Depression and acute myocardial infarction: A review and reinterpretation

SW. Sci. Med. Vol. 32, No. 9, pp. 1017-1027,1991

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DEPRESSION AND ACUTE MYOCARDIAL INFARCTION: A REVIEW AND REINTERPRETATION RICHARD FIELDING

Department of Community Medicine & Unit for Behavioural Sciences, University of Hong Kong, Pokfulam, Hong Kong Abstract-Depression is widely accepted as occurring in response to acute myocardial infarction (AMI), and to be an important determinant of recovery. A review of the literature reveals that three categories of patients with depressive symptomatology may be identifiable. First, many patients show depressive symptoms before admission with AMI; these may intensify during hospitalisation. For these patients, the depressive symptoms may contribute etiologically to the onset of AMI or derive from a common source along with AMI. The second group constitute patients with a history of AMI, and who on readmission with chest pain or suspected AM1 are more likely to report depressive symptoms. The third group of patients are non-depressed first time admissions for AMI. These patients appear to show transient depressive reactions, much of which it is argued, occurs as a reaction to hospitalisation and not to AM1 per se. This review considers the theoretical context whereby depressive symptoms may arise from the same circumstances that generate the coronary heart disease which underlies AMI, and links this to the generation of helplessness and cardiopathic processes. Key wordr-depression,

myocardial infarction, etiology, recovery

INTRODUCTION

Good reason exists for examining the nature of links between coronary heart disease (CHD) and depression. CHD is a major cause of death and disability in the industrialised world. For example, it is found to some extent in about one-third of all men under age 65 in the U.S.A. [ 11.Despite much opinion to the contrary, the proposed origins [2] and some treatments (e.g. Ref. [3]) of CHD are disputed. Depression is commonly related to acute myocardial infarction (AMI), being most frequently described as a response to AM1 and widely accepted as such [4]. Despite this, evidence exists suggesting important alternative roles for depression in AMI. Specifically, arguments are explored that suggest symptoms of depression may predate AM1 in a significant proportion of patients, and that for some patients depression seen post AM1 is due more to the effects of hospitalisation than to AMI. This review addresses four sets of questions regarding AM1 and depression. First, is there evidence that depression predates manifest AMI? If so, is depression a marker for AM1 or does depression contribute to AMI? Second, there is a high prevalence of depression following AM1 [4,5]. What is the relationship between AM1 and depression post AMI? Third, what is the relationship between depression and recovery from AMI? Finally, if depression is a risk factor for AMI, how might it exert a pathogenic effect? METHODOLOGICAL

ISSUES

i. Data collection

Searches were made of Medline and Psychinfo databases from 1980 onwards, supplemented by a

manual search of Index Medicus and Psychological Abstracts from 1960. All papers found on any depression predating any CHD were extracted. Papers focusing on depressive reaction to AM1 [but not Angina pectoralis (API], and on recovery from AMI published after 1969 were extracted. Attempts were made to trace references cited in papers not obtained by search, though this was often unsuccessful. Papers subject to meta-analytic review were not re-reviewed. Instead, the review itself is cited. Biochemical references were traced back to original sources from later publications. The literature on AP and sudden death was not searched, except in relation to CHD onset, nor that on Type A behaviour, given its intensive coverage elsewhere. ii. Definitional issues on assessment of depression

The various contributions to depression remain unclear. While the genetic/biochemical dimension may be important in Major Depressive Disorder (MDD) and Bipolar/Manic disorders, it may be less significant in dysthymia, [6] and unimportant in relation to depressive coping style [7,8]. Few published studies used Diagnostic and Statistical Manual (DSM) criteria for case finding, or distinguished between depression, melancholia or dysthymia. In the studies reviewed here, the most common means of assessing ‘depression’ were the Minnesota Multiphasic Personality Inventory ‘D’ subscale (MMPI), the Beck Depression Inventory (BDI), the Profile of Moods Scale (POMS) and the Centre for Epidemiological Studies Depression scale (CES-D). All of these scales probably tap a common dimension of ‘depressiveness’ in that the item similarity is high, often inter-correlations of more than +0.65 exist between these instruments, which suggests considerable conceptual equivalence.

