Introduction
The search for psychological factors involved in the development and/or progression of coronary heart disease (CHD) has been a fairly persistent, although not always fruitful, activity over the last few decades. Both the clinical observation that CHD patients seem to exhibit certain psychologi- cal profiles and the apparent failure of traditional risk factors, such as smoking, high blood pressure and cholesterol, and low levels of physical exer- tion, to predict anywhere near all new instances of CHD have helped fuel an expectation that there may be other, psychological, predisposing factors at work.
The earliest psychological research was con- cerned with what came to be called type A behav- ior. Briefly, individuals displaying the type A behavior complex were considered to be engaged in “chronic and excessive struggle to achieve more and more from their own environment in too short a period of time, and against the opposing efforts of other persons or things in the same envi- ronment.”1The subcomponents of the behavioral complex were regarded as excessive competitive striving, time urgency, and hostility. The strength of the evidence linking type A behavior to CHD reached its zenith in 1981 with the publication in the US of the Consensus Report2; type A behavior was agreed to be a risk factor of similar impor- tance to high blood pressure and high cholesterol.
Since that date, though, there has been increas- ing doubt expressed about such claims,3 and a number of large-scale and well-conducted prospective studies, such as the Multiple Risk
Factor Intervention Trial,4reported null findings.
However, from extensive sub-factor analysis of type A behavior emerged another potentially cardio-toxic psychological factor: hostility.
Whether or not type A behavior was indicated as a risk factor for CHD in prospective studies, one of its subcomponents, hostility, almost invariably was. In addition, studies specifically focusing on hostility, particularly cynical hostility, reported an association with subsequent incident CHD.5,6Evi- dence on hostility as a psychological risk factor has stood the test of time, unlike that of type A behavior. However, a substantial number of unan- swered questions remain. Hostility is strongly associated with the likelihood of engaging in unhealthy behaviors, such as smoking and physi- cal inactivity, that increase CHD risk.7 Hence it remains possible that variations in hostility are merely a proxy for variations in such behaviors, and it is the latter which have consequences for CHD. Further, hostility is steeply stratified by socioeconomic position, such that high hostility is more likely to characterize those in poorer social circumstances. Accordingly, it may be other expo- sures contingent on low socioeconomic position, and not hostility per se, that increase CHD risk.8 Thus, the question of causality remains problem- atic. It is important to appreciate that the issue of statistical confounding (i.e. when an association between an independent variable and a health outcome results from their mutual association with another variable) has not always been well understood. Even when prospective associations remain following statistical adjustment for poten- tial confounders, caution should still be exercised
32
Depression Following Myocardial Infarction:
Prevalence, Clinical Consequences, and Patient Management
Deirdre A. Lane and Douglas Carroll
269
in inferring a causal link. Residual confounding by a poorly measured or an unmeasured variable is still possible (see Christenfeld et al.9for a recent discussion). This is an issue to which we shall return.
More recently, attention on psychological factors has again shifted: this time to affective disposition, and especially depression. There is now a fair body of evidence linking depression prospectively with the onset of CHD (see Wulsin and Singal10 for a review), although there are exceptions to the generally positive relationship.11 There has also been substantial recent interest in the impact of depression following myocardial infarction (MI) on subsequent prognosis, and, in particular, whether patients who are depressed following their MI are at increased risk of subse- quent morbidity and mortality and whether the link between depression and prognosis is causal or not. This constitutes the focus of the rest of the chapter. Given the prevalence of depression in MI patients, this is an important public health matter.
It is also an issue that impacts substantially on how MI patients should be managed, that is, assessed and treated.
Prevalence and Persistence of Depression Following Myocardial Infarction
Depressive symptoms and major depression have been consistently reported as common psycho- logical reactions to MI. Major depression, a syn- drome characterized by persistently depressed mood, and/or loss of interest and pleasure, with symptoms lasting for a minimum of 2 weeks, occurs with an annual prevalence of between 1%
and 6% in the general population, with rates typically higher among patients following MI, at approximately 16–18%.12 Apart from major depression, depressive symptoms are quite preva- lent among the general population, with rates ranging from 10% to 29%. Earlier studies of MI patients reported levels of depressive symptoms varying markedly, from 18% to 60%, although the majority of more recent studies report relatively consistent prevalence rates ranging from 17% to 37%.12
Little is known about the persistence of depres- sion after an acute MI since few studies have repeatedly measured depression in the months following the event. However, it would appear that depressive symptoms first emerge between 48 and 72 hours following MI.12,13In the majority of post- MI patients, symptoms of depression are reported to abate after 5 or 6 days.14 However, in some patients distress persists for several months after discharge, with some patients only becoming depressed after discharge from hospital, in the first few months following the infarction.
