;

Causes of Death and Predictors of 5-Year Mortality in

Young Adults After First-Ever Ischemic Stroke
The Helsinki Young Stroke Registry
Jukka Putaala, MD; Sami Curtze, MD, PhD; Sini Hiltunen, MD; Heli Tolppanen, MD;
Markku Kaste, MD, PhD; Turgut Tatlisumak, MD, PhD

Background and Purpose—Data on mortality and its prognostic factors after an acute ischemic stroke in young adults are
scarce and based on relatively small heterogeneous patient series.
Methods—We analyzed 5-year mortality data of all consecutive patients aged 15 to 49 with first-ever ischemic stroke
treated at the Department of Neurology, Helsinki University Central Hospital, from January 1994 to September 2003.
We followed up the patients using data from the mortality registry of Statistics Finland. We used life table analyses for
calculating mortality risks. Kaplan–Meier method allowed comparisons of survival between clinical subgroups. We used
the Cox proportional hazard model for identifying predictors of mortality. Stroke severity was measured using the
National Institutes of Health Stroke Scale and the Glasgow Coma Scale.
Results—Among the 731 patients (mean age, 41.5⫾7.4 years; 62.8% males) followed, 78 died. Cumulative mortality risks
were 2.7% (95% CI, 1.5% to 3.9%) at 1 month, 4.7% (3.1% to 6.3%) at 1 year, and 10.7% (9.9% to 11.5%) at 5 years
with no gender difference. Those ⱖ45 years of age had lower probabilities of survival. Among the 30-day survivors
(n⫽711), stroke caused 21%, cardioaortic and other vascular causes 36%, malignancies 12%, and infections 9% of the
deaths. Malignancy, heart failure, heavy drinking, preceding infection, type 1 diabetes, increasing age, and large artery
atherosclerosis causing the index stroke independently predicted 5-year mortality adjusted for age, gender, relevant risk
factors, stroke severity, and etiologic subtype.
Conclusions—Despite the overall low mortality after an ischemic stroke in young adults, several recognizable subgroups
had substantially increased risk of death in the long term. (Stroke. 2009;40:2698-2703.)
Key Words: cerebral infarct 䡲 mortality 䡲 prognosis 䡲 risk factors 䡲 stroke in young adults

I schemic stroke is the second leading cause of death

worldwide.1 Although mortality rates in young adults with
ischemic stroke are low compared with similar older patients,
they still sustain clearly more deaths than the young in the
general population.2 Giving the potentially disastrous impact
of a stroke in a young adult, it is important that the treating
physician will be able to give as accurate prognostic infor-
mation as possible early in the course of the disease. In
addition, information on long-term outcome and factors
associated with mortality help in optimizing secondary pre-
vention strategies.
Earlier studies on long-term mortality in young adults after
an ischemic stroke have involved rather modest numbers of
patients, may have had incomplete follow-up, may have been
unpowered for multivariate analyses, or have not analyzed all
relevant factors affecting mortality risk.2–7 Models for pre-
dicting outcome after stroke have been developed,8 but
because young patients typically are underrepresented in
randomized trials and data sets—and because stroke charac-
teristics between younger and older patients differ—such
models may not apply to those of younger ages. Therefore,
we decided to analyze death rates, causes of death, and
predictors of 5-year mortality in a large, consecutive,
hospital-based defined cohort of young patients with first-
ever ischemic stroke.
Patients and Methods
This study was approved by the Ethics Committee and carried out at
the Department of Neurology, Helsinki University Central Hospital.
Our hospital has the only neurological emergency room for a defined
population of 1.5 million. In Finland, practically all patients with
stroke are treated in the hospital regardless of symptom severity. In
the present study, we included all consecutive patients aged 15 to 49
years with first-ever ischemic stroke from January 1994 to Septem-
ber 2003 entered into the Helsinki Young Stroke Registry according
to previously published, clearly defined inclusion and exclusion
criteria.9
All patients underwent a routine range of laboratory and other
diagnostic testing, which are described in detail elsewhere.9 Risk
factor information was obtained from the medical records. We

Received April 6, 2009; accepted May 1, 2009.

