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Department of Cardiology, Thoraxcenter, University Medical Center Groningen
Department of Internal Medicine and Department of Psychiatry, University Medical Center Groningen
Department of Psychiatry, St Lucas Andreas Hospital, Amsterdam
Department of Cardiology, University Hospital Maastricht
Department of Psychiatry, University Hospital Maastricht
Department of Psychiatry, Medical Center Leeuwarden
Department of Cardiology, University Medical Center Groningen
Department of Social Psychiatry and Psychiatric Epidemiology, University Medical Center Groningen, The Netherlands
Correspondence: Dr Peter de Jonge, Department of Internal Medicine and Department of Psychiatry, University Medical Center Groningen, P.O. Box 30.001, 9700 RB, The Netherlands. Email: p.de.jonge{at}med.umcg.nl
Declaration of interest None. Funding detailed in Acknowledgements.
See invited commentary, pp.
467–468, this
issue. 
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
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Aims To evaluate the effects of antidepressant treatment compared with usual care in an effectiveness study.
Method In a multicentre randomised controlled trial, 2177 myocardial infarction patients were evaluated for ICD–10 depression and randomised to intervention (n=209) or care as usual (n=122). Both arms were evaluated at 18 months post-myocardial infarction for long-term depression status and new cardiac events.
Results No differences were observed between intervention and control groups in mean scores on the Beck Depression Inventory (11.0, s.d.=7.5 v.10.2, s.d.=5.1, P=0.45) or presence of ICD–10 depression (30.5 v. 32.1%, P=0.68). The cardiac event rate was 14% among the intervention group and 13% among controls (OR=1.07, 95% CI 0.57–2.00).
Conclusions Antidepressant treatment did not alter long-term depression post-myocardial infarction status or improve cardiac prognosis.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
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Two intervention studies have assessed the effects of treatment of depression post-myocardial infarction. In the ENhancing Recovery in Coronary Heart Disease study (ENRICHD), the effects of cognitive–behavioural therapy (CBT) on depression and cardiac prognosis was evaluated (Berkman et al, 2003). In this large trial, no significant difference in cardiac outcomes was found between the intervention and the care as usual arms. Although substantial improvement in depression status was observed 6 months after initiation of CBT, the difference between the arms diminished over time and was no longer present after 30 months.
The SADHART study (Glassman et al, 2002) found sertraline to be a safe treatment for depression post-myocardial infarction, but there was little difference in depression status between groups receiving sertraline and placebo after 24 weeks of treatment. However, the effect of sertraline was greater in the patients with severe and recurrent depression. The study was not designed to assess the effects of treatment on cardiovascular prognosis, but severe cardiovascular events during the 6-month treatment tended to be less frequent in the sertraline group. The effects of sertraline on long-term depression status were not evaluated.
Thus, little is known about the effects of treatment for depression post-myocardial infarction on either long-term depression status or cardiac prognosis. We have conducted the Myocardial INfarction and Depression – Intervention Trial (MIND–IT) in order to determine, using a randomised controlled design, whether antidepressant treatment for depression post-myocardial infarction improves long-term depression status and cardiovascular prognosis (Van den Brink et al, 2002). The MIND–IT is an effectiveness study rather than an efficacy study, and compares the effects of an active treatment strategy with usual care.
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METHOD |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
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The institutional review board at each clinical centre approved the study protocol and all patients provided written informed consent before enrolment. In the study information pack it was emphasised that, although all participating patients were to be screened for depression, antidepressant treatment would be offered only to a random sample of patients and all were free to seek help for mood problems.
Design of the study
Patients admitted with an acute myocardial infarction were screened for
depressive symptoms during hospitalisation and at 3, 6, 9 and 12 months
post-myocardial infarction, using the Beck Depression Inventory (BDI;
Beck, 1979). Those with
depressive symptoms (i.e. BDI score 
10) underwent a psychiatric
evaluation using the WHO Composite International Diagnostic Interview (CIDI
auto version 2.1; World Health
Organization, 1990). The first CIDI interviews were performed at
least 3 months post-myocardial infarction to allow natural recovery of
depressive symptoms following a major life event. Both screening tools are
widely used and their feasibility and reliability have been described
elsewhere (Robins et al,
1988; Strik et al,
2001). Patients with a research diagnosis of ‘current
depressive episode’ (World Health
Organization, 1993) according to ICD–10 (further:
‘depression’) were randomised (1:1) to antidepressant treatment or
care as usual. The assignment was carried out at the Trial Coordination Centre
in Groningen with the use of computer-generated permuted blocks of four,
stratified according to clinical site and time of onset of depression (within
6 months v. 6 months or more post-myocardial infarction). Because the
number of patients actually treated with antidepressants was lower than
expected, the randomisation ratio was changed to 2:1 on 14 March 2001.