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RICIWRD

Because ofthe homogeneity amongst definitions of depression used in published studies, for the purposes of this review the term depressive symptoms is used to refer to the presence of dysphoric mood, and sleep, appetite or motivation disturbance, loss of self esteem, anergia, and difficulties in concentrating. Helplessness may be seen, with impaired coping and learning. Increased negative cognitions and a bias in favour of the recall of negative memories are also seen [9]. This bias is an important methodological issue in studies of depression. If, at the time of interview subjects were depressed, this may compound other retrospective biases. This is seldom mentioned in published studies and should be kept in mind by the reader. Hence, depressive symptoms represent a more enduring, less intense form of depression than MDD. By DSM-III-R criteria, depressive symptoms would approximate more to dysphoria/dysthmia than to MDD. It is assumed that depressive symptoms arise as a result of environmental rather than genetic/ biochemical causes. iii. Prevalence of depressive disorders

A prerequisite for a review of this nature is some linkage between the prevalence of CHD and that of depressive symptoms. Few recent epidemiological studies have addressed depressive conditions other than MDD (see Appendix for diagnostic criteria). Age, cohort and period effects have been claimed for MDD, with younger adults having higher prevalence than older; the birth cohort of 1935-1945 have higher rates than other cohorts; and period of onset rates increasing between 1960-1980. Mostly prevalence only is reported, with little attempt to identify etiologic variables. Also, many report on limited cohorts only (e.g. Ref. [lo]). Thus, these effects may be limited and as is often the case, different approaches to a problem have led to differing findings. Cumulative rates for MDD in U.S. Whites appear to remain low at 2-7% for males, and females born before 1934, but for females born after 1935 cumulative rates reach lO-20%, with younger persons having higher rates than older [lO-121. For depressive symptoms, simple prevalences between gender and ethnic groups range from lO-28.6% [13]. However, age [13, 141, sex [15-181, marital status [19], ethnicity [16,20] and life stress [12,21] effects associate with depressive symptoms inconsistently. Moreover, the role of cognitive factors is recognised as central to differentiating between individuals who report depressive symptoms in relation to particularly chronic stressors [22-241. The prevalence of CHD is well known to increase with age, and predominate in males. Though cohort effects are usually reported as absent in CHD, some have been identified [25]. It is over simplistic to argue that the proposed hypotheses are untenable because CHD affects mainly older men, whereas depression affects mainly younger females. Both of these propositions are equivocal. Given that the complex interplay of factors in both depression and CHD remains poorly understood (see below), and the inconsistent results from epidemiological studies of these conditions,

FIELDING reviewing their relationship these two conditions. UNRESOLVED ISSUES CORONARY

offers new insights into

IN THE EPIDEMIOLOGY HEART DISEXSE

OF

This section explores commonalities underlying the two conditions together with shortcomings of current etiological models, and sets the context for the review. CHD is a narrowing or obstruction of the coronary arteries which acutely interrupts blood supply to part of the myocardium (heart muscle), which may then die (myocardial infarction, AMI). Transient ischemia causes sporadic chest pain (AP) which resolves on resting or if angina1 drugs are taken. An unstable form of AP is resistant to these drugs, or occurs at rest. AMI usually presents as acute ischemic pain, with raised serum catalytic enzymes, enduring electrocardiographic (ECG) changes, systemic shock and often fatal collapse. Non-fatal AMI and fatal AMI may reflect differences in severity of arterial disease. Silent AM1 features asymptomatic enzyme and ECG changes. Sudden cardiac death seems to arise from chaotic electro-muscular activity in the heart, possibly with different origins to AMI. Only a minority of AM1 or sudden cardiac death cases have preexisting AP [26]. CHD trends vary over time [27], while the distribution of risk factors differs geographically and socially from that of CHD [28]; CHD decline among wealthy communities contrasts with comparable increases among poor communities [2,26,29-3 11. Hypertension, tobacco smoking and serum cholesterol are seen as the most important risks for CHD [27,32-371. Hypertension is the most important of these [38] deriving from several sources, including existing degree of artery occlusion, smoking, and coping with demanding situations [39-41]. Some decline in CHD rates may derive from reduced risk factors [42]. However, smoking, cholesterol intake and hypertension levels account for only about 30-50% of the observed variance in CHD rates [32-34,431, and large scale community intervention trials which reduced multiple risks have had little impact on CHD or overall mortality rates that have not been matched in control groups [3S-37,44,45]. Genetics and culture (e.g. Ref. [46]), Type A behaviour (e.g. Ref. [47]), life events and anxiety (see Refs [30,48-SO]) may also contribute to CHD risk, while improved housing and living standards generally may have helped to reduce CHD incidence [2]. One notable feature is that persistently higher CHD rates are seen in disadvantaged communities [2,26,29,30,51-531. (These are characterized by low occupational status, low educational level, unemployment, substandard housing, overcrowding, and the percentage of over 65 year olds with incomes below the poverty line [2].) This may lead to migration, marriage delay and breakdown, unemployment and overwork and may generate high levels of helplessness (and hypertension), all of which have been associated with excess CHD mortality [52]. Thus, while political expediency may favour individual over