From the Department of Neurology, Helsinki University Central Hospital, Helsinki, Finland.
Correspondence to Jukka Putaala, MD, Department of Neurology, Helsinki University Central Hospital, Haartmaninkatu 4, FIN-00290, Helsinki,
Finland. E-mail jukka.putaala@hus.fi
© 2009 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STROKEAHA.109.554998

2698
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 Putaala et al Mortality in Young Patients With Ischemic Stroke 2699

defined family history of any stroke as a history of ischemic or Table 1. Selected Baseline Variables of the Study Population
hemorrhagic stroke, or transient ischemic attack, in a first-degree (Nⴝ731)
relative. Dyslipidemia was defined as on lipid-lowering medication
or total cholesterol level ⱖ5.0 mmol/L (193 mg/dL), low-density Demographics
lipoprotein level ⱖ3.0 mmol/L (116 mg/dL), or high-density li- Age, years (⫾SD) 41.5 (⫾7.4)
poprotein level ⬍1.0 mmol/L (39 mg/dL). A patient was defined as
a smoker if smoking regularly ⱖ1 cigarettes per day within the year Age ⱖ45 years 348 (47.6)
before stroke. Hypertension was defined as treated with antihyper- Male gender 459 (62.8)
tensive medication or a history, or present diagnosis, of hypertension Risk factors
according to the 2003 World Health Organization criteria as systolic
blood pressure ⱖ140 mm Hg and/or diastolic blood pressure Family history of any stroke 91 (12.4)
ⱖ90 mm Hg. We defined obesity as body mass index ⱖ30 kg/m2 or Dyslipidemia 468 (64.0)
patient clearly stated as heavily obese in case body mass index data
Cigarette smoking 345 (47.2)
were not available. Recorded cardiovascular diseases included cor-
onary heart disease, heart failure (ejection fraction ⬍55%), previous Hypertension 280 (38.3)
myocardial infarction, and peripheral arterial disease. We recorded Obesity 76 (10.4)
separately diabetes mellitus Types 1 and 2 and defined them as
Coronary heart disease 41 (5.6)
treated or presently diagnosed according to the 1999 World Health
Organization criteria as fasting plasma glucose ⱖ7.0 mmol/L (126 Heart failure 33 (4.5)
mg/dL). Patients drinking an estimated amount of ⬎200 g of pure Myocardial infarction 29 (4.0)
alcohol per week regularly were considered heavy drinkers. We
defined preceding infection as documented symptoms of any infec- Peripheral arterial disease 16 (2.2)
tion or diagnosis of infectious disease within 1 month before stroke. History of transient ischemic attack 80 (10.9)
Obstructive sleep apnea was defined as apnea–hypopnea index ⱖ5 Diabetes mellitus, Type 2 49 (6.7)
with clinical symptoms. In addition, we recorded a history of
transient ischemic attack, presence of chronic or paroxysmal atrial Diabetes mellitus, Type 1 30 (4.1)
fibrillation, and migraine. The latter was defined according to the Atrial fibrillation 26 (3.6)
International Headache Society criteria.10 History of migraine 128 (17.5)
We measured stroke severity at admission for each patient by
using the National Institutes of Stroke Scale Stroke Scale (NIHSS) Heavy drinking 121 (16.6)
and the Glasgow Coma Scale (GCS). If a NIHSS score was not Preceding infection 86 (11.8)
available from the medical records, it was assessed by a single
Obstructive sleep apnea 31 (4.4)
investigator (J.P.) based on documented patient examination using a
previously published algorithm.11 Retrospective assessment of Active malignancy 11 (1.5)
NIHSS score has been validated and suggested to be reliable and Stroke severity
unbiased.12 Based on NIHSS, stroke severity was classified as
NIHSS score, mean (median; range) 5.3 (3; 0–27)
follows: mild (NIHSS score 0 to 6), moderate (7 to 14), or severe
(ⱖ15). Impaired consciousness was defined as GCS score ⬍15. Mild, NIHSS score 0–6 554 (75.8)
Stroke etiology was classified according to the Trial of Org 10172 Moderate, NIHSS score 7–14 101 (13.8)
in Acute Stroke Treatment criteria.13 Stroke subtype was assigned to
each patient by pairs of investigators and in case of discrepancy, the Severe, NIHSS score ⱖ15 76 (10.4)
patient records were reviewed by a senior investigator and the final GCS score, mean (median; range) 14.6 (15; 3–15)
categorization was based on a consensus agreement of all these. GCS score ⬍15 76 (10.4)
We followed up the patients using data from the mortality registry
at Statistics Finland, the central statistical office of the country. Each Acute treatment
death, its certificate, and the corresponding personal information in Intravenous alteplase 34 (4.7)
the computerized population register are crosschecked. Thus, due to Stroke etiology (TOAST)
legislation and death certification practices, Finnish mortality data
have been assessed to be exceptionally reliable.14 Onset of stroke Large artery atherosclerosis 60 (8.2)
symptoms was considered the starting point for follow-up. If the Cardioembolism 131 (17.9)
exact date of onset was unknown, we used the first day of the month
Small vessel disease 99 (13.5)
when the stroke was known to occur as the date of onset.
Deaths in the mortality register are classified according to the Other determined etiology 180 (24.6)
Finnish Edition of the International Classification of Diseases, 9th Undetermined etiology 261 (35.7)
Revision from 1994 to 1996 and the 10th Revision since 1997. In
addition to primary cause of death, we recorded the contributory Data are mean (⫾SD) or n (%) unless otherwise indicated.
causes on the death certificate. We categorized causes of deaths into TOAST indicates Trial of Org 10172 in Acute Stroke Treatment.
