EURO PEAN

SO CIETY O F
Original scientific paper CARDIOLOGY ®

European Journal of Preventive

Cardiology

Lifestyle interventions for secondary 2014, Vol. 21(8) 1026–1039

! The European Society of
Cardiology 2013
disease prevention in stroke and transient Reprints and permissions:
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ischaemic attack: a systematic review DOI: 10.1177/2047487313481756
ejpc.sagepub.com

Olive Lennon1, Rose Galvin2,3, Kathryn Smith4,

Catherine Doody1 and Catherine Blake1

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Abstract
Background and purpose: Secondary prevention in ischaemic stroke and transient ischaemic attack (TIA) is
dominated by pharmacological interventions with evidence for non-pharmacological interventions being less robust.
This systematic review and meta-analysis examines the impact of lifestyle interventions on secondary prevention in
stroke or TIA.
Methods: A systematic literature search was performed. Randomised controlled trials (RCTs) examining the effect-
iveness of intervention packages incorporating any key component of health education/promotion/counselling on lifestyle
and/or aerobic exercise compared to usual care  a sham intervention in participants with ischaemic stroke or TIA were
included. Outcomes of interest were mortality, cardiovascular disease (CVD) event rates, cardiovascular risk factors
including blood pressure, lipid profiles and physical activity participation. Methodological quality was assessed. Statistical
analyses determining treatment effect were conducted using Cochrane Review Manager Software.
Results: Seventeen RCTs were included. Data pooled from eight studies with a total of 2478 patients, demonstrated no
effect in favour of lifestyle interventions compared to routine or sham interventions on mortality (risk ratio (RR) ¼ 1.13
(95% confidence interval (CI), 0.85–1.52), I2 ¼ 0%). Data relating to CVD events were pooled from four studies (1013
patients), demonstrated non-significant findings (RR ¼ 1.16 (95% CI, 0.80–1.71), I2 ¼ 0%). Similar results were reported
for total cholesterol. Physical activity participation demonstrated significant improvement [SMD 0.24 (95% CI, 0.08–
0.41), l2 ¼ 47%]. Blood pressure reductions were noted but were non-significant when corrected for multimodal pack-
ages including enhanced pharmacotherapy compliance.
Conclusions: There is currently insufficient high quality research to support lifestyle interventions post-stroke or TIA
on mortality, CVD event rates and cardio-metabolic risk factor profiles. Promising blood pressure reductions were noted
in multimodal interventions which addressed lifestyle.

Keywords
Stroke, transient ischaemic attack, secondary prevention
Received 25 September 2012; accepted 18 February 2013

