many patient groups. Higher heart rate has been
linked to increased psychological stress, increased sym-
pathetic tone, decreased vagal tone, lack of physical
exercise, increased shear stress on arterial walls, inflam-
mation in arterial walls, arterial stiffness, endothelial
dysfunction, faster development of atherosclerotic
lesions, reduced angiogenesis and myocardial ischemia
due to a shorter diastolic time.26
Pirinen et al. 83

Figure 1. Kaplan–Meier plot of heart rate tertiles and all-cause mortality. Log rank P < 0.001.

Figure 2. Kaplan–Meier plot of QTc interval tertiles and all-cause mortality. Log rank P < 0.001.

A longer QTc interval is also associated with higher between longer QTc interval and cardiovascular mor-
mortality and cardiovascular mortality in the general tality, yet one would specifically think the causes of
population and even in older stroke patients,27–29 but death would be cardiovascular with this ECG
quite surprisingly we did not find an association abnormality.
84 European Stroke Journal 2(1)

Figure 3. Kaplan–Meier plot of P-wave duration tertiles and all-cause mortality. Log rank P ¼ 0.129.

Figure 4. Kaplan–Meier plot of heart rate tertiles and cardiovascular mortality. Log rank P < 0.001.

It is rather surprising that we did not find an asso- and cardiovascular) in the general population, and AF
ciation of any other ECG parameters with mortality, and pathological Q-waves have been associated with
since many of the parameters we analysed have earlier higher mortality also in older stroke populations.9–19
been associated with increased mortality (both all-cause As our patients’ causes of death were heterogeneous
Pirinen et al.
and the endpoint of cardiovascular death rather non-
specific, so it might be that other factors than cardiac
electrophysiological abnormalities explain the risk of
these endpoints.
The clinical factors associated with cardiovascular
mortality were as could be expected known cardiovas-
cular disease, heavy drinking, malignancy, markers of a
more severe stroke (higher NIHSS score, larger lesion)
and stroke aetiologies associated with existing cardio-
vascular disease (LAA, high-risk CE, other rare causes
and small vessel disease). The fact that T1D was asso-
ciated with all-cause mortality in this patient group was
expected based on earlier findings.1,5 T2D being asso-
ciated with cardiovascular, but not all-cause, mortality
was a rather surprising observation, because both T1D
and T2D increased both the all-cause and cardiovascu-
lar mortalities in the general population.30–32 T2D in
the young adults with IS may be a more aggressive,
early-onset form of T2D, and might have a poorer car-
diovascular prognosis compared with a later-onset
T2D.33 This finding needs, however, further investiga-
tions in young adults and in other populations.
Knowing that a higher heart rate means higher mor-
tality helps directing follow-up resources in stroke
patients. A high heart rate, among other clinical find-
ings could be a reason for taking a stroke patient to a
ward with more intense control and moreover, con-
sidered as a signal of having increased risk of death.
However, since the study was not an interventional
study, it does not reveal the possible beneficial effect
of lowering heart rate, e.g. with beta blockers.
Our study has its strengths and limitations. The
strengths include a relatively large population of
young IS patients with many variables considered for
multivariate analysis, systematic analysis of a large
scale of ECG parameters and a reliable database of
deaths and their causes. Limitations include the retro-
spective nature of this study and relatively unspe-
cific endpoints, representing various disease
mechanisms.
Conclusion
A higher heart rate during the subacute phase of stroke
is independently associated with a higher risk for death
from any cause and from cardiovascular disease in the
young with IS. Also, a longer QTc interval was asso-
ciated with higher all-cause mortality. The importance
of P-wave characteristics deserves to be further
investigated.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with
respect to the research, authorship, and/or publication of this
article.
85
Funding
The author(s) disclosed receipt of the following financial sup-
port for the research, authorship, and/or publication of this
article: The project was funded by the Heart Research
Foundation (Sydäntutkimussäätiö). Jani Pirinen also received
a grant from the Greta and Alfred Runeberg Foundation and
Finska Läkaresällskapet.
Ethical approval
Ethical approval for this study was obtained from the ethical
committee of the hospital district of Helsinki and Uusimaa
(approval number 73/13/03/00/11).
Informed consent
Written informed consent was obtained from all subjects
before the study.
Guarantor
JPi.
Contributorship
JPi: analysis of ECG strips, statistical analysis, obtaining
follow-up data and drafting the manuscript. JuP: building up
the patient registry and revising the manuscript. KA: obtaining
follow-up data and revising the manuscript. ALA: analysis of
ECG strips and revising the manuscript. SM: obtaining follow-
up data and revising the manuscript. JS: obtaining follow-up
data and revising the manuscript. MK: building up the patient
registry and revising the manuscript. EH: building up the
patient registry and revising the manuscript. TT: building up
the patient registry and revising the manuscript. ML: analysis
of ECG strips and revising the manuscript.
Acknowledgements
None.
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