Mortality at 12 and 24 Months After Stroke May Be Associated With

Transcription

Mortality at 12 and 24 Months After Stroke May Be
Associated With Depressive Symptoms at 1 Month
Allan House, DM, MRCPsych; Peter Knapp, RGN, PhD; John Bamford, MD, MRCP; Andy Vail, MSc
Downloaded from http://stroke.ahajournals.org/ by guest on August 1, 2017
Background and Purpose—Previous studies have reported mood symptoms after stroke to be a risk factor for later
mortality. The purpose of the study was to examine whether mood symptoms at 1 month after stroke may be a risk factor
for mortality at 12 and 24 months.
Methods—As a cohort within a randomized controlled trial, 448 hospital patients were seen at 1 month after stroke and
were randomized into a trial of psychological therapy. Follow-up was at 12 and 24 months. Mood symptoms were
assessed by the Present State Examination and the General Health Questionnaire (GHQ)-28. Measures of disability
before and after stroke and of cognitive impairment after stroke were also taken at 1 month. Mortality was determined
at 12 and 24 months after stroke.
Results—In logistic regression analyses, mortality at 12 months was associated unifactorally with scoring on the GHQ-D
subscale (odds ratio [OR] 2.4, 95% CI 1.3 to 4.5) and scoring in the highest quartile of the GHQ (OR 3.1, 95% CI 1.1
to 8.8). In multiple logistic regression analyses, only GHQ-D remained a significant predictor after controlling for other
known predictors. At 24 months, scoring on GHQ-D (OR 2.4, 95% CI 1.4 to 4.1) and in the highest GHQ quartile (OR
2.2, 95% CI 1.0 to 4.8) was significantly associated with mortality in unifactoral analyses. Scoring on the GHQ-D
remained a predictor of mortality after controlling for other variables. Psychiatric disorder, such as major depression
(according to International Classification of Diseases, 10th Revision), was not statistically significantly associated with
increased mortality at 12 or 24 months.
Conclusions—Mood symptoms on a self-reported rating scale were associated with 12- and 24-month mortality after
stroke, after adjustment for factors associated with stroke severity. The result is in keeping with other evidence that
depressive symptoms are a risk factor for death from vascular disease. (Stroke. 2001;32:696-701.)
Key Words: affect 䡲 cohort studies 䡲 depression 䡲 mortality
R
esearch in heart disease and stroke suggests that depression
may be an independent risk factor for vascular disease. For
example, 3 recent studies have reported that men with depression are more likely to develop ischemic heart disease.1–3 In
established coronary artery disease, major depression is associated with an increased risk of myocardial infarction4 and with
increased rates of angina after myocardial infarction.5 Major
depression may also be associated with increased mortality after
myocardial infarction, even after adjustment for cardiac risk
factors.6 Another study from the same group suggests that the
risk resides in general psychological distress (eg, as measured by
questionnaire) rather than a diagnosable psychiatric syndrome
such as major depression.7
There have been fewer studies examining depression as a
risk in stroke. A recently published cohort study from the
United States found an increased mortality from stroke in
people who had self-reported depressive symptoms at recruitment 29 years previously; this association remained signifi-
cant after adjusting for known clinical and behavioral risk
factors.8 Two small studies have reported that patients who
were depressed in the early weeks after stroke had higher
mortality at 15 months and at 10 years.9,10
If a causal link between depression and stroke mortality can
be established, then it has clinical and theoretical implications;
therefore, well-designed replications are needed. In the present
study, we report a cohort enrolled within a randomized controlled trial, in which we examined the effect of depression
identified 1 month after stroke on mortality at 12 and 24 months
after stroke. Because of the findings of Lesperance et al,7
suggesting a role for depression symptoms below diagnostic
criteria, we defined depression both by standardized clinical
interview and the application of research diagnostic criteria and
by scores on a self-reported questionnaire.
Subjects and Methods
The present study was undertaken in the context of a randomized
controlled trial of psychological treatment after stroke. In the trial,
Received July 8, 2000; final revision received November 20, 2000; accepted November 20, 2000.