Background 1
School of Public Health, Physiotherapy and Population Science,
Patients who survive a stroke or transient ischaemic University College Dublin, Republic of Ireland
2
School of Physiotherapy, Royal College of Surgeons in Ireland, Republic
attack (TIA) are at high risk of recurrent stroke and
of Ireland
other cardiovascular events including myocardial 3
HRB Centre for Primary Care Research, Royal College of Surgeons in
infarction.1 The five-year major cardiovascular event Ireland, Republic of Ireland
rate is estimated to be 24%,2 highlighting the increasing 4
The Library, University College Dublin, Republic of Ireland
need for disease management and secondary prevention
strategies. Secondary prevention in ischaemic stroke Corresponding author:
Olive Lennon, School of Public Health, Physiotherapy and Population
and transient ischaemic attack is dominated by Science, College of Life Sciences, University College Dublin, Belfield,
pharmacological interventions in the areas of Dublin 4, Republic of Ireland.
anti-hypertensive medications,3,4 lipid-lowering Email: olive.lennon@ucd.ie
Lennon et al.
medications5 and anti-platelet/anticoagulant medica-
tions.6 The evidence for non-pharmacological interven-
tions is less robust with national and international
guidelines drawing on primary prevention data, expert
opinion or data extrapolated from comparative popu-
lations such as coronary heart disease. Non-pharmaco-
logical or complex interventions, defined by the
Medical Research Council, are interventions that
include several, interconnecting, component parts.
A systematic review of non-pharmacological interven-
tions or complex interventions post-stroke was previ-
ously conducted in 2006.7 This review narrowed the
definition to educational or psychosocial interventions
aimed at changing knowledge, beliefs or behaviours.
This definition excluded specific rehabilitation or ther-
apy interventions including physiotherapy, occupa-
tional therapy, cognitive-behavioural therapy and
early discharge interventions, thus excluding cardiac
rehabilitation-based programmes. Furthermore the
review focussed on theoretical and methodological pro-
gramme development rather than intervention efficacy.
A more recent review of lifestyle interventions post
stroke listed primary outcomes of interest as changes
in behaviour and physiological outcomes.8 However,
the review included three studies with limited numbers
of participants. This systematic review and meta-analy-
sis examines the totality of evidence in relation to the
impact of lifestyle changes specifically on the secondary
prevention of vascular events post stroke or TIA.
Methods
Definitions
The Preferred Reporting Items for Systematic Reviews
and Meta-Analyses (PRISMA) guidelines standardised
the conduct and reporting of this study.9 Prior to sys-
tematically reviewing the literature, a number of oper-
ational definitions were defined by the authors (OL, CB
and KS) using methods based on the Cochrane hand-
book for systematic reviews of interventions.10 The popu-
lation of interest were study participants with ischaemic
stroke or TIA, defined by International Classification
of Disease codes, 10th revision (ICD 10): AM 163;
G45.0; G45.2; G45.3; G45.9).11 Interventions included
in the review were lifestyle intervention packages incor-
porating any key component of targeted health educa-
tion or health promotion on lifestyle-related issues,
lifestyle counselling and/or aerobic exercise and
broadly based on the cardiac rehabilitation model.
The comparison was with usual care which the authors
acknowledge includes routine pharmacotherapy and
advice as per guidelines, with or without an additional
sham intervention. The outcome of interest was second-
ary prevention and included measures of mortality,
1027
cardiovascular disease (CVD) event rates, cardiovascu-
lar risk factors including blood pressure, lipid profiles,
physical activity participation, healthy eating and
smoking cessation. Only randomised controlled trials
(RCTs) were included.
Literature search
The final literature search was conducted in February
2012 and included the following search engines:
PubMed, EMBASE, PsycINFO, CINAHL, Sport
Discus, Web of Science, Scopus, the Cochrane library
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and PEDro. The databases were searched using an
extensive string that included controlled vocabulary
terms specific to each database for stroke and TIA
populations. Expansive search strategies, including
singular/plural terms and English/American spellings
under each heading of exercise, diet, smoking, educa-
tion/health promotion and outcome, were conducted.
The following Boolean operators combined each
search string: [Stroke population string AND [exercise
string OR diet string OR smoking string OR educa-
tion/health promotion string] AND outcome string].
The entire search strategy is available as an online
supplementary table to this article (see
Supplementary Material, Table 1). The search was
supplemented by reference lists of guideline docu-
ments, reviews and relevant articles excluded in the
abstract review process because of study type.
Data extraction
The principal investigator extracted data. Data
extracted included participants’ demographic details,
study setting, intervention type and mode of delivery,
frequency and duration of the intervention, details of
the control arm of the trial and outcomes reported.
These included death, CVD event rates including recur-
rent stroke and/or cardiac events, cardiovascular risk
factors including blood pressure, lipid profiles, physical
activity participation, healthy eating, smoking cessation
and the incidence of adverse events.
Methodological quality
Two reviewers (OL and CB) independently docu-
mented the methodological quality of the studies to
be included. Studies were evaluated using the
Cochrane risk of bias tool under headings of sequence
generation, allocation concealment, blinding, incom-
plete data, selective outcome reporting and other poten-
tial threats to validity.10 Where all criteria were met, the
study was deemed to have low risk of bias. If one or
more criteria were partly met, the study was considered
to have moderate risk of bias and if one or more of the
1028
criteria were not met, the study was considered to have
high risk of bias.
Statistical analysis
Statistical analysis was conducted using the review man-
ager software package RevMan 5 (version 5.0.25
updated 2010, Cochrane Collaboration). Meta-analysis
of continuous variables analysed change scores with
standard deviation of the difference (sdDiff). Where
mean values were unavailable, the median was used as
proxy for the mean. A multiple of 0.75 times the inter-
quartile range, calculated from median values, was used
as proxy for the standard deviation.12 This method has
been used in previous studies of this nature.13 For con-
tinuous data, where different scales were employed by
different studies for assessment of the same outcome,
standardised mean differences (SMDs) with 95% confi-
dence intervals (CIs) were calculated. For dichotomous
variables, individual and pooled statistics were calcu-
lated and reported as risk ratio (RR) with 95% CI
using the Mantel-Haenszel statistical method. The I2
statistic was used to measure heterogeneity. Both
fixed-effect and random-effects models were applied:
non-identical results were considered indicative of stat-
istical heterogeneity, and the more conservative out-
come reported.
Sensitivity analysis assessed the effect, on the overall
results, of the inclusion of trials which the review
authors considered to be of high risk of bias.
Subgroup analysis was employed where possible to dis-
tinguish between lifestyle interventions alone and those
included in a multi-modal care pathway where
improvement in pharmacological compliance may
have, in part, contributed to the results.
Results
Study identification and selection
Figure 1 presents an overview of the identification and
selection process. Thirty-two full text articles were
obtained, reviewed and marked as relevant, irrelevant
or unsure by the principal investigator and independent
reviewer (CB). The authors of eight full text papers were
contacted during this process seeking clarity regarding the
intervention or to request stroke-specific data in studies
where participants were of a heterogeneous nature. Three
authors replied with stroke-specific data or further infor-
mation.14–16 Data was not available from five studies and
these studies were excluded. Eleven additional studies
were excluded, with reasons provided summarised in
Figure 1 and provided in detail in supplemental material
Table 2. Seventeen texts remained for analysis, 15 of
which contributed to the meta-analysis employed.
European Journal of Preventive Cardiology 21(8)
Study description
Table 1 summarises the studies included in the system-
atic review. Seven studies included data on both stroke
and TIA patients.16–22 Three studies fulfilled the key
intervention of aerobic exercise and healthy lifestyle
advice modelled on cardiac rehabilitation.19,23,24 Four
studies complied with evidence-based aerobic interven-
tions, sufficiently intense for cardiovascular train-
ing.23–26 Ten studies involved education, advice and/
or counselling,15–18,20–22,27–29 five of which included an
integrated care pathway for stroke patients, involving
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interdisciplinary teams.15,19,22,27,30 Improvements in
outcomes in these five studies cannot be attributed to
lifestyle interventions alone. They may also stem from
improved adherence to guidelines and pharmacother-
apy. These studies, included in meta-analysis were
removed during subgroup analysis, to eliminate pos-
sible confounding factors.
Interventions varied from less than one week16 to 33
months.15 Two studies reported adherence data that
varied between 71%18 and 93%.23 No adverse events
were noted as a direct consequence of the intervention
given. Two studies involved long-term follow-up of
patients: with follow-up at one year14 and 3.6 years29
post intervention.
Methodological quality
Table 2 illustrates the results of the methodological
quality of the studies included in the review. One
follow-up study had poor attrition and missing data
were not addressed or appropriately imputed.29
Meta-analysis
Mortality and CVD rate
Mortality data were pooled on 2478 patients (interven-
tion n ¼ 1243, control n ¼ 1235) from eight stu-
dies.15,17–19,27–30 Figure 2 demonstrates no effect in
favour of lifestyle interventions when compared to rou-
tine or sham interventions on mortality data (RR ¼ 1.13
(95% CI, 0.85–1.52), I2 ¼ 0%). Data relating to recur-
rent CVD events were pooled on a total of 1013 patients
(intervention n ¼ 501, control n ¼ 512) from four stu-
dies.15,19,28,29 There was no significant different in the
event rates reported in the intervention and control
groups (RR ¼ 1.16 (95% CI, 0.80–1.17), I2 ¼ 0%).
Blood pressure
Changes in blood pressure from baseline to post
intervention were pooled on a total of 1155 patients
(intervention n ¼ 569, control n ¼ 586) from six
Lennon et al. 1029

Identification
Records identified through
database search
(n =6,004)

Duplicates
(n =2,736)

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Screening

Records screened by
Records excluded by title
title
(n =2,518)
(n =3,268)

Stroke guidelines Records screened by Records excluded by title

(n =32) title and abstract and abstract
Reviews (n=28) (n =750) (n =657)

Full-text articles assessed
for eligibility
Eligibility
Full-text articles
excluded, with reasons
(n =16)

Population/Intervention
(n =33) /Outcome measures not
appropriate (n =8)
Not a RCT (n =2)
Request for stroke
Studies included in specific data or outcome
review synthesis data not complied with
(n =17) (n =5)
Subset of a study already
ncluded (n =1)
Included