Depression and acute myocardial infarction social etiologi& [2], CHD is clearly a disease of communities, and increasingly poor communities over wealthy ones. Intriguingly, different social groups show different CHD rates for a given level of risk factors [2,29,32]. Current risk factor models fail to explain such differences, suggesting some other variable(s) modulate risk. How people cope with demands in their life may account for additional variance in CHD [47+9,54]. Persons living in deprived circumstances face more problems in daily living, more life events [55], the consequences of which may be more aversive, while having fewer resources for coping with these [2,52]. Retaining control over important aspects of one’s life under difficult circumstances disrupts cardiovascular activity if the consequences of non-control are aversive [40,41,52]. People who perceive important aspects of their lives as uncontrollable tend to cope passively with demands [56, 371, while others (e.g. Type A [47-49,28,30]) aggressively strive to cope in extremis, then become passive [54,35]. No doubt other response patterns also exist. Where the absence of control over important aspects of life (employment, income, health) is chronic, greater stress is reported [57, 581, and helplessness may be experienced together with depressive symptoms. Vulnerability to depression increases with low education, poor perceived health, personal uncertainty, recent residential move, job loss, and chronic health conditions [ 131. Within these circumstances, depression is independent of age, income, origin, marital status, separation or divorce, or health practices [13]. With depression, perceptions of well-being are less [59-61], and more illness behaviour and symptoms are seen [56,62], with a greater tendency to seek medical care [56]. Depressed people may be less likely to believe that they can successfully carry out illnessalleviating behaviours [56], revealing a pessimistic explanatory style [63], associated with denial, distancing and emotion control coping [64]. Depression can predict poor health up to 25 years later [65,66], suggesting an enduring response style is implicated.

DEPRESSIVEDISORDERIN THE ETIOLOGYOF AMI Since 1960, depressive symptoms have rarely been considered in relation to AMI onset. The Western Electric Study reported higher MMPI depression scores prospectively gathered on a cohort of men who later developed AMI, compared to those who did not [67]. Later, the authors reported higher MMPI depression scores for men developing fatal AMI than for those developing non-fatal AMI [683. Most early studies had serious methodological shortcomings. For example G.P. patients prospectively identified as anxious or depressed (not specified) later received a cardiological examination and were found to have more possible and probable CHD than non-anxious, non-depressed patients [69]. One other study reported more unspecified ‘depression’ retrospectively in men manifesting CHD [701. Crisp, Queenan and D’Souza [71], reported on subjects screened three times over 5 years, 26

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of whom experienced AMI. AM1 patients were reportedly ‘significantly more depressed’ before the event. But, 11 of the 26 patients did not receive their third screening until after their AM1 and at the previous (second) screening simple ‘depression’ scores for the patients were no higher than for controls. Moreover, 62% of patients experienced chest pain before the AMI, a possible cause of depressive symptoms, but chest-pain influences on mood were not controlled for. All three of these studies are further biased by assessor or subject knowledge of the diagnoses and poor assessment of depression. Recent studies tend to be sounder. Booth-Kewley and Friedman [72] found a larger meta-analytical effect size between depressive symptoms and all CHD, than between all measures of Type A and CHD. Specifically for AMI, a larer effect size (r = 0.259) was seen for depressive symptoms than for any other variable examined (including 16 various Type A features) in seven studies which reported independent effect sizes for depressive symptoms. A comparison of cross-sectional with prospective studies (n = 3) for all CHD revealed smaller effect sizes for depressive symptoms in prospective studies (r = 0.168) compared to cross-sectional studies (r = 0.204; P < 0.00008). Criteria for inclusion were strict. Camey et al. [73] identified 9/52 patients as having DSM-III defined MDD prior to cardiac catheterization. Major cardiac events over the subsequent year were noted. MDD was the single most important predictor of major cardiac events, independent of CHD severity, left ventricular function, and smoking. But this depression may partly have been a response to ischemia, signs of which presumably led to angiography. AM1 sometimes follows other indicators of ischemic disease, rather than being the first manifestation [48,74], and up to 30% of patients who suspect they have, or who are investigated for CHD, report atypical chest pain of non-ischemic origin [74]. Many acquire a diagnosis of CHD nonetheless. Of patients with ‘generalized’ psychiatric diagnoses (including depression), 90% have negative angiogams compared to only 45% of patients without such psychiatric diagnosis [75]. ‘Emotional upset’ was retrospectively reported as present for over 6 months beforehand in 90/192 (47%) men admitted for suspected AM1 (of whom only 131 had confirmed AMI) [76]. This emotional upset was more likely in patients who continued to be upset during recovery (P < 0.0005). Unfortunately the numbers of patients with depressive symptoms are not known. Jenkins and Zyzanski [51] cited (but did not reference) four studies claiming ‘depression’ predated sudden cardiac death [2] and AM1 [2], only two of which were prospective, and of unknown methodological quality. A prospective link between (undifferentiated) ‘disturbing emotions’ and AM1 has been reported [77]. Depressive symptoms predicted AM1 and death amongst patients receiving electrophysiological studies for cardiac arrhythmias. Depressed patients (S/88) showed either ventricular tachycardia or fibrillation on testing. Though the overall mortality rate was 14.5%, for patients with depressive symptoms, it was 75% [78].