From the Academic Unit of Psychiatry and Behavioural Sciences (A.H.) and the Division of Academic Pharmacy Practice, School of Healthcare Studies
(P.K.), University of Leeds, Leeds, UK; the Department of Neurology (J.B.), St James’ University Hospital, Leeds, UK; and Hope Hospital (A.V.),
University of Manchester, Manchester, UK.
Correspondence to Allan House, MD, MRCPsych, Professor in Liaison Psychiatry, Academic Unit of Psychiatry and Behavioural Sciences, University
of Leeds, 15 Hyde Terrace, Leeds LS2 9LT, UK. E-mail [email protected]
© 2001 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org
696
House et al
TABLE 1.
Two-Year Mortality and Depression After Stroke
697
Characteristics of the Sample at Initial Interview 1 Month After Stroke
All
Patients
(N⫽448)
Patients With Major
Depression
(N⫽100)
Patients Without Major
Depression
(N⫽348)
Difference
Age, y
70.7⫾11.6
70.1⫾11.9
70.9⫾11.5
t⫽0.65, P⫽0.51
Female, n (%)
207 (46.2)
53 (53.0)
154 (44.2)
␹2⫽2.39, P⫽0.12
94 (21.0)
24 (24.0)
70 (20.1)
␹2⫽0.71, P⫽0.40
Prestroke Barthel ⬍20, n (%)
132 (29.5)
41 (41.0)
91 (26.1)
␹2⫽8.24, P⫽0.004
Prestroke Frenchay ⬍27, n (%)
245 (54.7)
49 (49.0)
154 (44.2)
␹2⫽0.71, P⫽0.40
Poststroke Barthel ⬍12, n (%)
155 (34.6)
40 (40.0)
115 (33.0)
␹2⫽1.66, P⫽0.20
Poststroke Barthel ⬍20, n (%)
367 (71.9)
92 (92.0)
275 (79.0)
␹2⫽8.83, P⫽0.005
MMSE ⬍24, n (%)
124 (27.7)
35 (35.0)
89 (25.6)
␹2⫽3.45, P⫽0.06
30 (6.7)
9 (9.0)
21 (6.0)
␹2⫽1.09, P⫽0.30
Previous stroke, n (%)
Urinary incontinence, n (%)
Values are mean⫾SD or as indicated.
patients who had been admitted to the hospital in Leeds and Bradford
were randomized to receive treatment as usual, volunteer visits, or
problem-solving therapy11 delivered by a psychiatric nurse. The
primary aim of the trial was to evaluate the effect of problem-solving
therapy on depression at 6 and 12 months after stroke; we have
described the study therapy elsewhere.12 Because all the subjects
were assessed for depression at recruitment and followed up at 12
and 24 months, we were able to analyze the cohort to examine the
effect of depression as an independent risk factor for mortality.
Patients were assessed at 1 month after stroke and recruited if they
met the following criteria: definite clinical diagnosis of stroke (not
subarachnoid hemorrhage), sufficient speech and use of English for
interview (as judged by interviewer), sufficient cognitive abilities to
benefit from therapy (we defined this as Mini-Mental State Examination [MMSE] score of ⱖ20 rather than the usually quoted
threshold13 because we were interested in the ability to participate in
a simple psychological therapy rather than in the presence of
diagnosable but mild cognitive impairment), local residence and
living independently before stroke, no concurrent illness likely to
dominate the pattern of care (approximately equivalent to Rankin
handicap scores of 4 or 514), and written consent. We did not recruit
patients with subarachnoid hemorrhage, because the trial was an
evaluation of psychological intervention in patients admitted to
general medical and neurology wards rather than those admitted
under the care of neurosurgeons.
From an original stroke population of 1387 consecutive admissions, we excluded those with severe cognitive impairment (n⫽210)
or language disorder (n⫽179) and those who were too ill to
participate in the psychological therapy (n⫽269). Other exclusions
were based on place of residence and involvement in other trials
(n⫽187), and there were 92 refusals of consent to participate in the
trial. There were 2 protocol violations leading to exclusion; therefore, the sample was composed of 448 hospitalized stroke patients
who had been recruited to the trial.