Studies included in
quantitative synthesis
(meta-analysis)
(n =15 )

Figure 1. Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) flow diagram.
RCT: randomised controlled trial.

studies.15–17,22,24,29 The mean difference in the change in

blood pressure (BP) from baseline to post intervention
was significantly higher in the intervention group
when compared to the control group for both systolic
blood pressure (SBP) (1.34 mmHg (95% CI, 2.54
to 0.14 mmHg), I2 ¼ 80%) and diastolic blood pressure
(DBP) (1.40 mmHg (95% CI, 2.43 to 0.37 mmHg),
I2 ¼ 91%). This is displayed in Figure 3. Subgroup ana-
lysis of lifestyle interventions, excluding multimodal
care-pathways demonstrated no change with respect to
SBP or DBP (p ¼ 0.42 and p ¼ 0.84 respectively).
Total cholesterol
Changes in total cholesterol from baseline to post inter-
vention were pooled on a total of 806 patients (inter-
vention n ¼ 397, control n ¼ 409) from five
studies.15,16,22,24,29 There was no significant difference
between the groups with respect to the mean change
in total cholesterol levels from baseline to post interven-
tion (2.06 mmol/l (95% CI, 5.21 to 1.09 mmol/l),
I2 ¼ 99%). However, the point estimate is large, the
95% CI is very wide and there is significant heterogeneity
 1030

Table 1. Summary of studies included in the systematic review

Study Setting Participants Intervention Outcome measures Time to follow-up

Allen 2002 Recruited in acute care prior n ¼ 93 (3 lost to follow-up); 41 men, 52 Post-discharge care management Mortality Three month follow-
to discharge to the women. Intervention n ¼ 47. Mean age model including referral to car- Stroke event rate up at end of
community 70.5 years. Sub-acute stroke and TIA with diac rehabilitation vs usual care. % hypertensive intervention
mild to moderate disability.
Mean NIHSS: intervention 2.1, usual care
1.9.
Co-morbidities: not reported.
Allen 2009 Recruited in acute care prior n ¼ 380 (190 in each group); 190 men, 190 Post-discharge care management Mortality Six month follow-up
to discharge to the women. Mean age 68.5 years. Sub-acute model vs organised stroke care %hypertensive(systolic) at end of
community stroke with mild to moderate disability. discharge planning. Acute stroke %hypertensive (diastolic) intervention
No data missing on mortality. (15 missing patients followed on discharge. %total cholesterol >180 mg/dl
in intervention % smoking
25 missing in self report variables, 25 missing % exercising
in intervention, 36 in control for per-
formance measures).
Mean NIHSS: intervention 2.0, usual care
1.7.
Co-morbidities included: diabetes, previous
MI or stroke, hypertension and
dyslipidaemia.
Boysen 2009 Recruited in acute care n ¼ 314 (157 in each group); 177 men, 137 Repeated verbal instruction to exer- Mortality Two year follow-up at
Intervention on discharge to women. Mean age 69 years. Sub-acute cise vs usual care. Acute patients Stroke event rate the end of
the community stroke patients with mild disability. recruited during in-patient stay. MI event rate intervention.
Mean NIHSS: unavailable. Physical Activity Scale for the
Modified Rankin score 0–3. Elderly (PASE)
Co-morbidities included: diabetes, previous
MI or stroke, atrial fibrillation, CABG,
PTCA, hypertension and dyslipidaemia.
Brotons 2011 Community n ¼ 1224 (642 in intervention, 600 in control Intervention included one visit every Mortality Three year follow-up
group). Mixed group of CVD patients. four months for 21 months with Hospital cardiovascular admis-
(n ¼ 414 with stroke or TIA) Average age information, lifestyle education sion
and gender not available. and supervision of prophylactic Smoking
NIHSS or alternate stroke severity score and targeted risk factors. The Blood pressure
unavailable. control group continued with BMI
Co-morbidities included coronary heart usual care. Waist
disease, stroke, peripheral vascular dis- Glucose
ease, diabetes, COPD, renal failure, Cholesterol
hypertension and dyslipidaemia. Golberg Scale
QoL SF36
(continued)
European Journal of Preventive Cardiology 21(8)

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Table 1. Continued
Study Setting Participants Intervention Outcome measures Time to follow-up
Lennon et al.

Ellis 2005 Community n ¼ 192(intervention 94; control 98); 106 Health education and motivational Change in systolic BP 3 month intervention;
men, 86 women. Stroke or TIA patients counselling vs usual care. Change in diastolic BP follow-up at 5
with mild to moderate disability. Mean Change in number of cigarettes/ months.
age 65 years. day
Community dwelling stroke patients. Change in total cholesterol
NIHSS or alternate stroke severity score
unavailable.
Comorbidities included: hypertension, dia-
betes, dyslipidaemia, previous stroke,
TIA, atrial fibrillation.
McManus 2009 Community n ¼ 192 for mortality data Intervention group received Mortality Follow-up long term
n ¼ 102 (intervention 49; control 53). enhanced including further infor- Stroke event rate (3.6 years)
NIHSS or alternate stroke severity score mation on stroke pathology, Change in systolic BP
unavailable. explanation of individual risk fac- Change in diastolic BP
Comorbidities extrapolated from Ellis et al. tors, motivational interviewing Change in number of smokers
(2005) included: hypertension, diabetes, about behaviour change inten- Change in total cholesterol
dyslipidaemia, previous stroke, TIA, atrial tions and development of a plan, if
fibrillation. appropriate. Telephone support
follow-up at two and six weeks.
Control received usual care.
Gillham 2010 Outpatient clinic n ¼ 52 (26 in intervention; 26 in control). Readiness to change Three month follow-
Mean age 68.3 years, 44 women. Hospital Anxiety and Depression up
NIHSS or alternate stroke severity score Scale
unavailable Alcohol consumption
Co-morbidities not reported. Smoking behaviour
Exercise frequency
Fruit and vegetable consumption
Green 2007 Community n ¼ 200 (100 in each group); 114 men, 83 Brief one-to-one interview with Mortality Three month follow-
women. Acute/subacute minor stroke motivational counselling and one Class attendance up
and TIA subjects. Mean age 66.5 years. 28 lifestyle class within two months Change from passive to active
patients in intervention group lost to vs usual care with Community stage of change(dichotomised
follow-up, eight in the control group. dwelling TIA and minor stroke variable)in:
NIHSS unavailable. patients. Smoking
Modified Rankin Score 0–2. Dietary change
Comorbidities included: hypertension, dia- Physical activity
betes, dyslipidaemia, previous stroke, Weight loss
TIA, atrial fibrillation, ischaemic heart
disease and obesity.
(continued)
1031