Patients with a significant risk of suicide were excluded from randomisation
and referred for treatment outside the study. To compare both strategies, we
used the Zelen design (Zelen,
1979): patients allocated to the ‘care as usual’ arm
were not informed about their research diagnosis of depression to avoid
influencing usual care. Data management was independently performed at the
Trial Coordination Centre, Groningen, The Netherlands.
Baseline variables
Data were collected on demographics, medical history, clinical variables
and medication use during hospitalisation for the index myocardial infarction.
The cumulative burden of medical comorbidity was assessed with a modified
version of the Charlson Comorbidity Index
(Watkins et al,
2003). Higher scores on this scale indicate more comorbidity. To
account for a possible relationship between depression post-myocardial
infarction and cardiac disease severity, the following parameters of risk
stratification were assessed: Killip class at admission, maximum values of
serum aspartate transaminase during hospitalisation, left ventricular ejection
fraction (as measured by either echocardiography or radionuclide
ventriculography) and wall motion score index (WMSI) according to the
recommendations of the American Society of Echocardiography
(Schiller et al,
1989). Independent analysis was performed at the core
echocardiography laboratory by technicians who were unaware of the
patients’ randomisation status.
Antidepressant intervention
The MIND–IT study was designed as an effectiveness study comparing
active antidepressant treatment with usual care. In the intervention arm, the
research diagnosis provided by the CIDI interview was confirmed by a
psychiatrist prior to the patient starting antidepressant treatment. Several
treatment modalities were possible. Flexibility in treatment was permitted
because the main research question was whether implementing any active
depression treatment strategy would be associated with better outcomes than
usual care in which antidepressant treatment is almost negligible
(Frasure-Smith et al,
1993). However, allocation to these modalities was strictly
defined in the protocol. First-choice treatment was double-blind
placebo-controlled treatment with the selective noradrenaline reuptake
inhibitor mirtazapine (a non-tricyclic, presynaptic
2-antagonist which enhances both noradrenergic and
serotonergic neurotransmission; De Boer,
1996). In case of refusal or insufficient treatment response after
8 weeks, open treatment with the selective serotonin reuptake inhibitor (SSRI)
citalopram was offered (Montgomery &
Djarv, 1996). Sufficient treatment response was defined as at
least 50% reduction on the Hamilton Depression Rating Scale (HDRS;
Hamilton, 1960) compared with
baseline score or a HDRS score at 8 weeks of 
9. Thus, patients who were
initially treated with placebo and who did not improve within 8 weeks were
subsequently treated with an SSRI. The third option was ‘tailored
treatment’ which was at the discretion of the clinical psychiatrist
(e.g. SSRI, psychotherapy, etc.). Patients were scheduled to visit the
psychiatrist on average once a month during the treatment period of 6 months.
In the care as usual arm, psychiatric treatment outside the study was recorded
but no treatment was offered by the MIND–IT investigators. Whether the
patient was referred for cardiac rehabilitation was left to the discretion of
the patient’s cardiologist (who was masked to the psychiatric screening
results).
Long-term depression status and quality of life
At approximately 18 months post-myocardial infarction, the course and
outcome of the depressive episode was assessed in a CIDI interview. The BDI
was administered to evaluate the severity of depressive symptoms. In addition,
health-related quality of life was assessed with the RAND 36-item Health
Survey, which consists of 36 items organised into eight scales
(Ware et al, 1993;
Essink-Bot et al,
1997). Somatic health complaints were assessed with the Health
Complaints Scale (HCS), a self-report measure to assess common health
complaints in patients with coronary heart disease
(Denollet, 1994). Disability
was assessed according to Broadhead et al
(1990). Patients were asked to
indicate with a time frame of the past month: ‘how many days were you
not able to do your daily activities (for example your work, housework,
studies, leisure activities) owing to physical or emotional problems?’
and ‘apart from the above, on how many days were you able to do your
daily activities for less than half of the time owing to physical or emotional
problems?’ Both complete and partial disability were categorised as
having been present for either less than 1 week or for 1 week or more during
the previous month.
Cardiac events
The occurrence of any significant cardiac event served as the primary
end-point for the study. Cardiac events included cardiac death or hospital
admission for documented non-fatal myocardial infarction, myocardial
ischaemia, coronary revascularisation (coronary angioplasty or bypass
surgery), heart failure or ventricular tachycardia occurring in the time
between randomisation and 18 months post-myocardial infarction. Time to
follow-up (6–15 months) depended on the time of randomisation (range 3
months to 12 months post-myocardial infarction). Other cardiac-related
hospital admissions (defined as admissions with an initial evaluation by a
cardiologist or hospitalisations at the cardiology ward) were considered as
secondary end-points. Potential end-points were recorded at 12 months and 18
months post-myocardial infarction, and were reviewed and classified according
to pre-specified, established criteria
(Cannon et al, 2001)
by an independent end-point committee that was unaware of patients’
treatment assignments. Discrepancies were discussed until agreement was
reached.