The majority of the more recent studies of MI patients have limited the formal assessment of symptoms of depression to the period prior to dis- charge from hospital. However, there are at least two compelling reasons why the assessment of depression should be continued beyond discharge.
First, there is the proposed prognostic significance of post-MI depression. Some, although by no means all studies, have found that depressive symptomatology following MI increases the risk of death and/or recurrent cardiac events (see Table 32-1). Second, depression also significantly impairs quality of life and reduces the likelihood of participation in cardiac rehabilitation. Third, it is necessary to establish whether symptoms of depression experienced in hospital are associated with cardiac disease severity or are largely a reac- tion to hospitalization per se.
Review of the Evidence Linking Depression Following MI and
Subsequent Mortality and Morbidity
Observational Studies
Many observational studies have now examined the association between depression following MI and subsequent cardiac events (fatal and nonfatal) and/or cardiac and all-cause mortality (Table 32-1). Of these, nine studies have reported a pos- itive relationship between depression and one or more of these outcomes: cardiac events,15–17,20,23
cardiac mortality,16,17,19,21,23,24,29and all-cause mor- tality.19,29,36Further, after adjustment for potential confounders, such as age, sex, and markers of disease severity, eight studies concluded that depression was an independent (i.e. causal) risk
factor for at least one outcome: cardiac events35 (Table 32-1), cardiac mortality,17,21,24,29,33 and all- cause mortality.29,36 In contrast, 11 reports found no significant association between depression and prognosis18,22,27,28,31,32,39 or describe equivocal findings.25,26,30,38
In the absence of compelling evidence from randomized controlled trials, the case for depression as an independent risk factor for prognosis following MI necessarily rests with the evidence from these observational epidemio- logical studies. Accordingly, it is important to determine the strength of that evidence. Two recent meta-analyses40,41have sought to determine whether the evidence strongly implicates depres- sion as an independent risk factor for mortality (cardiac and all-cause) and recurrent cardiac events, and to provide a quantitative estimate of the magnitude of the independent association between depression and prognosis following MI.
The unadjusted pooled analyses of both meta- analyses indicate that depression following MI is associated with a 2-fold increased risk of death and recurrent cardiac events. This was true irre- spective of whether depression was assessed by clinical diagnosis or questionnaire, and the strength of the association was not influenced by length of follow-up. However, the year of data col- lection (prior to and after 1992) influenced the magnitude of the link between depression and subsequent mortality; earlier studies reported a stronger association between depression follow- ing MI and clinical prognosis (OR, 3.22; 95% CI, 2.14–4.86) than later studies (OR, 2.01; 95% CI, 1.45–2.78).40
However, only the latter meta-analysis41under- took formal analyses using adjusted odds ratios, to assess the association between depression and outcome after controlling for possible con- founders. In such analyses, depression was no longer a statistically significant predictor of cardiac mortality (OR, 1.95; 95% CI, 0.81–4.73).
The associations between all-cause mortality and recurrent cardiac events were also attenuated, but remained statistically significant (OR, 1.66; 95%
CI, 1.20–2.29 and OR, 1.41; 95% CI, 1.11–1.79, respectively), indicating that depression following MI conferred a 41% and 66% increased risk of death from any cause and of recurrent cardiac
events, respectively. van Melle et al.40 also con- ceded that in those studies reporting multivariate analyses, the adjusted odds ratios were generally smaller than the corresponding unadjusted odds ratios.
Why are there differences in study outcomes exploring the link(s) between depression follow- ing MI and prognosis? The inconsistency in previous findings may be due, in part, to the dis- similar MI populations studied and other methodological differences. The sample popula- tions varied markedly, with highly selected MI populations (e.g. patients with arrhythmias or significant left ventricular dysfunction), which may have heightened their mortality risk. Studies also vary markedly in the time delay between the occurrence of MI and measurement of depression. The variety of diagnostic instruments and standardized ques- tionnaires used may also have contributed to the variations in the outcomes of studies. Further, small sample sizes and the failure to report mul- tivariate analyses controlling for other risk factors suggests that caution should be exercised in inter- preting the results. With such variations in popu- lation measurement, design, and statistical control, it might be expected that results would vary considerably.