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 1032
Table 1. Continued
Study Setting Participants Intervention Outcome measures Time to follow-up

Hornnes 2011 Community intervention n ¼ 349 (172 in intervention group; 48% Home visits at 1, 4, 7 and 10 months Change in blood pressure One year follow-up
Recruited at discharge female, mean age 70.2 years; 177 in con- after inclusion. Blood pressure GP visits
from hospital or from day trol group, 50% female, mean age 68.5 monitoring, referral to GP if ele- Medication compliance
clinics years) 46 patients excluded from final vated, medication compliance and
analysis. lifestyle counselling versus usual
NIHSS unavailable. care.
Modified Rankin Score 0–5.
Comorbidities included: hypertension, dia-
betes, atrial fibrillation.
Joubert 2009 Acute care at enrolment n ¼ 233 (intervention 123, control 110); 102 Integrated care of collaboration Change in systolic BP 12 month follow-up at
Followed to the commu- men, 84 women. Subacute stroke and between stroke specialist service, Change in diastolic BP end of intervention
nity on discharge TIA patients. Mean age 66 years. 47 sub- hospital co-ordinator and general Change in cholesterol
jects lost to follow-up. practitioner (smoking and physical Change in BMI
NIHSS or alternate stroke severity score activity among the targets) from Number of walks
unavailable at baseline. Rankin scores discharge to continued commu-
reported at follow-up, nity care vs usual care.
Co-morbidities not reported at baseline.
Atrial fibrillation reported at follow-up.
Lee 2008 Community n ¼ 24 (12 in each group analysed); 12 men, Aerobic training versus aerobic plus Change in VO2 Three month follow-
12 women. Sub-acute and chronic stroke resistance training versus sham up at end of
patients (3 months to 57 months post exercise. Intervention time 10–12 intervention
stroke) with mild to moderate disability. weeks.
Mean age 66 years.
NIHSS or alternate stroke severity score
unavailable
Comorbidities included: coronary artery
disease, hypertension, diabetes and mean
number of chronic illnesses.
Lennon 2008 Community n ¼ 48(24 in each group); 28 men, 20 Aerobic exercise classes twice per Change in waist girth 10 week follow-up at
women. Chronic stroke patients >I year week and life management skills Change in total cholesterol end of intervention
post stroke with mild to severe disability. class vs usual care. Intervention Change in cardiac risk score
Mean age 60 years. duration eight weeks. Change in systolic BP
NIHSS unavailable. Change in diastolic BP
Oxfordshire Stroke subtype classification Change in BMI
employed and Functional Ambulatory Change in VO2
Categories 0–5.
Comorbidities included: ischaemic heart
disease and MI, CABG, previous stroke,
TIA, atrial fibrillation.
(continued)
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Table 1. Continued
Study Setting Participants Intervention Outcome measures Time to follow-up

Maasland 2007 Community n ¼ 57 (Intervention 30; control 27); 34 men, Individualised multimedia computer Change in systolic BP Three month follow-
Lennon et al.

Rimmer 2000 Community
Rimmer 2009 Community
Van der Ploeg 2007 In-patient and out-patient mix
Follow-up on discharge from
rehabilitation of commu-
nity dwelling patients
23 women. Acute-subacute minor stroke
and TIA patients with mild disability.
Mean age 64 years.
NIHSS or alternate stroke severity score
unavailable.
Co-morbidities not reported.
n ¼ 35 (intervention 18; control 17); 9 men ,
26 women. All participants had chronic
stroke of >6 months. were predomin-
antly African-American, female patients.
Mean age 53 years.
NIHSS or alternate stroke severity score
unavailable. Patients were independently
mobile >50 feet.
Co-morbidities included: number of chronic
conditions, hypertension, diabetes, dysli-
pidaemia, back pain, arthritis, depression
and obesity.
n ¼ 3655(moderate ex 18; therapeutic
exercise 18. Chronic stroke patients >6
months post stroke with mild to moder-
ate disability. Mean age 59 years.
Predominately female and African-
American.
NIHSS or alternate stroke severity score
unavailable.
Participants were independently mobile.
Comorbidities included: hypertension, dia-
betes and congestive heart failure.
n ¼ 171 subacute-chronic stroke patients
(intervention 35; control 136) from a
total of 1202 participants with mixed
diagnosis. . Breakdown data on age and
gender unavailable .
NIHSS or alternate stroke severity score
unavailable.
Co-morbidities not available.
programme for health education
(weight, smoking and exercise
included
12 week health promotion interven-
tion three days per week post
stroke vs usual care.
14 week intervention of moderate
intensity, low intensity or thera-
peutic exercise three days per
week.
Active after rehabilitation group
involved a 40 min counselling ses-
sion based on the transtheoretical
model of change six weeks before
discharge from rehabilitation and
telephone counselling 2, 5 and 8
weeks after discharge. Control
group received individual session
with a sport counsellor and one
follow-up phone call six weeks
after discharge vs usual care.
Change in diastolic BP up
Change in total cholesterol
Change in triglyceride
Change in LDL
Change in BMI
Change in number of cigarettes
smoked
Change in number engaging in
regular physical activity
Attendance Three month follow-
Change in total cholesterol up post
Change in LDL intervention
Change in HDL
Change in triglycerides
Change in VO2
Physical Activity Disability Scale
(PADS)
Diet (Rate your plate)
Change in systolic BP 14 weeks follow-up
Change in diastolic BP post intervention
Change in total cholesterol
Change in HDL
Change in LDL
Change in triglycerides Change in
VO2
Change in BMI
Physical Activity Scale for One year follow-up
Individuals with Physical
Disabilities (PASIPD)
Number participating in sport
Sport score incorporating inten-
sity and average duration per
week
Number meeting requirement of
physically active for 30 min
five days per week
1033

(continued)

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1034 European Journal of Preventive Cardiology 21(8)

density lipoprotein; LDL: Low density lipoprotein; NIHSS: Nottingham Institutes of Health Stroke Scale; MI: Myocardial Infarct; PTCA: Percutaneous transluminal coronary angioplasty; QoL SF36; Quality of
BP: blood pressure; TIA: transient ischaemic attack; BMI: Body mass index; CABG: Coronary artery bypass graft; COPD: Chronic obstructive pulmonary disease; GP: General Practitioner; HDL: High
indicating that further work is needed to establish the

One year follow-up

Time to follow-up
impact of lifestyle interventions on cholesterolaemia in
secondary disease prevention post stroke and TIA.