ischemic or hemorrhagic strokes, cardioaortic causes, other vascular
causes (eg, pulmonary embolism), malignancies, infections, and ses. All statistical analyses used SPSS 17.0 for Macintosh (SPSS Inc,
miscellaneous causes. Chicago, Ill). Two-sided values of P⬍0.05 were considered
We estimated cumulative mortality risks and 95% CIs with significant.
Kaplan–Meier analysis. Actual annual risks were calculated from
Kaplan–Meier data with the Life Tables function. Average annual
rate was calculated using the formula 1⫺[(1⫺Ic)1/n], where Ic is Results
cumulative mortality rate at n years. Only patients who survived the Table 1 shows the baseline data of the 731 consecutive
first 30 days after the index stroke were included in the subsequent patients with complete 5-year follow-up. Of these, 78 had
analyses. ␹2 and Fisher exact tests allowed comparisons of propor- died. During the first 30 days, 20 patients died giving a
tions of causes of death. We used the Cox proportional hazards
model for univariate and multivariate risk factor analyses. A predic-
case-fatality rate of 2.7% (95% CI, 1.5% to 3.9%). One-year
tion model using a backward stepwise method was constructed by cumulative mortality risk was 4.7% (95% CI, 3.1% to 6.3%),
selecting significant or relevant variables from the univariate analy- but annual mortality fell to a level ranging from 1.4% to 1.9%
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2700 Stroke August 2009
in the subsequent years. Average annual mortality was 2.2%.
Cumulative 5-year mortality risk was 10.7% (95% CI, 9.9%
to 11.5%) in the study population. In contrast to roughly 2
times higher risk of death in those aged 45 to 49 compared
with those ⬍45 (cumulative 5-year risk 14.7% [95% CI,
13.1% to 16.3%] versus 7.0% [6.4% to 7.6%]), mortality
curves showed no gender difference (Figure 1). Those with
large artery atherosclerosis or cardioembolism had overall
higher risks of death compared with patients with small
vessel disease, undetermined etiology, or other determined
etiology (Figure 2).
Proportions of causes of death in those surviving the first
30 days, but who died within the 5-year observation (n⫽58),
are shown in Figure 3. Ischemic (n⫽9) or hemorrhagic (n⫽3)
strokes caused more than one fifth of the deaths, 18 died from
cardioaortic causes, and 3 from other vascular causes (2
pulmonary embolisms, one intestinal necrosis). Overall, acute
or chronic alcohol-related condition, or an alcohol-
attributable disease, was present in 14 (18%) deaths. All
patients dying of malignancies were ⱖ45 years of age.
Otherwise, we found no significant differences in the spec-
trums of causes of death between males and females and
between those aged 15 to 44 and ⱖ45 years (data not shown).
Previous myocardial infarct and severe index stroke were
factors associated with death within 5 years only in the crude
univariate analysis. After adjustment for age and gender, the
strongest predictor of death in the long-term was malignancy,
followed by heart failure, large artery atherosclerosis under-
Figure 2. Kaplan–Meier estimates depicting cumulative 5-year
mortality risks stratified by etiologic subgroups (log rank
P⬍0.001).
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Figure 1. Kaplan–Meier estimates show-
ing cumulative 5-year mortality risks (A) in
the entire patient population and stratified
by (B) gender and (C) age group.
lying the index stroke, peripheral arterial disease, heavy
drinking preceding infection, and age ⱖ45 years (Table 2).
Malignancy, heart failure, large artery atherosclerosis,
Type 1 diabetes, heavy drinking, preceding infection, and
increasing age were all independent factors in the Cox
proportional hazards model associated with risk of death
within 5 years from the index stroke (Table 3).
Discussion
The overall risk of long-term death after an acute ischemic
stroke in young adults is low. However, apart from patients
with malignancies, several subgroups are at notably higher
risk of death and therefore need special attention. Multifactorial
assessment, including demographics, risk factors, stroke severity
as well as stroke subtype, is a key role in identifying those
young adults who have a high risk of death after their first
ischemic stroke.
The 30-day case-fatality rates in young adults with ische-
mic stroke ranged from 2.3% to 3.4% in prior studies from the
last 2 decades.3,6,15,16 The first-year mortality rates varied
from 4.5% to 6.3%,2,5–7 and the average rates were between
0.8% and 1.8% during the subsequent years.2,5–7 These
figures are closely similar to ours despite the variation in the
chosen upper age limit between the studies or whether
patients with earlier stroke were included. The overall risk of
death is clearly highest during the first month and year after
ischemic stroke in young adults but reduces considerably
thereafter.
In earlier studies, which included sufficient information on
causes of death during long-term follow-up in young adults,
recurrent strokes caused 0% to 33% of deaths, 13% to 55%
died due to cardiac causes and 23% to 33% due to malignan-
cies.4,6,7 The variability in the proportions of vascular causes
in these studies is perhaps related to referral bias, small
sample sizes, or incomplete data on causes of death. Based on
our consecutive patient series and reliable mortality data,
Figure 3. Causes of death in 30-day survivors (n⫽58) within the
5-year follow-up.
 Putaala et al Mortality in Young Patients With Ischemic Stroke 2701