However, as we have highlighted previously,42 there is one other fairly consistent difference between prospective observational studies report- ing a relationship between depression and cardiac events and mortality following MI and those that do not find such an association. This has to do with the issue of disease severity and its relation- ship with depression. Depression would appear to predict clinical prognosis following MI mainly in studies that have either not controlled for cardiac disease severity or in which disease severity is significantly correlated with depression. Others researchers have also noted that one of the main problems with attributing a causal role to depres- sion in clinical prognosis following MI is the potential confounding of depression with disease severity in such patients.9,11,42,43In the prospective observational studies that have adjusted for mea- sures of disease severity,17,20,21,24–29,31–33,35–36,38 the association between depression and outcome was either no longer statistically significant20,25,26 or was attenuated.17,21,29,33,35,36,38
TABLE32-1.Observational studies assessing the relationship between depression following myocardial infarction and mortality and recurrent cardiac events Baseline Sample size,nprevalence of Author,year,place(% women)Depression measuredepression (%)OutcomesLength of follow-upAssociation between depression and outcome(s) Silverstone (1987),UK15108 (25.0)MADRS44.4Cardiac events1 weekDepression measured within 24 hours of MI was predictive of increased ACMrisk of ACM or cardiac events Ladwig (1991),Germany16553 (0)KSb-SHigh:14.5Cardiac events6 monthsDepression predicted CM (P=0.035) and cardiac events (P=0.001) in Med:22.2CMbivariate analyses only Low:63.3 Frasure-Smith (1993),222 (22.1)Modified DIS15.8CM6 monthsMajor depression predicted CM in both bivariate (HR,5.74;95% CI Canada174.61–6.87) and multivariate analyses (HR,4.29;95% CI,3.14–5.44) Jenkinson (1993)*,UK181376 (22.0)Investigator tailored scale5.7ACM6,12,and 36 monthsDepression did not predict ACM (P=0.48) Denollet (1995) Belgium19105 (0)MBHI46.7ACM2–5 yearsDepression predicted ACM (P<0.005) and CM (P=0.01) in bivariate CManalyses only Frasure-Smith (1995),222 (22.1)Modified DISMDD:15.8Cardiac events12 monthsBoth major depression (OR,2.67;95% CI,1.22–5.85) and depressive Canada20BDIBDI ≥10:31.2symptoms (OR,3.32;95% CI,1.69–6.53) were predictive of cardiac events in bivariate analyses only.After adjustment,depression did not predict cardiac events Frasure-Smith (1995),222 (22.1)Modified DISMDD:15.8CM18 monthsDepressive symptoms predicted CM in bivariate (OR,7.82;95% CI, Canada21BDIBDI ≥10:31.22.42–25.26) and multivariate (OR,6.64;95% CI,1.76–25.09) analyses. However,major depression only predicted CM in bivariate analyses (OR, 3.64;95% CI,1.32–10.05) Carinci (1997),Italy222449 (12.4)CBAF depression scale1.3ACM6 monthsDepression did not predict ACM (HR,1.7;95% CI,0.9–3.1) Denollet (1998),Belgium2387 (6.9)MBHI50.6Cardiac events6–10 yearsDepression predicted CM (OR,7.5;95% CI,1.5–36.4) and cardiac events CM(OR,4.3;95% CI,1.4–13.3) in bivariate analyses.Multivariate analyses not reported Frasure-Smith (1999),896 (31.6)BDI32.4CM12 monthsDepressive symptoms predicted CM in both bivariate (OR,3.23;95% CI, Canada241.65–6.33) and multivariate (OR,3.66;95% CI,1.68–7.99) analyses Irvine (1999),Canada25634 (17.2)BDI†Cardiac events2 yearsDepression predicted cardiac events in those receiving placebo medication after controlling for previous MI and congestive heart failure (OR 2.45;95% 1.14 = 5.35.However,after additional adjustment for dyspnea,depression did not predict cardiac events (RR,1.73;95% CI,0.75–3.98). Kaufmann (1999),US26331 (34.4)DIS27.2ACM6 and 12 monthsMajor depression only predicted ACM at the 12 month follow-up in bivariate analyses (p=0.04) Lane (2000),UK27288 (25.3)BDI29.8Cardiac events12 monthsDepression did not predict cardiac events in either bivariate (OR,0.97; 95% CI,0.55–1.70) or multivariate (OR,0.79;95% CI,0.43–1.43) analyses Mayou (2000)*,UK28347 (27.0)HADS-D7.6ACM6 and 18 months andDepression did not predict ACM or CM in either bivariate (OR,1.95;95% CM6 yearsCI,0.83–4.56 and OR,1.34,0.44–4.10,respectively) or multivariate (OR,2.69;95% CI,0.97–7.48 and OR,2.07;95% CI,0.53–8.09, respectively) analyses