Physical activity participation and fitness

Five studies reported outcomes of physical activity par-
ticipation as a result of the intervention allowing data
therapy, antiplatelet therapy
Management of key modifiable

respect to antihypertensive
risk factors for stroke with

to be pooled for a total of 657 patients (intervention

and smoking cessation

n ¼ 280, control n ¼ 377).14,20,22,23,28 There was a signifi-

cant difference between the groups with respect to par-
Outcome measures

ticipation in physical activity at follow-up (SMD 0.24

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(95% CI, 0.08–0.41), I2 ¼ 47%). Four studies had a
documented intervention of sufficient moderate aerobic
activity and reported an index of aerobic fitness.23–26
Two studies found that levels of aerobic fitness signifi-
cantly improved following the intervention.23–24
mised to receive patient and gen-

months post stroke versus usual

However, it was not possible to pool the data due to

Cluster trial with practices rando-

evidence based management

advice at 10 weeks, 5 and 8

the heterogeneous nature of the outcomes examined.

eral practitioner tailored,

Smoking
Five studies reported smoking status at follow-up but
the variety of measures employed, including number
Intervention

and percentage of individuals smoking,15,27 number of

care.

cigarettes smoked per day,16 change in smoking status29

and absolute risk reduction,30 prohibited synthesis of
data. However no significant difference between groups
Comorbidities included: hypertension, dia-
n ¼ 523 (247 in intervention group; 249 in

was reported in any study included in this review. Only

NIHSS or alternate stroke severity score
control) 244 were female. Mean age

one study confirmed the self-reported status by monitor-

ing the participants blood nicotine levels and indicated
that self-report was not an accurate measure with 9.8%
of participants at follow-up giving false information.30
betes, dyslipidaemia.

Diet
unavailable.

unavailable.

Only two studies used measures of dietary intake. One

Participants

study23 used an adapted version of the Rate your Plate

Eating Pattern Assessment to assess fat intake with no
significant difference between groups noted. A further
Life Short Form 36; VO2: Volume of oxygen (ml/sec/kg).

study20 used self-reported fruit and vegetable portions

consumed per week with an improvement in the inter-
vention group by comparison with controls observed
(p ¼ 0.03).
Community

Discussion
Setting

From the present meta-analysis, it can be concluded

that there is currently insufficient high quality evidence
Table 1. Continued

in support of lifestyle interventions targeting individ-

uals with ischaemic stroke or TIA on mortality, CVD
event rates and total cholesterol. Further research in
Wolfe 2010

this area is warranted with longer follow-up and more

detailed reporting of mortality, morbidity and cardio-
Study

vascular profiles. It is acknowledged by the authors that

Lennon et al. 1035

Table 2. Methodological quality of the included studies (n ¼ 17)

Sequence Allocation Incomplete outcome Free of selective

Study generation concealment Blinding data addressed outcome reporting Risk of bias

Allen 2009 yes yes unclear yes yes moderate

Allen 2002 unclear yes unclear yes yes moderate
Boysen 2009 yes yes yes yes yes low
Brotons 2011 yes yes no yes yes moderate
Ellis 2005 yes yes yes yes yes low
Green 2007 unclear yes yes yes yes moderate
Gillham 2010 yes unclear yes yes yes moderate
Hornnes 2011 yes yes yes yes yes low

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Joubert 2009 no unclear unclear yes yes high
Lee 2008 yes yes yes yes yes low
Lennon 2008 yes yes yes yes yes low
Maasland 2007 Yes unclear yes yes yes moderate
McManus 2009 yes yes yes no yes high
Rimmer 2000 unclear unclear unclear yes yes moderate
Rimmer 2009 no unclear unclear yes yes high
Van der Ploeg 2007 no yes yes yes yes high
Wolfe 2010 yes yes yes yes yes low

Lifestyle intervention Control Risk Ratio Risk Ratio

Study or Subgroup Events Total Events Total Weight M-H, Fixed, 95% CI M-H, Fixed, 95% CI
2.1.1 Mortality
Allen 2002 1 47 4 46 5.2% 0.24 [0.03, 2.11]
Allen 2009 9 190 7 190 9.0% 1.29 [0.49, 3.38]
Boysen 2009 11 157 9 157 11.5% 1.22 [0.52, 2.87]
Brotons 2011 11 203 13 211 16.3% 0.88 [0.40, 1.92]
Green 2007 1 100 0 100 0.6% 3.00 [0.12, 72.77]
Hornnes 2011 10 172 5 177 6.3% 2.06 [0.72, 5.90]
McManus 2009 11 100 14 105 17.5% 0.82 [0.39, 1.73]
Wolfe 2010 35 274 25 249 33.6% 1.27 [0.78, 2.06]
Subtotal (95% CI) 1243 1235 100.0% 1.13 [0.85, 1.52]
Total events 89 77
Heterogeneity: Chi² = 4.97, df = 7 (P = 0.66); I² = 0%
Test for overall effect: Z = 0.84 (P = 0.40)

2.1.2 CVD event rate

Allen 2002 1 47 0 46 1.2% 2.94 [0.12, 70.30]
Boysen 2009 16 157 13 157 29.6% 1.23 [0.61, 2.47]
Brotons 2011 26 203 25 211 55.9% 1.08 [0.65, 1.81]
McManus 2009 7 94 6 98 13.4% 1.22 [0.42, 3.49]
Subtotal (95% CI) 501 512 100.0% 1.16 [0.80, 1.71]
Total events 50 44
Heterogeneity: Chi² = 0.44, df = 3 (P = 0.93); I² = 0%
Test for overall effect: Z = 0.78 (P = 0.43)

0.01 0.1 1 10 100

Favours experimental Favours control

Figure 2. Mortality and cardiovascular event data post-intervention.