Table 2. Cumulative 5-Year Mortality Rates (From Kaplan–Meier Functions) Stratified by Presence or
Absence of Demographic Factors, Selected Risk Factors, Stroke Severity, Thrombolysis, and Etiology in
30-Day Survivors With Complete 5-Year Follow-Up (nⴝ711) and Respective Univariate Hazard Ratios (From
Cox Proportional Hazard Functions)
Cumulative Mortality Rate
Crude Univariate Hazard Adjusted Univariate Hazard
Present Absent Ratio (95% CI) Ratio (95% CI)†
Demographics
Age ⱖ45 years 12% 5% 2.56 (1.47–4.47)* 2.47 (1.41–4.33)*
Male gender 9% 6%‡ 1.55 (0.87–2.76) 1.36 (0.76–2.44)
Risk factors
Family history of any stroke 6% 9% 0.63 (0.25–1.58) 0.57 (0.23–1.43)
Dyslipidemia 9% 7% 1.33 (0.76–2.34) 1.09 (0.61–1.95)
Cigarette smoking 10% 7% 1.47 (0.87–2.46) 1.38 (0.82–2.33)
Hypertension 11% 7% 1.61 (0.96–2.69) 1.27 (0.75–2.16)
Obesity 12% 8% 1.56 (0.77–3.18) 1.41 (0.69–2.87)
Coronary heart disease 16% 8% 2.10 (0.90–4.88) 1.68 (0.72–3.95)
Heart failure 32% 7% 5.22 (2.64–10.32)* 5.25 (2.63–10.49)*
Myocardial infarction 21% 8% 2.84 (1.13–7.10)* 2.27 (0.90–5.74)
Peripheral arterial disease 27% 8% 4.03 (1.46–11.14)* 2.96 (1.06–8.30)*
History of transient ischemic attack 13% 8% 1.72 (0.87–3.40) 1.65 (0.83–3.26)
Diabetes mellitus, Type 2 12% 8% 1.57 (0.68–3.66) 1.23 (0.52–2.90)
Diabetes mellitus, Type 1 17% 8% 2.27 (0.91–5.69) 2.19 (0.88–5.48)
Atrial fibrillation 13% 8% 1.68 (0.52–5.36) 1.48 (0.46–4.73)
History of migraine 4% 9% 0.42 (0.17–1.04) 0.51 (0.20–1.30)
Heavy drinking 19% 6% 3.34 (1.97–5.68)* 2.85 (1.64–4.98)*
Preceding infection 18% 7% 2.70 (1.48–4.93)* 2.95 (1.61–5.41)*
Obstructive sleep apnea 6% 8% 0.78 (0.19–3.17) 0.63 (0.15–2.59)
Active malignancy 56% 8% 13.81 (5.51–34.62)* 20.54 (7.41–56.92)*
Stroke severity
Mild, NIHSS score 0–6 7% NA 1 1
Moderate, NIHSS score 7–14 9% NA 1.25 (0.61–2.57) 1.25 (0.61–2.56)
Severe, NIHSS score ⱖ15 13% NA 1.85 (0.87–3.94) 1.70 (0.80–3.64)
GCS score ⬍15 13% 8% 1.77 (0.84–3.73) 1.89 (0.89–3.99)
Acute treatment
Intravenous alteplase 6% 8% 0.72 (0.18–2.96) 0.76 (0.18–3.10)
Stroke etiology
Large artery atherosclerosis 21% NA 4.60 (1.62–13.04)* 4.42 (1.56–12.56)*
Cardioembolism 11% NA 2.20 (0.79–6.18) 2.79 (0.99–7.89)
Small vessel disease 5% NA 1 1
Other determined etiology 7% NA 1.47 (0.52–4.12) 2.00 (0.70–5.67)
Undetermined etiology 6% NA 1.18 (0.43–3.24) 1.48 (0.53–4.09)
*P⬍0.05.
†Adjusted for age and gender.
‡Females.
NA indicates not applicable.