hc~wu,

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Studies fYorn the Netherlands report consistent associations between ‘vital exhaustion’ (VE) and AMI. VE includes dysphoria, tiredness, hopelessness, and sleep disturbance, but not guilt or loss of self esteem [26]. This, the authors argue, makes VE different from clinical depression. However, healthy people at high risk of AM1 (by standard risk factor profile) had elevated levels of depressive symptoms, compared to AM1 patients [79]. A prospective study of 3877 males over 4.2 years found VE predicted future angina, particularly unstable AP (Relative Risk = 1.86) and non-fatal AM1 (RR = 2.28), when standard risk factors were controlled [80]. This level of relative risk is less than that attributable to smoking, but slightly greater than that for cholesterol. The authors concluded that vital exhaustion preceded AMI, particularly in younger AM1 patients. It is worth noting the similarity between vital exhaustion, and older concepts such as emotional drain and neurasthenia. Many reports of sleep disturbance preceding AM1 can be found in the literature (e.g. Refs [48,51,81]). Sleep disturbances are seen both in depressive disorders and VE [26,81]. Pre-hospitalisation depressive symptoms are reported in other medically ill groups, and were one of several psychosocial variables related to in-patient depressive symptoms in a group of 71 hospitalised (non-CHD) medical patients, of whom 38% were diagnosed as clinically depressed by standard assessments [82]. Two other retrospective studies [83,84] have reported depressive symptoms predating AM1 in up to 40% of patients. To summarise, there is some evidence for a doseresponse relationship between depressive symptomatology and infarct size 167,681, though negative findings [65] indicate a need for clarification. The small number of prospective studies (n = 3) of depressive symptomatology and AM1 means care must be taken when interpreting meta-analytic data [72] which again indicate a small, but significant effect. The Dutch studies of VE [26,79-8 l] also provide evidence for an antecedent depression-like condition. Retrospective studies tend to suggest that 3848% of hospitalised patients have depression predating admission [76,83,84], though the reliability of these data must be suspect. Prevalence rates for depressive symptoms in the general population are significantly lower than those reported in some of the studies outlined above, being in the region of lO-20% [57] supporting the contention that depressive coping style and symptoms rather than clinical depression may be culpable in this area. Methodologically, the standard of these studies varies from marginal to very good, with poorer methodologies identified as such. The varied criteria for ‘depression’ adopted in the studies makes interpretation more problematic. However, together, these data support the hypothesis that depressive symptoms predate AM1 for a significant proportion of patients. DEPRESSION FOLLOWING

AMI

Because depressed persons have more symptoms and rate their health as worse, compared to the non-depressed [56,61], and because depressed

FIELDING

mood acts as a powerful context for recalling moodcongruent material [9], there is a greater risk of patients being classified as depressed pre-AM1 on the basis of recalled events, or as more ill when in hospital. These two sets of problems obscure the depression-AM1 relationship post AMI. I. Depression as reaction to AMI Depressive reaction to AM1 in previously nondepressed patients is implied in most of the literature [4,5,61], though the foregoing section indicates this may not necessarily be the best interpretation. Available studies seldom controlled the tendency for hospitalised patients generally to develop depressive symptoms. Previous reviews [4,85,86] suggest that depressive symptoms appear on the second or third day post AM1 (e.g. Ref. [5]). However, some studies report no change in the distribution of depressive symptoms over the course of hospitalisation for AM1 from levels at 48 hr post admission [87], others that depressive symptoms are seen at 24 hr post admission [82]. Also, depressive symptoms are not significantly fewer in patients who show ‘denial’ (881. Cay et al. [76] reported 62% of post AMI patients were ‘emotionally upset’ (a term including both anxiety and depression). However, more patients who were later found not to have had AM1 were ‘upset’ than those with confirmed AMI. Patients who had had previous AM1 were more likely to report depressive symptoms. A statistical test of Cay et al.‘s data (Table 3) is not possible, but there appears to be a greater incidence of psychiatric disturbance in men confirmed not to have AMI. This may refIect greater symptom reporting leading to more admission in psychiatrically disturbed patients [75]. Forty-seven percent of the cohort remained depressed after discharge from the Coronary Care Unit. More depression was seen in patients with a history of AM1 independent of whether or not the current AMI was confirmed, and in those with ‘upset’ pre-dating the onset of AM1 [89]. More recently, 52/283 patients were diagnosed as having MDD and 76/283 as having ‘minor depressive disorder’ 8-10 days post-AMI. Non-depressed, minor depressed and major depressed groups were distinguished by reporting a decreasing sense of control over their lives. The degree of depression was not significantly associated with extent of cardiac impairment [83]. Lloyd and Cawley identified two groups of patients with unspecified psychiatric morbidity at one week post AMI. One group had morbidity predating the AMI, the other had morbidity ‘in reaction to’ their AMI. Patients’ (30/100) with pre-existing AP had more morbidity post AM1 than others. Those with symptoms in reaction to AM1 more closely resembled normal patients [go]. Thus, two groups of depressed patients can be identified: those with major depressive disorders who are more likely to have been depressed prior to AM1 and report more stressful life events in the year preceding AMI, and those with less intense depressive symptomatology. This again suggests that a chronic depressive coping style may characterize these former individuals.