1036 European Journal of Preventive Cardiology 21(8)

Lifestyle intervention Control Mean Difference Mean Difference

Study or Subgroup Mean SD Total Mean SD Total Weight IV, Random, 95% CI IV, Random, 95% CI
2.8.1 Systolic blood pressure
Brotons 2011 -0.45 1.841 203 1.38 1.75 211 46.4% -1.83 [-2.18, -1.48]
Hornnes 2011 0.1 2.1 172 0.7 1.97 177 45.5% -0.60 [-1.03, -0.17]
Joubert 2009 -6 20.1 91 1.8 24.2 95 3.3% -7.80 [-14.18, -1.42]
Lennon 2008 -1.7 14.04 24 -1.1 17.35 23 1.7% -0.60 [-9.65, 8.45]
Maasland 2007 -8.43 17.35 30 -6.88 16.71 27 1.8% -1.55 [-10.40, 7.30]
McManus 2009 -2.8 26.3 49 -8.3 25.1 53 1.4% 5.50 [-4.49, 15.49]
Subtotal (95% CI) 569 586 100.0% -1.34 [-2.54, -0.14]
Heterogeneity: Tau² = 0.78; Chi² = 24.96, df = 5 (P = 0.0001); I² = 80%
Test for overall effect: Z = 2.19 (P = 0.03)

2.8.2 Diastolic blood pressure

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Brotons 2011 -0.15 1.12 203 1.21 1.16 211 41.0% -1.36 [-1.58, -1.14]
Hornnes 2011 -0.1 1.1 172 2.4 1.1 177 40.9% -2.50 [-2.73, -2.27]
Joubert 2009 -1 12.3 91 -2.8 13 95 6.8% 1.80 [-1.84, 5.44]
Lennon 2008 -1.78 8.49 24 -1.1 9.52 23 3.6% -0.68 [-5.84, 4.48]
Maasland 2007 -5.37 9.73 30 -6.16 9.89 27 3.7% 0.79 [-4.31, 5.89]
McManus 2009 -3.9 11.2 49 -5.2 14 53 4.0% 1.30 [-3.60, 6.20]
Subtotal (95% CI) 569 586 100.0% -1.40 [-2.43, -0.37]
Heterogeneity: Tau² = 0.66; Chi² = 56.05, df = 5 (P < 0.00001); I² = 91%
Test for overall effect: Z = 2.66 (P = 0.008)

-20 -10 0 10 20
Favours intervention Favours control

Figure 3. Changes in blood pressure from baseline to post-intervention.

CI: confidence interval; SD: standard deviation; IV: Instrumental variables.