more than one fifth of the deaths in 30-day survivors were association between age and mortality.7 In our study, the risk
caused by recurrent stroke, nearly one third by cardiac or of death was clearly higher in those ⱖ45 years compared with
aortic cause, and in total 58% by a vascular cause within the younger patients. In addition, increasing age independently
first 5 years from the index stroke. predicted death after adjusting for gender and other relevant
In young patients with ischemic stroke, aged 15 to 45 factors, akin to general knowledge. Higher mortality in
years, age ⬎35 years was reported as a predictive variable for patients ⱖ45 years likely also reflects their higher prevalence
increased risk of death,2,6 whereas a Norwegian study, which of well-defined vascular risk factors.9 We did not find an
included patients aged 15 to 49 years, did not find an association between male gender and higher mortality within
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2702 Stroke August 2009

Table 3. Multivariate Cox Proportional Hazards Model for exclusion of those dying within the first 30 days. Having such
Predicting of 5-Year Mortality in 30-Day Survivors (nⴝ711) an impact on long-term prognosis, preceding infections
Hazard Ratio (95% CI) P should be routinely screened for every patient with stroke.
However, due to methodological limitations of our study, the
Demographics
association between infection preceding stroke and long-term
Age per year 1.07 (1.01–1.12) 0.021 risk of death—and particularly whether the risk could be
Male gender 0.78 (0.40–1.52) 0.458 modified—should be further investigated in large-scale pro-
Risk factors spective trials.
Heart failure 6.83 (2.21–21.12) 0.001 NIHSS score is widely used and rapid to assess and
Myocardial infarction 1.11 (0.38–3.24) 0.844 strongly predicts functional outcome and death after stroke at
Peripheral arterial disease 2.11 (0.70–6.33) 0.185 3 months.8,23 In young adults, high NIHSS score predicted
combined unfavorable outcome or death at 3 months.15 In
Diabetes mellitus, Type 1 3.25 (1.18–8.90) 0.022
older patients, severe index stroke predicts long-term mortal-
Heavy drinking 2.29 (1.28–4.10) 0.005
ity,17 but this issue has not been analyzed in young patients,
Preceding infection 2.32 (1.24–4.36) 0.009 who generally have better likelihood to survive. In our
Active malignancy 15.75 (6.03–41.14) ⬍0.001 analysis, stroke severity measured with the NIHSS or GCS
Stroke severity had no impact on long-term mortality in patients who
Mild, NIHSS score 0–6 1 survived the first 30 days. According to prior literature and
Moderate, NIHSS score 7–14 0.77 (0.35–1.67) 0.506 our results, severe stroke thus affects survival in young adults
Severe, NIHSS score ⱖ15 1.62 (0.77–3.42) 0.209 merely during the very early phase after the stroke.
In our study, patients with large artery atherosclerosis and
GCS score ⬍15 1.20 (0.43–3.31) 0.733
cardioembolism underlying the index stroke were at clearly
Stroke etiology
higher risk of long-term death compared with those with
Small vessel disease 1 index strokes of other etiologic subtypes (Figure 2). The
Large artery atherosclerosis 4.17 (1.35–12.90) 0.013 former was also observed in an earlier study on young
Cardioembolism 1.03 (0.26–4.11) 0.969 patients with stroke.4 After adjustment for age, gender, and
Other determined etiology 1.90 (0.62–5.84) 0.263 clinical variables, large artery atherosclerosis was a strong
Undetermined etiology 1.56 (0.52–4.72) 0.428 independent predictor of long-term mortality in our study. In
contrast, cardioembolism lacked such predictive value, prob-
ably because more deaths attributable to cardioembolic index
our 5-year observation period as was suggested earlier in stroke occurred within the first 30 days. In older patients with
studies involving young patients with stroke with longer stroke, both cardioembolism and large vessel disease were
mean follow-up times (8 to 12 years).2,6 associated with low probability of survival during the first
Coronary atherosclerosis, active tumor disease, and excess years after the stroke compared with that of small vessel
consumption of alcohol were risk factors that predicted death disease.24 –26 These differences most likely arise from the