Depression and acute myocardial infarction Clarification-both of the role of different subtypes of depressive features, and of the effects of previous AM1 on depressive symptomatology after subsequent AM1 is needed. If AMI patients with concurrent non-CHD illness are more likely to report depressive symptoms, then patients with previous cardiac illness would also be expected to do so. Depressive symptoms seem to form very early, usually being transient if in reaction to AMI in first time CHD patients, or more intense and prolonged in patients with a history of CHD. Reports indicate depressive symptoms post-AM1 remain unaffected by denial [69]. 2. Depression symptoms arising from hospitalisation An alternative explanation for depressive symptoms post-AM1 is that they arise in reaction to hospitalisation rather than AM1 per se. Loss of control over most tasks and forced reliance on staff during hospitalisation generates personal helplessness, leading to depression [91,22,23]. About 40% [82] of medical inpatients report increasing depressive symptoms, that are independent of illness severity [92] over the course of hospitalisation, plus increased impairment on cognitive tasks and more susceptibility to helplessness when exposed to inescapable noise [93]; key characteristics of helplessness [94]. Higher cortisol levels found over three days following onset of AM1 may reflect sudden loss of behavioural control on admission [95]. Notably, no association between numbers of previous hospitalisations and depressive symptoms was found among general medical patients (821, suggesting these are independent of hospitalisation history. The only known study comparing home versus hospital care of AMI did not report on psychological reactions to AM1 [74], but such a future study could help to clarify the contribution of hospitalisation in depressive symptoms post-AMI. There is substantive evidence that depressive states pre-date AMI. Do patients already showing depressive symptoms on admission experience more depressive symptoms post-AM1 than otherwise? The answer seems to be affirmative. Crisp et al. [71] reported patients who were depressed prior to their AM1 were more likely to have higher post-AM1 depression scores than the general population, while Cay’s studies [76,89] indicate a greater depression score for patients readmitted with AM1 and more ‘upset’ postAMI in patients with pre-existing ‘upset’. However, van Doomen [79] reported high risk healthy persons to have a higher depression score than AMI patients (though this may indicate a survivor effect for the less depressed, e.g. Ref. [68]). Finally, a 9 year prospective study found depressive symptomatology at baseline accounted for a relative risk of 4.10 (95% limits 3.23-5.19) for depressive symptoms at follow up [13]. In summary, the available evidence indicates that depressive symptoms post-AM1 may not arise solely in reaction to AMI, but may be a reaction to the effects of hospitalisation. More severe depression is seen in patients with a past history of CHD, in those admitted for chest pain, irrespective of whether AMI is confirmed [76,89], implying more of a reaction to the illness.