Measures
Initial assessments were undertaken by a trained research interviewer, who collected basic biographical data, including age and
whether the patient lived alone and could name a career. History of
previous stroke was obtained from the patient and the medical
record.
Physical functional status was assessed by using the Barthel
Index,15 a measure of activities of daily living, which is scored 0 to
20, with higher scores indicating greater independence. An assessment was made of the patient’s poststroke and prestroke abilities.
The Barthel Index may be recoded to form categories: a score of 20
indicates no disability, and scores of ⱖ12 are generally taken to
indicate an ability to live independently in the community.16
The Frenchay Activities Index17 measures social function and is
scored 0 to 45, with higher scores indicating greater social activity.
Patients were asked to rate their prestroke activity. There are no
published threshold scores, so we used the median score to categorize patients.
The MMSE is a measure of cognitive ability, designed originally
to screen for dementia in the elderly. The measure is scored 0 to 30,
with a lower score indicating greater cognitive impairment. A
threshold score of ⬍24 may be used to categorize patients as
cognitively impaired.13
The General Health Questionnaire (GHQ)-2818 is a measure of
general psychological distress and is scored 0 to 28, with higher
scores indicating greater distress. In neurological inpatients, scores
of ⱖ12 are taken to indicate the probable presence of psychiatric
disorder.19 Because this threshold masks much variation, we also
analyzed the GHQ-28 by quartiles (scores 0 to 1, 2 to 5, 6 to 9, and
10 to 28). The GHQ-28 also has 4 subscales: somatic (A), anxiety
and insomnia (B), social dysfunction (C) and severe depression (D).
There are no “caseness” thresholds for the subscales, so we categorized patients by the median score on each.
The short-form Present State Examination is a standardized
semistructured psychiatric interview,20 which allows the reliable
identification of psychiatric symptoms when it is administered by a
trained interviewer, as in the present study. With minor additions to
the interview, International Classification of Diseases, 10th Revision
(ICD-10) psychiatric diagnoses can be derived from Present State
Examination ratings; we used the ICD-10 research diagnostic
criteria.21
Patient survival at 12 and 24 months was determined through
general practitioners and checked, for untraceable patients, through
the Office for National Statistics, which also provided certified
causes of death. Data were analyzed by using SPSS 9.0.22
Results
The sample had a median age of 72 years, with slightly more
men (54%) than women. Almost 40% of the patients lived
alone before the stroke, although only 10% were unable to
name a career. Most patients were functionally independent
before the index stroke, although 21% had suffered a previous
stroke (see Table 1).
Similar rates of depression were obtained by using the
different criteria used in the present study: 100 (22.3%)
patients met ICD-10 research criteria for major depression;
85 (19.1%) patients scored above the probable “caseness”
cutoff of ⱖ12 on the GHQ-28. Depression at 1 month after
stroke was significantly associated, at the 95% level, with
lower prestroke and 1-month poststroke Barthel scores (see
Table 1). Depression was also associated with being female,
with lower MMSE scores, and with being incontinent at 1
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March 2001
TABLE 2. Risk of Death Within 12 and 24 Months of Stroke for Mood-Related
Variables Identified at Assessment 1 Month After Stroke
Risk of Death by 12
Months: Unifactorial Analysis
Risk of Death by 24 Months:
Unifactorial Analysis
OR
95% CI
P
OR
95% CI
1.1
0.51–2.4
0.78
1.5
0.82–2.8
0.18
GHQ 2nd quartile
2.1
0.72–6.1
0.18
1.1
0.50–2.5
0.78
GHQ 3rd quartile
2.1
0.71–6.4
0.18
1.2
0.51–2.8
0.68
GHQ 4th quartile
3.1
1.1–8.8
0.037
2.2
1.0–4.8
0.048
GHQ-A ⱖ2
1.3
0.70–2.4
0.41
1.1
0.68–1.9
0.61
GHQ-B ⱖ1
1.6
0.86–3.1
0.12
1.3
0.80–2.3
0.26
GHQ-C ⱖ3
1.4
0.78–1.9
0.24
1.5
0.88–2.5
0.14
GHQ-D ⱖ1
2.4
1.3–4.5
0.007
2.4
1.4–4.1
ICD-10 major depression
1.3
0.65–2.7
0.42
1.7
0.95–3.0
0.07
ICD-10 any depression
1.3
0.70–2.5
0.39
0.73
0.28–1.9
0.53
GHQ total ⱖ12
P
GHQ quartiles (compared with
lowest quartile)
0.0015
OR indicates odds ratio.