Welin (2000),Sweden29275 (16.4)Zung SRDS36.7ACM10 yearsDepression predicted ACM and CM in both bivariate (OR,2.45;95% CI CM1.49–4.02 and OR,3.54;95% CI,1.85–6.79,respectively) and multivariate (OR,1.75;95% CI,1.02–2.99 and OR,3.16;95% CI, 1.38–7.25,respectively) analyses Bush (2001),US30267 (58.0)SCIDMood disorder:17.2ACM4 monthsOnly mood disorder ±depressive symptoms were predictive of ACM in BDIBDI ≥10:19.0bivariate analyses (RR,3.8;95% CI,†;P=0.008).Multivariate Mood disorder ±BDIanalyses were not reported ≥10:27.3 Lane (2001;2002)*,288 (25.3)BDI30.9ACM4,12,and 36 monthsDepression did not predict ACM or CM in either bivariate (OR,1.04;95% UK31,32CMCI,0.50–2.16 and OR,0.84;95% CI,0.37–1.90) or multivariate (OR, 0.77;95% CI,0.33–1.76 and OR,0.56;95% CI,0.22–1.43) analyses Lespérance (2002),896 (31.6)BDI≥10:32.4ACM5 yearsBDI scores ≥10 predicted a 2- to 4-fold increased risk of ACM and CM in Canada33CMbivariate and multivariate analyses.Depression was associated with a Cardiac events1.6- to 2.4-fold greater risk of cardiac events in bivariate analyses only.BDI scores <10 only predicted CM in bivariate analyses Luutonen (2002),Finland3485 (23.5)BDI21.2ACM18 months† Shiotani (2002),Japan351042 (19.6)Zung SRDS42.0CM12 monthsDepression predicted cardiac events in both bivariate (OR,1.46;95% CI, Cardiac events1.11–1.92) and multivariate (OR,1.41;95% CI,1.03–1.92) analyses. However,depression did not predict CM Carney (2003),US36766 (39.6)DSM-IVAny:46.7ACM30 monthsDepression (MDD/minor/combination) was associated with a 2- to 3-fold DISHMDD:45.5increased of ACM in bivariate and multivariate analyses BDIMinor:54.5 Lauzon (2003),Canada37587 (19.8)BDI34.7ACM12 monthsDepression did not predict ACM (HR,1.3;95% CI,0.59–3.05) in bivariate analyses Strik (2003),The318 (0)SCL-90 depression47.1Cardiac events1–70 monthsDepression did not predict cardiac events in bivariate analyses.After Netherlands38subscaleadjustment for age,LVEF,and antidepressant use,depression was predictive of cardiac events (HR,2.32;95% CI,1.04–5.18).However, after additional adjustment for anxiety and hostility,depression did not predict cardiac events (P=0.45) Steeds (2004),UK39131 (32.8)BDI (version II)47.3ACM25–37 monthsDepression did not predict ACM (OR,1.8;95% CI,0.56–6.0) in bivariate analyses ACM =all-cause mortality;BDI =Beck Depression Inventory;Cardiac events =fatal and nonfatal cardiac events combined;CI =confidence intervals;CM =cardiac mortality;CBAF =Cognitive-Behavioural Assessment Form;DIS =Diagnostic Interview Schedule;DISH =Depression Interview and Structured Hamilton;DSM-IV =Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition);HADS-D =Hospital Anxiety and Depression Scale-Depression subscale;HDRS =Hamilton Depression Rating Scale;HR =hazard ratio;KSb-S =Kleinische Selbstburteilungsskalen;LVEF =left ventricular ejection fraction;MADRS =Montgomery-Asberg Depression Rating Scale;MBHI =Millon Behavioural Health Inventory;MDD =major depressive disorder;MI =myocardial infarction;NS =not significant;OR =odds ratio;PVCs =premature ventricular contractions;RR =relative risk;SADS =Schedule for Affective Disorders and Schizophrenia;SCID =Structured Clinical Interview for DSM-III-R;SCL-90 =Symptom Checklist-90;SD =standard deviation;SRDS =Self-Rating Depression Scale;<=less than;≥=greater than or equal to;† =not reported;* =the results from the longest follow-up period available are presented.