since usual care should incorporate pharmacotherapy
and lifestyle advice as per international best practice
guidelines,31 the margins for improvement by targeted
interventions, in either lifestyle alone or combined with
enhanced care pathways, may be difficult to extrapolate
or prove. However, a recent systematic review and
meta-analysis of lifestyle modification programmes in
coronary heart disease, testing whether improvements
in routine cardiac care would offset the incremental
benefit of older programmes, has confirmed the benefits
of lifestyle modification programmes over and above
routine care for mortality, cardiovascular events and
risk behaviours.32
A statistically significant reduction in blood pressure
scores, in favour of the intervention, is noted here. While
this difference may not be clinically meaningful on an
individual basis,33 it may be of relevance with respect to
population effects where a 2 mmHg reduction in systolic
blood pressure is estimated to lower mortality from
stroke by 10% and ischaemic heart disease and other
vascular causes by 7%.34 The reduction noted is evident
only when specific care-pathways, including medication
and medical guidelines adherence, are included and sug-
gests, as with most secondary prevention strategies, a
multipronged approach accrues maximal benefit.
Insufficient reporting of lipid profiles limited a full ana-
lysis of the efficacy of the programmes included in this
review with regard to cholesterol changes. One must
consider that the total cholesterol results reported here
may mask favorable changes in High density lipoprotein
(HDL) cholesterol (a sub-fraction which can be
increased) and LDL cholesterol (which can be decreased).
The evidence in favour of comprehensive cardiac
rehabilitation and exercise-based interventions in the
Coronary Heart Disease (CHD) population is robust.35
Broadly examining the successful outcomes in our
review, the cardiac rehabilitation paradigm was success-
ful in all three interventions that employed this method
of delivery.19,23,24 Four of the five studies that used an
integrated care pathway also reported significantly
favourable outcomes.15,19,22,27 A recent Cochrane
review pooled data from 47 studies from this population,
randomising 10,794 patients to exercise-based cardiac
rehabilitation or usual care. In studies with >12
months follow-up, exercise-based cardiac rehabilitation
reduced overall and cardiovascular mortality (RR 0.87
(95% CI, 0.75–0.99) and 0.74 (95% CI, 0.63–0.87),
respectively) and hospital admissions (RR 0.69 (95%
CI, 0.51–0.93)) in the shorter term (<12 months
follow-up), with no evidence of heterogeneity noted
across trials. Lack of long-term follow-up and varied
duration/content of interventions in studies included in
this review may have in part contributed to the results
obtained. No study included was adequately powered to
detect a change in mortality or cardiovascular event rate
in stroke. In a mixed population trial by Brotons and
Lennon et al.
colleagues,15 the authors calculated that a 5% reduction
in overall event rates over a three-year period would
require a minimum of 1554 subjects, again pointing to
limited numbers and insufficient follow-up length for
mortality/morbidity meta-analysis in this review.
Only three studies in this review fulfilled the key
intervention of aerobic exercise and healthy lifestyle
advice modelled on cardiac rehabilitation.19,23,24
These trials varied in the outcomes assessed and
meta-analysis of cardiac rehabilitation post-ischaemic
stroke and TIA alone was not possible. Further studies
are required to test these programme types with the
stroke population and longer follow-up data is
required. Interventions of education and counselling
on physical activity levels did demonstrate improve-
ment in physical activity participation. This is promis-
ing as a recent meta-analysis of 21 prospective cohort
studies 36 concluded that that high levels of leisure time
physical activity (2–5 hr per week) and moderate level
of occupational physical activity have a beneficial effect
on cardiovascular health by reducing the overall risk of
incident coronary heart disease and stroke among men
and women by 20–30% and 10–20%, respectively.
Other outcomes that focus on the secondary preven-
tion of cardiovascular disease include smoking cessa-
tion methods, counselling, and dietary advice. Results
were not conclusive in this review, due either to the
heterogeneous nature of the data reported or to
under-reporting of the variable. Recent stroke-specific
research suggests that a brief intervention is as effective
as intensive smoking cessation counselling.37
Interventions by nurses,38 physicians39 and individual
behavioural counsellors40 have demonstrated signifi-
cantly positive changes in the likelihood of stopping
smoking. However, from a narrative perspective, no
study identified in our review demonstrated a signifi-
cant effect on smoking rates or habits. Given the
robustness of evidence that smoking increases all
CVD risk, further testing is warranted on smoking ces-
sation post-stroke as part of a multifaceted risk reduc-
tion intervention. Given the discrepancy between the
literature demonstrating efficacy of targeted interven-
tions for smoking cessation and that no study in this
review shows demonstrable change, it may be possible
that behavioural change with respect to smoking
requires specific intervention and the message may
become lost in a multi-modal package.
Evidence to date also indicates that dietary advice
for reducing cardiovascular risk has significantly
reduced total serum cholesterol in intervention
groups.41 In our systematic review, where three studies
broadly fit the comprehensive cardiac rehabilitation
model and dietary advice was included in a number
of other studies, only two studies included outcome
measures of dietary intake.20,23 This may represent a
1037
lack of focus on this aspect of care in the studies
included and in post-stroke secondary prevention in
general. Furthermore, our meta-analysis of lifestyle
interventions post-ischaemic stroke and TIA demon-
strated no change in serum cholesterol levels, where
reported. However, this finding needs to be interpreted
in the context of the small number of trials pooled and
the heterogeneity in these pooled studies.
This review used a comprehensive and systematic
search strategy to identify all relevant trials but it has
a number of limitations. Firstly, data was not available
from five studies and these studies were excluded which
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may subject the review to selection bias. In addition,
several of the included studies exhibited methodological
problems or lack of clarity with randomisation, blind-
ing of assessors, inadequate sample sizes and lack of
intention to treat which may have contributed to bias.
Where possible, these methodological issues were
addressed with sensitivity analysis. In addition, the lim-
ited numbers of studies prohibited testing of some
aspects of interventions: for example group versus indi-
vidual interventions, supervised versus unsupervised
exercise or specific lifestyle counselling methodologies.
Outcomes such as patient satisfaction, self-efficacy,
health related quality of life, reduction in hospital
admissions or medication dependence were poorly
reported and some potential benefits of these interven-
tions may be missed. Finally, we only pooled data from
a small number of studies and in many cases the pooled
estimates were heterogeneous and the CIs wide. Further
research is needed using methodologically sound study
designs and robust and valid outcome measures to
determine the impact of lifestyle interventions on sec-
ondary prevention of stroke.
Conclusions
The totality of evidence from this systematic review and
meta-analysis targeting individuals with ischaemic
stroke or TIA suggests that currently there is limited
evidence to support lifestyle interventions, alone or as
part of an integrated care-pathway, based on mortality,
CVD event rates and the cardio-metabolic risk factor
profile of total cholesterol. There is some support for
lifestyle interventions for increased exercise participa-
tion and when delivered as part of a comprehensive
care-package post-stroke for minor reductions in BP.
Given the relatively small numbers available in
this review, the short follow up periods reported and
a possible methodological difficulty extrapolating
improvements in intervention from usual care
(including pharmacotherapy and advice), results must
be interpreted with a degree of caution. High-quality,
robust trials are required with longer term follow-up
and clear documentation of mortality, morbidity and
1038
cardiovascular risk profile outcomes. Studies targeting