Statistical analysis
Study power was calculated for long-term depression outcomes and cardiac
events. With respect to the long-term depression status, a sample of 320
randomised patients would result in a study power of 80%, assuming a drop-out
rate of 20% and a small-to-medium effect size (0.35). With respect to cardiac
events, we expected a 12-month incidence of 38% for patients with depression
and 19% for patients without depression
(Frasure-Smith et al,
1995). If psychiatric treatment could reduce the risk for patients
with depression from 38 to 25% (i.e. reduction of the attributable risk by
two-thirds), 190 patients in the intervention arm and 130 in the care as usual
arm would give a statistical power of 0.84 to detect this effect with a
log-rank test (=0.05).
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2-test was used to compare categorical
data. Time-to-event data were analysed with the Kaplan–Meier method and
differences between care as usual and intervention groups in the incidence of
cardiac events were assessed with the log-rank test. Outcome data were
considered at 18 months post-myocardial infarction, the time of last contact,
withdrawal from the study, or at the time of a primary end-point. All
P values were two-tailed. |
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
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Antidepressant intervention
Of the 196 patients assigned to the intervention and not lost to follow-up,
45 (23%) did not receive antidepressant treatment, either because they refused
to accept the proposed therapy or because the psychiatrist did not confirm the
diagnosis of depression at the time of the visit. The median length of time
from the randomisation date to the first visit to the psychiatrist was 13 days
(interquartile range 7–21 days). The majority of patients in the
intervention arm received clinical management of depression and 94 (45%) were
enrolled in the double-blind placebo-controlled medication treatment
sub-study. Of these patients, 47 initially received mirtazapine and 44
initially received placebo. Three patients received no treatment because they
failed to keep their appointment. Twenty patients originally treated with
mirtazapine and 26 who received placebo subsequently received 16 weeks of
open-label treatment with citalopram because of an insufficient response after
8 weeks of the initial treatment. The remaining patients continued to receive
their original treatment. Seventeen (8%) received immediate open-label
antidepressant treatment with citalopram and 40 (19%) received
non-pharmacological antidepressant treatment (i.e. psychotherapy, counselling,
etc.). Patients in the intervention arm who received these different
treatments did not significantly differ on severity of depressive symptoms
during hospitalisation (mean BDI score for those receiving double-blind
treatment 11.6, s.d.=6.9; open label treatment 13.8, s.d.=8.7); other
treatment 11.6, s.d.=6.6; no treatment 11.0, s.d.= 6.7; F=0.66;
P=0.58). Moreover, these patient groups did not differ significantly
on ICD–10 depression characteristics.
In contrast, only 8 patients (7%) in the care as usual arm received antidepressant medication and 12 (10%) received non-pharmacological treatment for their depression (Fig. 1).
Effects on long-term depression status
Of the 307 patients who were alive at 18 months and available for
follow-up, depression assessments were obtained for 218 patients (71%), which
was comparable for patients in the intervention (69%) and care as usual arm
(74%). The prevalence of ICD–10 depression was 30.5% in the patients
assigned to the intervention and 32.1% in the care as usual arm
(P=0.68; Table 4). No
significant differences were observed between patients assigned to
intervention or care as usual with respect to depressive symptoms, health
complaints, disability and quality of life.
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The total rate for cardiac-related hospitalisations between randomisation and 18 months post-myocardial infarction was 127 out of 314 (40%). The incidences of these secondary end-points were comparable between patients allocated to intervention and care as usual 77 of 196, 39% v. 48 of 118, 41%, P=0.34).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
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Limitations
The lack of positive results in our trial might be a result of either
suboptimal antidepressant treatment in the intervention arm or better than
expected treatment in the care as usual arm. This possibility is not supported
by our secondary analyses because comparing treated patients in the
intervention arm with untreated patients in the care as usual arm still
yielded no differences in the incidence of cardiac events. However, the data
needed to determine whether optimal dosage and continuation of antidepressant
treatment were provided in the intervention arm were not collected.