Further, the inference that some exposure or characteristic constitutes an independent, causal, risk factor for some health outcome is usually based on multivariate analyses in which a statisti- cally significant bivariate association between the exposure or characteristic and the health outcome remains after adjustment for potential confound- ing variables. However, declarations of indepen- dence on this basis may be premature.44 The ability of multivariate statistical models to deter- mine independence depends on the accuracy of measurement of the potentially confounding variables; any inaccuracy will inevitably lead to underestimation of their true impact.44 Therefore, “it can appear that a risk factor is related to disease after the adjustment for confounding factors, but this residual relationship only exists because of under-adjustment for these confounding factors” (Davey Smith and Phillips,44 p. 257).
The indices of disease severity employed in observational studies in this area have been various and all are imperfect. Accordingly, char- acteristics such as depression can appear to have an independent association with mortality or recurrent cardiac events but this could arise as a consequence of the residual confounding of depression with disease severity, where disease severity is measured imprecisely. Since no single precise measure of cardiac disease severity exists, composite indices assessing the severity of the MI, degree of heart failure, left ventricular dysfunc- tion, medication, presence of arrhythmias, and length of index hospital admission, among others, may be a better method of capturing exactly how ill patients are.45
Experimental Studies
The issue of whether depression is a cause of mor- tality, through some as yet identified pathway, or is a marker for some other cause, is an impor- tant one. If depression is a cause, its appropriate treatment should reduce subsequent mortality.
However, if depression is only a marker of some other underlying cause, for example disease sever- ity, the treatment of depression per se should not affect prognosis.
The reported association between depression and mortality and recurrent cardiac events has
helped to initiate interventions aimed at reducing depression and thus mortality and morbidity.
To date, two randomized controlled trials, one large-scale cognitive-behavioral trial, supple- mented where necessary with antidepressant medication (Enhancing Recovery In Coronary Heart Disease: ENRICHD),48 and one phar- macological trial (Myocardial INfarction and Depression-Intervention Trial: MIND-IT),46 have examined the impact of reducing depression post- MI on subsequent morbidity and mortality (Table 32-2). Another pharmacological trial, SADHART (Sertraline Antidepressant Heart Attack Ran- domised Trial: SADHART),47assessed the safety and efficacy of SSRI antidepressants in unstable cardiac patients (Table 32-2). Both SADHART47 and ENRICHD48observed a relative reduction in depression with treatment.
However, the interventions had no significant effect on nonfatal reinfarction or mortality48or on indices of disease severity, such as left ventricular ejection fraction, ventricular arrhythmias, or elec- trocardiogram profile.47We await the results of the MIND-IT trial.46
Summary of the Evidence Concerning Depression and Prognosis
The balance of evidence and argument suggests that it is right to be skeptical about a causal link between depression following MI and sub- sequent cardiac events and mortality. The recent meta-analyses suggest that depression following MI is associated with a slightly elevated risk of all-cause mortality and recurrent cardiac events after adjustment for potential confounders, including disease severity. However, few studies included in these meta-analyses reported statistical outcomes following adjustment. In addition, the possibility of residual confound- ing remains even in those studies which have undertaken multivariate analyses, given the difficulties surrounding the accurate assessment of disease severity in this context. Further, the one experimental study, to date, to have its findings published, found that an intervention effective in ameliorating depression did not influence mortality or recurrent nonfatal cardiac events.48