DEPRESSIVE SYMPTOMS

1021 AND OUTCOME

The relation between depressive symptoms and outcome from AM1 appears unequivocal. Depression has been identified as a significant predictor of mortality amongst post-AM1 patients [65,68,96-991. AfReck et al. [loo] reported more causal attributions (which may reflect perceptions of control [loll) to ‘stress’, more responses ‘blaming’ others, and fewer benefits perceived from the AM1 at 7 weeks after the event as predictive of eight year morbidity post-AMI. Unfortunately, the authors did not assess mood. Similar blaming responses predicted nonadherence with rehabilitation programmes post AM1 [95]. However, preliminary reports suggest accepting personal responsibility in non-depressed patients is associated with active coping responses for the AMI [84], consistent with AfIleck et al.‘s findings. These data are consistent with depressed patients ascribing cause to uncontrollable events [22,23,94]. Blaming responses for AM1 associate with helplessness and nonadherence to self-help [95], but not to drug treatments [loll, though depressed patients are less likely to adhere to medical regimens [87, 1021,and persons attributing causality to uncontrollable sources seem more likely to become depressed [92]. So, self-dependent behaviour change should occur less in depressed than in non-depressed patients. A confirmation of this prediction would be important in tying together this area. Levels of cardiac damage sustained during the AMI have little, if any bearing 6 months to 1 year later on return to previous occupational and social activity levels [103-1051. By contrast, the presence of depression is consistently reported as a major predictor of poor long-term outcome [63,83,85,86,95, 106-1081. Depressed AM1 patients are less likely to return to normal occupational and social activity levels [83,104]. Expectation of reduced work capacity, depressive symptoms and anxiety during hospitalisation, and low cardiac knowledge predicted poor return to work (as did place of residence) [ 107. Though not reporting on depression per se, Wicklund and colleagues [109] showed that ‘sedative use’ was a significant predictor of risk of reinfarction, and the authors argue this reflects chronic emotional disturbance, though perhaps more anxiety-related than depressive in nature. Interventions that have targeted reducing General Health Questionnaire scores, of which depressive symptoms are a key component in patients post AMI, have reported significant reductions in mortality and non-fatal AMI lasting several years after the brief intervention programme 1110, 11I]. This and similar studies show that morbidity and mortality rates post AM1 are significantly influenced by changing levels of depressive symptomatology. In summary, depression is arguably the key obstacle to effective and full recovery from AMI. PROCESSES RELEVANT TO DEPRESSION IN AMI 1.

Coping with AMI

Patients perceive work pressure, worry and smoking to be the principal causes of AMI [ 101, 1121, while most treatments are aimed at standard risk

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RICHARD FIELDING

factors, which AM1 patients view as more controllable, but less pathogenic than overwork, worry and stress [loll. Uncontrollable problems, like financial worries, work demands, or reinfarction after adherence to treatment may lead to helplessness, more so when medical advice has been complied with [113]. From this view, patients’ perceptions of AM1 etiology are the more realistic [2, 113, 1141. Notably, when AM1 patients perceive health as determined by personal efforts, personal culpability for the AM1 is more likely, together with active coping to minimize future risk [84]. But, some AM1 patients blame others for the life events before AM1 [115], and even for the AM1 itself [75,80]. Believing themselves to be unable to control causes, passive coping may come to predominate [84,95, 116-l 181. Causal attributions may determine strategies for coping [I 191. Many AMI patients ‘make sense’ of what has happened over the first 48 h or more after diagnosis. Control of emotional reactions to the event ‘anesthetizes’ patients. Then, frequent but brief ‘peeking’ gives controlled exposure to the event, allowing its implications to be dealt with. This seems always to be something the patient is aware and in control of [84]. By contrast ‘denial’ implies a fear-driven refusal to face the event. Making sense (permitted by ‘denial of impact’) is desirable in that it permits adaptation while consciously controlling emotions. A better outcome is seen with transitory ‘denial of impact’ post AM1 [120,121] which is similar to the concept outlined above. A similar coping pattern has been proposed for breast cancer patients [122]. There is good evidence for an interaction between coping style, perceived controllability of life events [llS, 1161, and depression [22,23, 117, 1231. Weaker evidence links depressed mood, low controllability of health and the perception of AM1 as a chance event [84], and coping to control emotions [124], as opposed to coping to control threat [118, 1251. After a first AMI, attributing causes for AM1 to controllable sources would be expected to prompt active treatment adherence and lifestyle change. Subsequent AM1 should produce more noncontrollable attributions (since attempts to prevent recurrence have failed), and depressive symptoms. So far, this has not been tested, but depressive symptoms occurs more after subsequent AMI than first AMI. Causal attributions for AM1 may interact with depressive cognitions in a two way manner. Perceptions of noncontrollability lead to depressive symptoms [94], while depressed AM1 patients are more likely to attribute non-control to causal attributions post AMI, and be less likely to take steps to confront and actively cope with the problems they face, implying poorer outcome. Ability to cope with difficult situations in premorbid life predicts survival following first AM1 [126]. 2. Depression as a cardiopathic process By what means might depression (as indicated by the presence of depressive symptoms) predispose a person to CHD? The literature suggest two pathways may link depression with potentially cardiopathic changes. The first involves changes in lipid metabolism. Serum concentrations of lipids are highly