It could also be argued that perhaps these findings are the result of a large rate of spontaneous recovery from depression which has been observed previously in both ENRICHD and SADHART clinical trials. Although this is plausible, our study was not designed to evaluate this possibility in detail since we used a Zelen design in which the care as usual patients were not informed about their depression and randomisation status. The advantage of this design is that usual care was truly representative but the disadvantage is that we cannot evaluate the (short-term) spontaneous recovery. However, the fact that both arms were comparable in depression outcomes at 18 months does support this possibility. This stresses the need to improve the identification of patients with persistent depression post-myocardial infarction in future clinical trials.
An important limitation is the power of the study. When the trial was initiated the results of the ENRICHD and SADHART trials had not been published and we had to rely on data that in retrospect may have been too optimistic (e.g. Frasure-Smith et al, 1995). First, the expected incidence of cardiac events was substantially higher than the observed incidence. Second, the association between depression and cardiac outcomes might have been overestimated and third, the anticipated effects of treatment on depression were overly optimistic. As a result, we believe that our study had sufficient power to detect differences in long-term depression outcomes (standardised effect size >0.35) but was underpowered to detect differences in cardiac outcomes. However, the nearly identical long-term depression status in the two arms and the similar rates of cardiac events offer little evidence that a significant difference would have emerged if more patients had been included. Thus, although we believe that our trial was underpowered, the observation that there were no consistent differences suggests that more study power would very likely not have yielded different conclusions.
Implications
The MIND–IT produced null findings in terms of long-term depression
outcomes and was inconclusive about the effects of depression treatment on
cardiac outcomes. We were unable to substantially alter long-term depression
status, and as a result we still do not know whether effective treatment of
depression would result in a better cardiac prognosis. Future efforts should
focus on the identification and effective treatment of patients with
depression post-myocardial infarction with different antidepressant treatment
modalities. In the absence of such knowledge, we did not choose one specific
antidepressant therapy but rather compared an active psychiatric intervention
arm with care as usual. Unfortunately, this has resulted in a considerable
proportion of patients that did not receive antidepressant medication although
being in the intervention arm. When the efficacy of one antidepressant
treatment has been proven, the next step should be to investigate whether that
treatment might improve the impaired cardiac prognosis in this patient
group.
Some recent findings suggest that particular subtypes of depression post-myocardial infarction might be specifically related to impaired prognosis. We have found that only somatic/affective symptoms are associated with a worsened cardiac prognosis (De Jonge et al, 2006a). Other studies have found that only incident post-myocardial infarction depression (Grace et al, 2005; De Jonge et al, 2006b) is related to poor cardiac outcomes, and that even minimal symptoms can have an effect (Bush et al, 2001). We believe that the validity and homogeneity of the diagnosis and treatment of depression in acute coronary syndromes need to be reconsidered (Frasure-Smith & Lesperance, 2003). This might lead to treatment strategies that might be quite different from treatment for depression in the general population (American Psychiatric Association, 2000) but be better adapted to cardiac care.
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ACKNOWLEDGMENTS |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
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The following investigators and institutions in The Netherlands participated in the MIND-IT study: Steering committee, J. Ormel, PhD (principal investigator), A. H. Schene, MD, PhD, A. Honig, MD, PhD, H. J. G. M. Crijns, MD PhD; Study coordination, P. de Jonge, PhD, J. P. van Melle, MD PhD; Data management, Trial Coordination Centre, Groningen, The Netherlands; Clinical centres, Flevo Hospital, Almere: A. S. J. M. Sadee, MD, L. M. Konijnenberg, MD; Academic Medical Centre, Amsterdam: G. Casteelen, MD, A. M. G. Kuyper, MD, R. J. G. Peters, MD, PhD; Slotervaart Hospital, Amsterdam: M. Bax, MD; Nij Smellinghe Hospital, Drachten: M. van der Linde, MD, PhD; H. Teunenbroek, MD; Medical Spectrum Twente, Enschede: D. G. Buiten, MD, G. P. Molhoek, MD, PhD; University Hospital Groningen: J. A. den Boer, MD, PhD, J. F. May, MD, PhD; Tjongerschans Hospital, Heerenveen: H. P. den Daas, MD, D. G. Jochemsen, MD; Atrium Medical Centre, Heerlen: L. H. B. Baur, MD, PhD, C. J. M. van den Berg, MD, PhD; Medical Centre Leeuwarden: D. M. Tulner, MD, C. J. de Vries, MD; University Hospital Maastricht: A. Honig, MD, PhD, P. M. J. C. Kuijpers, MD, A. Schins, MD, PhD; Endpoint committee, P. M. J. C. Kuijpers, MD, PhD, J. F. May, MD, PhD, R. J. G. Peters, MD, PhD.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
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Received for publication July 12, 2006. Revision received January 3, 2007. Accepted for publication January 22, 2007.
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, care as usual;
, intervention; vertical
ticks indicate censored data.