TABLE32-2.Experimental studies examining the impact of interventions to reduce depression on outcomes in MI/unstable angina patients Sample size,n (% women);studyLength of Trial,year,countryperiodInterventionOutcome(s)follow-upSummary MIND-IT (2002),The320 (†) MI patientsMirtazapine (or open-labelCardiac events (cardiac death12–27 monthsOngoing trial – results available late 2005/early 2006 Netherlands46enrolled Septembercitalopram**) (n=190) vs.or hospital admission for 1999 to March 2002usual care (n=130) for 24nonfatal MI,unstable weeksangina,heart failure,or ventricular tachyarrhythmia) SADHART† (2002),US,369 (36.6) MI andSertraline (n=186) vs.Change in baseline LVEF ECG6 monthsNo significant differences between two groups in LVEF,ECG Europe,Canada,Australia47unstable anginaplacebo (n=183) for 24parameters (e.g.PVCs)parameters,death,or recurrent cardiac events patients enrolledweeksReduction in depressionSertraline significantly reduced depression compared to placebo April 1997 to April 2001 ENRICHD (2003),US482481 (43.7) MICognitive-behavioral Death or nonfatal MI30 monthsAll events:HR (95% CI) =1.01 (0.86–1.18) patients enrolledtherapy* (n=1238) vs.ACMACM:0.98 (0.79–1.21) October 1996 tousual care (n=1243) forCVMCVM:0.83 (0.64–1.10) October 1999maximum of 6 monthsRecurrent nonfatal MIRecurrent nonfatal MI:0.90 (0.71–1.14) Reduction in depressionCognitive-behavioral therapy significantly reduced depression ACM =all-cause mortality;CI =confidence interval;CVM =cardiovascular mortality;ECG =electrocardiogram;ENRICHD =Enhancing Recovery In Coronary Heart Disease;HR =hazard ratio;LVEF =left ventricular ejec- tion fraction;MI =myocardial infarction;MIND-IT =Myocardial INfarction and Depression Intervention Trial;PVC =premature ventricular complexes;SADHART =Sertraline Antidepressant Heart Attack Randomised Trial; * =given if mirtazapine was refused or not tolerated;** =249 patients received adjunctive antidepressant medication;† =SADHART was designed to assess the safety and efficacy of sertraline use in unstable cardiac patients.
Depression Following MI and Quality of Life
Whatever the case regarding depression following MI and clinical prognosis, it is clear that depres- sion has substantial lifestyle consequences for MI patients. Several studies have now demonstrated a link between depression and subsequent quality of life.28,31 In this context, it is worth noting that cardiology has started to embrace outcomes other than morbidity and mortality, such as quality of life. As an influential editorial argued, “We should not lose sight of the fact that an intervention that improves well-being, but fails to change survival, is still a very valuable treatment” (Lespérance and Frasure-Smith,49p. 20). Quality of life is discussed in more detail in Chapter 31. Aside from overall quality of life and subjective well-being, depres- sion has been linked to a range of behavioral out- comes in MI patients: non-attendance at cardiac rehabilitation,50 delayed return to work,51 and poor adherence to medication.52
Implications for Patient Management
The research on depression following MI has clear implications for patient management. As soon as MI patients are medically stable, as determined by a cardiologist, they should undergo routine screening to identify those that are severely dis- tressed. There are many self-report questionnaires available53 to assess depression, with the Beck Depression Inventory,54and the Hospital Anxiety and Depression Scale55being among those most commonly employed. Symptoms of depression should be assessed using a self-report instrument during hospitalization (3 to 7 days post-MI), and 6 weeks or so after discharge (usually when formal cardiac rehabilitation classes begin), to identify those patients who are experiencing significant emotional distress. Appropriate referral to a mental health professional should be considered for those patients demonstrating persistent ele- vated symptoms of depression, to allow for assess- ment of clinical depression and appropriate treatment. For those patients who are depressed or have a history of depression, therapy, in addi- tion to health education and exercise rehabilita-
tion, should be made available. For most, intervention with cognitive behavior therapy, supplemented where appropriate with selective serotonin reuptake inhibitors, is advised. Cogni- tive behavior therapy has proved to be an effective treatment for depression in the general popula- tion, and in the ENRICHD trial,48relative to usual care, it significantly improved levels of depression following MI. In addition, treatment with selec- tive serotonin reuptake inhibitors, regardless of treatment arm, was associated with decreased mortality.48
Conclusions
The issue of whether depression following MI is a causal factor in subsequent mortality and cardio- vascular morbidity remains to be resolved. Only further randomized control trials will truly advance our understanding. In addition, future observational studies should report multivariate analyses in which adjustment is made for poten- tial confounders, most importantly measures of disease severity. Better composite measures of disease severity need to be employed.45Irrespec- tive of the implications of depression following MI for mortality and morbidity, the high incidence of depression in this population and the link between depression and quality of life should be sufficient to suggest changes to patient manage- ment practices.
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