labile, and are elevated by dietary intake of fats and other foodstufs, and by acute exercise [127-1291. Although level of activity discriminates between depressed and non-depressed men, depressed men have the lower activity levels [130]. Coping demand [ 131-1341, also elevates lipid levels. A few studies have reported associations between depression and free fatty acid (FFA) levels [135-1381. One explanation for these data is catecholamine-stimulated hyperlipolysis of adipose tissue. Mueller et al. [136] found no correlation between serum FFA concentrations and urinary catecholamines, whereas others reported correlations between cholesterol and noradrenaline levels and argue for this mechanism, making the point that noradrenaline also inhibits enzymes associated with reducing cholesterol levels [138]. Decreased glucose utilization, reported in depression [139, 1401, is often associated with increased FFA metabolism [141]. Pryce [142] reported that decreased glucose utilization persists after resolution of depression. This explanation is preferred by Mueller [136] for their data. A third mechanism is that FFA levels are stimulated via raised steroid production [ 136, 1441. Steroid elevation is seen in threatening situations where outcome is dependent on controlling acts, or where control is suddenly lost [143], or in passive distress [40]. But van Doomen and van Blokland argue only prolonged demand elevates cholesterol independently of FFA. Helplessness in the face of repetitive aversive stimulation elevates cholesterol (1441 and should also activate adreno-cortical response. Thus an enduring depressive coping style (or precursor state) with passivity, such as helplessness, would be required for a cholesterol-elevating effect which might contribute significantly to atherosclerosis. The major criticism of such cholesterol-led models is that high serum LDL levels do not equate with atheromatous deposition [ 1451, hence high serum cholesterol concentrations alone are probably insufficient to generate CHD. The second pathway involves sympathetic arousal. Sympathetic catecholamines at high levels directly cause diffuse necrotic lesions in the myocardium with accompanying inflammation and fibrous scarring, and small myocardial blood vessels contain aggregated platelets [146]. Catecholamines regulate complex interrelationships between vasoconstriction, localized pressor effects, lipid metabolism, mechanical strain and ischemia which are strikingly similar to those seen in AM1 [146]. Such lesions can be prevented by beta-adrenergic medication [147], a major approach in the treatment of AM1 [148]. Several reports of raised sympathetic activity in depressed patients have been published. van Doornen reported higher heart rate both at rest and during a reaction time test, and an inverse relation between depression and diastolic blood pressure (DBP) amongst depressed, compared to non-depressed subjects [79]. Reduced DBP is associated with a decrease in peripheral resistance to blood flow, consistent with a greater blood supply to muscles. FFA fuels muscle activity. However, as depressed persons are more sedentary than non-depressed, yet have higher serum FFA levels (which are converted into low density lipoproteins (LDL) by the liver), adding to already

Depression and acute myocardial infarction raised resting LDL cholesterol levels, then greater vascular deposition is possible. One report [149] found a high correlation between depression and degree of vessel obstruction on angiography, which relates to the severity of the atherotic process. This was independent of AP intensity or frequency. Direct cardiopathic effects of sympathetic activity are facilitated by steroids, [145]. Blood pressure changes respond to demanding situations in complex ways [40,41,79]. Deficits in coping with aversive stimuli have been linked to Type A behaviour and VE [81]. VE and depression correlated with reported life changes, particularly to do with serious marital conflicts, continuous problems with children and considerable financial troubles [81]; all aversive situations which are not easy to control. By comparison, Type A behaviour seems to be more associated with poorly controllable chronic work-related demand [81]. Life events have reportedly a greater impact, being more distressing for MI patients than for patients admitted with chest pain of non-ischemic origin [150]. Thus, the evidence for depressive symptoms being etiologically important in AMI and even AP and sudden cardiac death is substantial. Links can be made between life circumstances characterised by personally important demanding situations which are difficult, if not impossible to influence positively, and the evidence that lipid, pressor, and sympathetic systems are more active under these situations. We can then link inability to cope with demanding and aversive circumstances to helplessness, and thence to the appearence of depressive symptoms, and to shorter survival times after AMI. Depression is in turn associated with greater lipid activation and sympathetic arousal, lower activity, and often steroid elevation. Depressive states therefore are associated with increased cholesterol and increased cardiac demand at a time of reduced activity and helplessness. Under such circumstances, electrical and vascular led changes in myocardial integrity are prone to occur [29, 146, 147, 1511. Depressive symptoms seem to arise from circumstances which also give rise to other CHD risk [2], and the changes accompanying depressive symptoms may compound such risk by a variety of mechanisms outlined above. Johnston [ 1521has made the point that risk factors are multiplicative, not additive, but current epidemiological approaches make no allowance for this, treating risk variables as independent and additive.