in the long term in young adults in the Norwegian study.7 overall higher prevalence of atrial fibrillation and other
Only cardiac diseases and previous stroke were predictors of high-risk cardiac sources among the elderly versus relatively
long-term mortality in a multicenter Italian study,2 whereas larger proportion of low-risk cardiac causes, eg, patent
diabetes predicted unfavorable outcome or death at 3 months foramen ovale, in the young.9 In addition, our data suggest
in a more recent study.15 These earlier results tally with ours: that mortality rates are generally low in the young with stroke
malignancy, heavy drinking, and Type 1 diabetes predicted attributable not only to small vessel disease, but also to
all death in our patients after multivariate analysis. We undetermined and other determined etiologies. Moreover, our
analyzed cardiovascular diseases separately, which led to mortality data apply in part also to patients with cervicoce-
observation that heart failure was the cardiac factor particu- rebral artery dissection, because they comprised 59% of those
larly related to long-term death in young adults. This, in turn, with other determined etiology.9
is consistent with the findings from prior studies involving Our nonselected consecutive patients came from a well-
older patients with stroke.17 defined population, nearly all patients in the studied age
Preceding infection is a significant risk factor and trigger groups were treated in our hospital, and complete mortality
for stroke, possibly in all age groups, and the risk seems data were obtained from a reliable national crosschecked
generic.18 Despite emerging literature on this topic, data on register. Yet, our study has potential limitations. Baseline
impact of infection on long-term outcome or survival are data were obtained retrospectively and we included patients
scarce. Greater stroke severity was associated with recent from a very long time period. We may have underestimated
infection in a few studies.19 –21 In a recent study, neurological the prevalence of risk factors that are often based on self-
stage was worse on Day 4 after stroke in patients with reporting such as family history of stroke, drinking, or
infection during the week before stroke compared with those smoking. Because of overall low mortality in our young
without infection.22 Long-term outcome or mortality were patients, we could not perform reliable subgroup analyses on
analyzed in none of the previous studies. In our study, any deaths due to vascular causes. We also could not analyze the
preceding documented infection within the month before effect of secondary prevention with respect to risk of death
stroke independently associated with long-term death after due to lacking data of medication used. Furthermore, stroke
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 Putaala et al
therapy has made considerable advances during the last 2
decades, which might have improved the survival along the
years. These problems are common to most longitudinal
observational studies on patients with stroke, however.
Conclusions
Despite the overall low risk of death in the young after the
first-ever ischemic stroke, several easily recognizable factors
associate independently with the long-term mortality. Re-
garding young adults with a long expected lifespan ahead,
detecting these factors are important, because in most pa-
tients, they can be modified by lifestyle changes, strictly
controlled medication, or invasive interventions, when
indicated.
Acknowledgments
We are indebted to Marja Metso, RN, and Jaana Valkeapää, RN, for
their dedication and technical support.
Source of Funding
This work was supported by the Helsinki University Central Hospital
(TYH2008253).
Disclosures
None.
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 Causes of Death and Predictors of 5-Year Mortality in Young Adults After First-Ever
Ischemic Stroke: The Helsinki Young Stroke Registry
Jukka Putaala, Sami Curtze, Sini Hiltunen, Heli Tolppanen, Markku Kaste and Turgut
Tatlisumak

Stroke. 2009;40:2698-2703; originally published online July 9, 2009;

doi: 10.1161/STROKEAHA.109.554998
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
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