patients in the acute phase and those with severe dis-
ability post-stroke are lacking. Future research in these
areas is also warranted.
Funding
This work is supported by the Irish Health Research Board
(HRB) Clinical Services fellowship grant (Ref HSR/2007/6)
and by University College Dublin (UCD) Seed Fund Grant
SF-109 2006.
Conflict of interest
The authors declare that there is no conflict of interest.
References
1. Touze E, Varenne O, Chatellier G, et al. Risk of myocar-
dial infarction and vascular death after transient ischemic
attack and ischemic stroke: A systematic review and
meta-analysis. Stroke 2005; 36: 2748–2755.
2. Hackam DG and Spence JD. Combining multiple
approaches for the secondary prevention of vascular
events after stroke: A quantitative modeling study.
Stroke 2007; 38: 1881–1885.
3. Lawes CM, Bennett DA, Feigin VL, et al. Blood pressure
and stroke: An overview of published reviews. Stroke
2004; 35: 776–785.
4. Yusuf S, Diener HC, Sacco RL, et al. Telmisartan to
prevent recurrent stroke and cardiovascular events.
N Engl J Med 2008; 359: 1225–1237.
5. Amarenco P, Benavente O, Goldstein LB, et al. Results
of the Stroke Prevention by Aggressive Reduction in
Cholesterol Levels (SPARCL) trial by stroke subtypes.
Stroke 2009; 40: 1405–1409.
6. Baigent C, Blackwell L, Collins R, et al. Aspirin in the
primary and secondary prevention of vascular disease:
Collaborative meta-analysis of individual participant
data from randomised trials. Lancet 2009; 373:
1849–1860.
7. Redfern J, McKevitt C and Wolfe CD. Development of
complex interventions in stroke care: A systematic review.
Stroke 2006; 37: 2410–2419.
8. Lawrence M, Kerr S, McVey C, et al. The effectiveness of
secondary prevention lifestyle interventions designed to
change lifestyle behavior following stroke: Summary of
a systematic review. Int J Stroke 2011; 7: 243–247.
9. Moher D, Liberati A, Tetzlaff J, et al. Preferred reporting
items for systematic reviews and meta-analyses: The
PRISMA statement. Int J Surg 2010; 8: 336–341.
10. Higgins J and Green S. Cochrane handbook for systematic
reviews of interventions version 5.1.0.The Cochrane
Collaboration 2011. Available at: http://www.cochrane.
org/training/cochrane-handbook.
11. Investigators WMP. The World Health Organization
MONICA Project (monitoring trends and determinants
in cardiovascular disease): A major international collab-
oration. WHO MONICA Project Principal Investigators.
J Clin Epidemiol 1988; 41: 105–114.
European Journal of Preventive Cardiology 21(8)
12. Hozo SP, Djulbegovic B and Hozo I. Estimating the
mean and variance from the median, range, and the size
of a sample. BMC Med Res Methodol 2005; 5: 13.
13. Galvin R, Murphy B, Cusack T, et al. The impact of
increased duration of exercise therapy on functional
recovery following stroke – what is the evidence? Top
Stroke Rehabil 2008; 15: 365–377.
14. Van der Ploeg HP, Streppel KR, van der Beek AJ, et al.
Successfully improving physical activity behavior after
rehabilitation. Am J Health Promot 2007; 21: 153–159.
15. Brotons C, Soriano N, Moral I, et al. Randomized
clinical trial to assess the efficacy of a comprehensive
programme of secondary prevention of cardiovascular
Downloaded from https://academic.oup.com/eurjpc/article/21/8/1026/5925803 by guest on 16 March 2024
disease in general practice: The PREseAP study. Rev
Esp Cardiol 2011; 64: 13–20.
16. Maasland E, Koudstaal PJ, Habbema JD, et al. Effects of
an individualized multimedia computer program for
health education in patients with a recent minor stroke
or transient ischemic attack – a randomized controlled
trial. Acta Neurol Scand 2007; 115: 41–48.
17. Hornnes N, Larsen K and Boysen G. Blood pressure 1
year after stroke: The need to optimize secondary preven-
tion. J Stroke Cerebrovasc Dis 2011; 20: 16–23.
18. Green T, Haley E, Eliasziw M, et al. Education in
stroke prevention: Efficacy of an educational counselling
intervention to increase knowledge in stroke survivors.
Can J Neurosci Nurs 2007; 29: 13–20.
19. Allen KR, Hazelett S, Jarjoura D, et al. Effectiveness of a
postdischarge care management model for stroke and
transient ischemic attack: A randomized trial. J Stroke
Cerebrovasc Dis 2002; 11: 88–98.
20. Gillham S and Endacott R. Impact of enhanced second-
ary prevention on health behaviour in patients following
minor stroke and transient ischaemic attack: A rando-
mized controlled trial. Clin Rehabil 2010; 24: 822–830.
21. Ellis G, Rodger J, McAlpine C, et al. The impact of
stroke nurse specialist input on risk factor modification:
A randomised controlled trial. Age Ageing 2005; 34:
389–392.
22. Joubert J, Reid C, Barton D, et al. Integrated care
improves risk-factor modification after stroke: Initial
results of the Integrated Care for the Reduction of
Secondary Stroke model. J Neurol Neurosurg Psychiatry
2009; 80: 279–284.
23. Rimmer JH, Braunschweig C, Silverman K, et al. Effects
of a short-term health promotion intervention for a pre-
dominantly African-American group of stroke survivors.
Am J Prev Med 2000; 18: 332–338.
24. Lennon O, Carey A, Gaffney N, et al. A pilot randomized
controlled trial to evaluate the benefit of the cardiac
rehabilitation paradigm for the non-acute ischaemic
stroke population. Clin Rehabil 2008; 22: 125–133.
25. Lee MJ, Kilbreath SL, Singh MF, et al. Comparison of
effect of aerobic cycle training and progressive resistance
training on walking ability after stroke: A randomized
sham exercise-controlled study. J Am Geriatr Soc 2008;
56: 976–985.
26. Rimmer JH, Rauworth AE, Wang EC, et al. A prelimin-
ary study to examine the effects of aerobic and thera-
peutic (nonaerobic) exercise on cardiorespiratory fitness
Lennon et al.
and coronary risk reduction in stroke survivors. Arch
Phys Med Rehabil 2009; 90: 407–412.
27. Allen K, Hazelett S, Jarjoura D, et al. A randomized trial
testing the superiority of a postdischarge care manage-
ment model for stroke survivors. J Stroke Cerebrovasc
Dis 2009; 18: 443–452.
28. Boysen G, Krarup LH, Zeng X, et al. ExStroke Pilot
Trial of the effect of repeated instructions to improve
physical activity after ischaemic stroke: A multinational
randomised controlled clinical trial. Brit Med J 2009; 339:
b2810.
29. McManus JA, Craig A, McAlpine C, et al. Does behav-
iour modification affect post-stroke risk factor control?
Three-year follow-up of a randomized controlled trial.
Clin Rehabil 2009; 23: 99–105.
30. Wolfe CD, Redfern J, Rudd AG, et al. Cluster rando-
mized controlled trial of a patient and general practi-
tioner intervention to improve the management of
multiple risk factors after stroke: Stop stroke. Stroke
2010; 41: 2470–2476.
31. European Guidelines on cardiovascular disease preven-
tion in clinical practice (version 2012). The Fifth Joint
Task Force of the European Society of Cardiology and
Other Societies on Cardiovascular Disease Prevention in
Clinical Practice (constituted by representatives of nine
societies and by invited experts). Eur J Prev Cardiol
2012; 19: 585–667.
32. Janssen V, Gucht VD, Dusseldorp E, et al. Lifestyle
modification programmes for patients with coronary
heart disease : A systematic review and meta-analysis of
randomized controlled trials. Eur J Prev Cardiol 2013; 20:
620–640.
1039
33. Rashid P, Leonardi-Bee J and Bath P. Blood pressure
reduction and secondary prevention of stroke and other
vascular events: A systematic review. Stroke 2003; 34:
2741–2748.
34. Lewington S, Clarke R, Qizilbash N, et al. Age-specific
relevance of usual blood pressure to vascular mortality: A
meta-analysis of individual data for one million adults in
61 prospective studies. Lancet 2002; 360: 1903–1913.
35. Heran BS, Chen JM, Ebrahim S, et al. Exercise-based
cardiac rehabilitation for coronary heart disease.
Cochrane Database Syst Rev 2011: CD001800.
36. Li J and Siegrist J. Physical activity and risk of cardio-
vascular disease – a meta-analysis of prospective cohort
Downloaded from https://academic.oup.com/eurjpc/article/21/8/1026/5925803 by guest on 16 March 2024
studies. Int J Environ Res Public Health 2012; 9: 391–407.
37. Brunner Frandsen N, Sorensen M, Hyldahl TK, et al.
Smoking cessation intervention after ischemic stroke or
transient ischemic attack. A randomized controlled pilot
trial. Nicotine Tob Res 2012; 14: 443–447.
38. Rice VH and Stead L. Nursing intervention and smoking
cessation: Meta-analysis update. Heart Lung 2006; 35:
147–163.
39. Stead LF, Bergson G and Lancaster T. Physician advice
for smoking cessation. Cochrane Database Syst Rev 2008:
CD000165.
40. Lancaster T and Stead LF. Individual behavioural coun-
selling for smoking cessation. Cochrane Database Syst
Rev 2005: CD001292.
41. Brunner EJ, Rees K, Ward K, et al. Dietary advice for
reducing cardiovascular risk. Cochrane Database Syst
Rev 2007: CD002128.