IMPLICATIONS FOR THE ROLE OF DEPRESSION IN AMI

Depressive symptoms often precede AMI, and with indications of a dose-response relationship, a causal interpretation is attractive. However, before this conclusion can be accepted, there are some points to consider. First, a degree of comparability between the depressive symptoms described preceding AMI (vital exhaustion-depression) and that seen post AMI (‘helplessness’ induced depression?) has been assumed. This may not be so. The failure of nearly all published studies to explore diagnostic subtypes of depression, or even to agree on what those are makes

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answering this question difficult. Is this one condition or two, or more? Second, by what extent must the depressive symptoms predate AMI to be- considered contributory? Lebovits allowed an eight year delay between collection of depression data and AMI [68]. This contrasts with the Dutch studies which imply a snowballing loss of vitality intensifying over only a few months preceding the AMI, of which depression is a component [79,80]. More enduring depression pre-AM1 would, according to current models of etiology, presumably be needed if depression is to be considered as a distinct etiological agent akin to smoking, hypertension and cholesterol. This would indicate a persistent type of depressive symptoms or depressive coping style, more akin to dysthymia rather than MDD. However, intensification with MDD overlaying dysthymic/depressive coping processes could produce a sudden cardiopathic effect. Sudden cardiopathic processes are not without precedent [151], and identification of one causal pathway does not exclude others acting concurrently. Work should in future focus more on the role and identification of depressive features and coping in AMI. CONCLUSIONS

In conclusion, this review supports hypothesis that complex interactions between demanding situations and restricted coping probably results in the emergence of depressive symptoms concurrently with changes in physiological systems consistent with those evoked by the standard risk factors for CHD. These demanding situations and coping restrictions are more likely seen in persons living in disadvantaged circumstances. One effect of limited coping may be to encourage or oblige use of other cardiopathic behaviours which compound risk further. Such a model could account for the differing CHD levels in communities with the same level of risks. The following conclusions can be drawn from this review: 1. The patterns of prevalence of CHD are consistent with those for deprived communities. Persons in these communities not only tend to have higher incidences of standard risk factors, but also of aversive demands, which they may be less able to influence through limitations on available coping. 2. Under situations of marginal or non-control, persons may be obliged to make more extended efforts to minimize aversive consequences. The failure of such efforts may trigger chronic maladaptive depressive coping styles resulting in helplessnessinduced depressive symptoms. 3. Depressive symptoms are associated with physiological changes consistent with cardiopathic processes, namely increased serum lipid levels, greater sympathetic arousal, changes in smoking behaviour, and decreases in activity levels and restful sleep. 4. Depressive symptoms have been consistently reported as often well established before the onset of AMI and in many cases, before the onset of prodroma1 symptoms of AM1 such as chest pains.

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5. There is tentative evidence for a doseresponse relationship between level of depressive symptoms and non-AM& fatal AM1 and sudden cardiac death, but this is in need of both confirmation and clarification. If confirmed, it strongly suggests either an etiological role for depressive symptoms in AMI, or that depressive symptoms and CHD arise from common origins. At least one study has equated the relative risk for AM1 associated with depressivelike states as slightly greater than that seen for cholesterol. 6. Following admission to hospital for chest pain, depressive symptoms are seen to be more transient in patients with first AM1 or no history of AMI and no confirmed AMI. Depressive symptoms are more intense and more likely to have pre-dated AMI in patients with a history of AMI, irrespective of whether the latest admission confirms m-infarction. Minor depressive symptoms post-AM1 in individuals not reporting pre-morbid depressive symptoms are most probably a response to hospitalisation than to AMI per se. 7. Depressive disorders are the major obstacle in return to fully functional lifestyle following AMI, and of eventual outcome, with depressed patients having poorer prognoses than non-depressed patients. Subsequent AMI may be associated with high levels of depressive symptoms. High levels of depressive symptoms predict an increase future AMI risk, and continue to be etiologically important post AMI. Acknowledgement-The author acknowledges the helpful comments on drafts of this manuscript by anonymous reviewers of Social Science and Medicine. REFERENCES 1. Moore F. Forward. In Cardiac Surgery (Edited by Norman J.). Appleton-Century-Croft, New York, 1972. 2. Research Unit in Health & Behavioural Change. Changing The Public Health. Wiley, Edinburgh, 1989. 3. Bates M. S. A critical perspective on coronary artery disease and coronary bypass surgery. Sot. Sci. Med. 30, 249-260,

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APPENDIX Criteria for

D$erent

Depressive

Disorders

Major depressive disorders The criteria for which include prominent and persistent dysphoric mood and at least four other other symptoms daily for at least two weeks, e.g. appetite and sleep disturbance, agitation, retardation, loss of interest, fatigue, feelings of worthlessness, diminished ability to think, recurrent thoughts of death. Dysthymia

Depressed mood for at least 2 years, together with at least two of the following; poor appetite or overeating, insomnia or hypersomnia, low energy or fatigue, low selfesteem, poor concentration/difficulty in decision making; feelings of hopelessness. There should be no evidence of equivocal major depressive episode during first two years of disturbance, no history of mania, psychotic disorder, or organic pathology (including pharmacological agents).