month after stroke, but these associations did not reach
statistical significance.
sion analysis, the statistically significant effects of GHQ
quartiles were lost after controlling for other predictors (see
Table 4).
Mortality at 12 Months
At 12 months, we were unable to establish the status of 2
patients who had moved abroad, leaving no contact details.
Of the 446 traceable patients, 45 (10.1%) had died. Causes of
death were as follows: recurrent stroke in 17 (37.8%),
cardiovascular disease in 10 (22.2%), and other causes in 18
(40.0%). No patient died as a result of suicide, and there was
no statistically significant difference between depressed and
nondepressed patients in the cause of death.
The relationship between independent variables assessed at
1 month and mortality at 12 months was examined by logistic
regression. Independent variables were categorized (see Subjects and Methods) and were assessed individually. All the
mood measures showed a trend for higher scores to be
associated with increased mortality, but only 2 measures
(GHQ-D “severe depression” and GHQ quartiles) were statistically significant. The odds ratio for mortality was 3.1
between the lowest and highest scoring quartiles (see Table
2), with the rate of mortality 5% in the lowest quartile and
14% in the highest (see Figure 1). Those scoring ⱖ1 on the
GHQ-D severe depression subscale had an odds ratio for
mortality of 2.4 compared with those scoring 0.
We conducted multiple logistic regression analyses to
assess whether impaired mood was associated with increased
mortality after controlling for the effects of recognized
physical predictors (older age, lower MMSE scores, lower
poststroke Barthel score, having suffered a previous stroke,
and urinary incontinence). We did this separately for the
GHQ quartiles and the GHQ-D subscale.
Multiple logistic regression showed that higher GHQ-D
score, greater age, lower MMSE scores, and lower poststroke
Barthel scores were all associated with an increased risk of
dying within 12 months of stroke (see Table 3). Other
variables, including treatment condition in the trial, were not
significantly associated with mortality. In a separate regres-
Mortality at 24 Months
A further 20 patients had died between 12 and 24 months
after stroke, giving a total of 65 (14.6%) deaths for 446
patients in 24 months. As at 12 months, no patient had died
as a result of suicide.
As at 12 months, the relationship between independent
variables assessed at 1 month and mortality at 24 months was
examined by logistic regression. The GHQ quartiles and
subscale GHQ-D were statistically significantly associated
with mortality; major depression at 1 month was associated
with mortality, but the result was not statistically significant
(see Table 2). Mortality among those in the lowest GHQ
quartile was 11% compared with a mortality of 23% among
those in the highest quartile (see Figure 2).
A multiple regression analysis assessed whether impaired
mood was an independent predictor of increased mortality
Figure 1. Mortality (%) at 12 months after stroke, by GHQ-28
score at 1 month. Q indicates quartile.
House et al
Figure 2. Mortality (%) at 24 months after stroke, by GHQ-28
score at 1 month.
after controlling for the effects of recognized physical predictors, as at 12 months. This showed that the effects of
scoring ⱖ1 on the GHQ-D subscale remained statistically
significant, even after controlling for the effects of age,
cognitive status, and known physical predictors (see Table 3).
The effects of the GHQ quartiles did not remain statistically
significant after controlling for other predictors (see Table 4).
Discussion
We have found that mood symptoms, as measured by the
GHQ, reported within 1 month of stroke, were associated
with 12- and 24-month mortality after adjustment for other
risk factors identified in the present study: age, cognitive
impairment, urinary incontinence, and level of physical disability after stroke. Major depression diagnosis and mortality
were not associated statistically, although the data showed a
trend in that direction. One possible explanation for the
absence of a statistical relationship is a lack of statistical
power associated with binary variables, such as major
depression.
The strength of association between mood and mortality is
considerably lower than that reported by Morris and colleagues.9,10 Does this result represent a true association, or
could it be due to chance, bias, or confounding? We used
several measures of mood in the analyses, raising the possibility of a false-positive result from multiple testing. The use
of ⬎1 mood measure was unavoidable if we were to test
alternative hypotheses on the nature of depression, which
predicts mortality, because previous research has suggested
that either major depression or general psychological distress
may be important. However, we cannot entirely exclude
multiple testing as an explanation for our finding.
A second possibility is that bias may have affected the
results. Observer bias is unlikely, because the significant
mood measure was self-rated. Bias may result from studying
hospital samples, when a spurious association can be found
between variables that are both independently associated with
risk of hospitalization (Berkson’s bias)23; this is unlikely,
since multiple regression showed that the GHQ-D score was
a predictor of mortality independent of measures of stroke
severity. Mortality data were obtained for all but 2 patients,
thus excluding bias from incomplete follow-up.
The third possibility is that there was residual confounding,
particularly arising from an association between severity of
physical illness and depressive symptoms, which was not
detected through the available measures. Against this interpretation is our finding that the one significant GHQ subscale
measured depressive thinking, whereas confounding of phys-
TABLE 3. Multiple Logistic Regression Analysis of GHQ-D Subscale and Other Predictors of
12- and 24-Month Mortality
12 Months
GHQ-D subscale ⱖ1
24 Months
OR
95% CI
P
OR
95% CI
P
2.0
1.0–4.1
0.0499
2.2
1.2–4.0
0.0097
3.3
0.36–30
0.29
2.0
0.48–7.9
9.8
1.2–77
0.03
5.1
1.4–18
0.011
1.4–96
0.021
5.7
1.5–21
0.01
Age (compared with ⬍60-y group)
60–69 y
70–79 y
80⫹ y
12
699
0.34
Urinary incontinence
4.0
1.5–11
0.006
2.6
0.99–6.7
0.052
MMSE ⬍24
2.5
1.2–5.0
0.01
2.3
1.3–4.2
0.005
12–19
0.90
0.42–1.9
0.79
1.1
0.58–2.1
0.76
⬍12
0.16
Poststroke Barthel (compared with
patients scoring 20)
1.4
0.48–5.0
0.51
1.9
0.77–4.8
Prestroke Frenchay ⬍27
1.2
0.58–2.4
0.64
1.3
0.70–2.3
0.41
Sex (female)
1.1
0.54–2.2
0.79
1.1
0.6–2.0
0.73
Previous stroke
0.80
0.33–1.9
0.63
1.5
0.77–2.4
0.24
Problem-solving therapy
1.1
0.49–2.6
0.78
1.1
0.55–2.3
0.75
Volunteer visits
1.1
0.50–2.6
0.75
1.2
0.60–2.4
0.59
Random group allocation (compared
with treatment as usual)
700
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March 2001
TABLE 4. Multiple Logistic Regression Analysis of GHQ-28 Quartile and Other Predictors of
12- and 24-Months Mortality
12 Months
24 Months
OR
95% CI
P
OR
95% CI
P
2nd
1.6
0.52–5.0
0.40
0.84
0.35–2.2
0.71
3rd
1.6
0.50–5.3
0.41
0.91
0.39–2.4
0.85
4th
2.4
0.74–7.7
0.14
1.8
0.73–4.2
0.20
60–69 y
3.1
0.34–29
0.31
1.8
0.46–7.3
70–79 y
9.6
1.2–75
0.031
4.9
1.4–17
0.012
GHQ quartiles (compared with lowest quartile)
Age (compared with ⬍60-y group)
80⫹ y
11
0.39
1.3–89
0.025
5.3
1.4–20
0.012
Urinary incontinence
4.1
1.5–11
0.005
2.7
1.0–7.1
0.044
MMSE ⬍24
2.5
1.3–5.1
0.009
2.5
1.4–4.5
0.003
12–19
0.87
0.41–1.9
0.73
1.0
0.53–1.9
0.97
⬍12
1.4
0.46–4.5
0.53
1.7
0.59–4.4
0.25
Prestroke Frenchay ⬍27
1.2
0.61–2.5
0.55
1.4
0.75–2.5
0.30
Sex (female)
1.1
0.53–2.1
0.87
1.1
0.53–2.1
0.83
Previous stroke
0.77
0.32–1.9
0.56
1.5
0.77–3.0
0.23
Poststroke Barthel (compared with patients
scoring 20)
Random group allocation (compared with
treatment as usual)
Problem-solving therapy
1.1
0.49–2.5
0.80
1.1
0.56–2.3
0.74
Volunteer visits
1.1
0.49–2.5
0.80
1.1
0.59–2.4
0.63
ical illness and somatic mood symptoms would be more
likely in subscales A and C (somatic and social dysfunction
items). Because of the nature of the study design, we were not
able to assess all the stroke-related variables (eg, not every
patient had a brain scan).
One possibility that we have not been able to explore is the
confounding arising from a link between depressive symptoms after stroke and prior life events. It is possible that
stressful life events might be a risk both for depression and
for recurrent stroke or myocardial infarction.24
The mechanisms by which mood symptoms may be associated with increased mortality are behavioral or physiological. Suggested physiological explanations include alterations
in autonomic control of cardiac rhythm (eg, those manifested
by reduced heart rate variability)25 and increased platelet
reactivity26 in depressed patients. Some support for this idea
is provided by a meta-analysis of psychological treatments
after myocardial infarction,27 which found that treatment not
only reduced distress but also apparently led to lower blood
pressure, heart rate, and cholesterol levels. Possible behavioral explanations include continued higher levels of smoking
and alcohol consumption among depressed patients and lesser
adherence to medical treatment.28 We were not able to
measure all these factors (because of funding restrictions and
problems of rater burden in a psychological treatment trial);
therefore, the present study offers no evidence about the
nature of any link that does exist.
One interesting implication of our results is that the
psychological factor most strongly associated with mortality
after stroke may not be depressed mood, per se, but general
psychological distress or negative thoughts, such as feeling
that life is not worth living or a feeling of personal worthlessness (items on the GHQ-D subscale). This finding is
broadly in keeping with recent work into psychological
predictors of mortality after myocardial infarction.6
This is the largest cohort study of mortality and depression
after stroke. Its findings are ambiguous and therefore need
replication, with further attempts to identify and adjust for
confounders and more detailed characterization of psychological variables that might act as risk factors. At the same
time, a descriptive study of the frequency of possible mediating variables (physiological and behavioral) in depressed
and nondepressed stroke patients would help to clarify their
possible involvement in any process whereby depressive
symptoms have an impact on mortality after stroke.
Acknowledgments
The Stroke Outcome Study was funded through the National Health
Service Research and Development Initiative in Cardiovascular
Disease and Stroke. The grant holders were Allan House, John
Bamford, Anne Forster, Graham Mulley, Trevor Sheldon, Ken
Wright, and John Young. We should like to thank those who worked
on the study (Kathy Cambridge, Margaret Clegg, Eve Cowdell,
Carrie Dempster, Felicity Garbett, and Carein Todd) and the staff of
the Leeds Stroke Database.
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Mortality at 12 and 24 Months After Stroke May Be Associated With Depressive
Symptoms at 1 Month
Allan House, Peter Knapp, John Bamford and Andy Vail
Stroke. 2001;32:696-701
doi: 10.1161/01.STR.32.3.696
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Mortality at 12 and 24 Months After Stroke May Be Associated With

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