Anxiety, Depression, and Psychological Adjustment After an Acute Cardiac Event

  • Barbara M. MurphyEmail author
  • Rosemary O. Higgins
  • Alun C. Jackson
Living reference work entry


Psychological adjustment following acute cardiac events such as acute myocardial infarction (AMI) and coronary artery bypass graft surgery (CABGS) has received increasing attention in the last three decades. While physical recovery remains the highest priority, psychological recovery is now considered a primary concern for health professionals working in cardiac rehabilitation and secondary prevention. The prevalence of anxiety and depression in people who have had a cardiac event is up to four times higher than in the general population. Post-event anxiety and depression both confer an increased mortality risk, highlighting the importance of identifying these patients early in order to ensure appropriate treatment. In recent years it has been recommended that all cardiac patients be screened for depression after a cardiac event. However, there are some inherent problems with routine depression screening, particularly if undertaken soon after the event. There are risks of both unnecessary treatment of patients with transient symptoms and non-identification of patients whose symptoms appear later after physical recovery. This chapter outlines evidence regarding the prevalence and impacts of anxiety and depression in cardiac patients and issues regarding depression screening. Some alternative ways of identifying patients at risk of depression are discussed.


Anxiety Depression Emotional adjustment Distress Screening 

Prevalence of Anxiety and Depression

Many studies document high levels of both anxiety and depression in patients at the time of or soon after an acute cardiac event (Andrew et al. 2000; Barefoot et al. 2000; Berkman et al. 2003; Frasure-Smith and Lesperance 2003; Thombs et al. 2006). A 2006 review of 24 studies involving over 14,000 patients reported prevalence of depression in patients hospitalized after acute myocardial infarction (AMI). Prevalence rates varied depending on the assessment method. Across the eight studies that used a standardized diagnostic interview, the prevalence of major depression varied from 16 % to 27 %, with a weighted prevalence of 19.8 % (Thombs et al. 2006). The largest of the included studies – the Enhancing Recovery in Coronary Heart Disease (ENRICHD) study, which involved over 9,000 patients – reported a prevalence of 20 % (Berkman et al. 2003). Across the 17 studies that used a validated questionnaire, the prevalence of “clinically significant depression” varied from 10 % to 47 %, with variation depending on the instrument used (Thombs et al. 2006). When depression was classified as Beck Depression Inventory (BDI) scores ≥10, the prevalence rates were relatively high, ranging from 20 % to 37 %, with a weighted prevalence of 31 %. In contrast, when depression was classified as Hospital Anxiety and Depression Scale – Depression (HADS-D) scores ≥8, the prevalence was considerably lower, ranging from 11 % to 17 %, with a weighted prevalence of 15.5 % (Thombs et al. 2006). Given these variations, it is difficult to categorically report prevalence rates for in-hospital depression post-cardiac event. However, it is generally agreed that 15–20 % of patients meet diagnostic criteria for major depression while in hospital after acute myocardial infarction (AMI) or coronary artery bypass graft surgery (CABGS) (Colquhoun et al. 2013; Lichtman et al. 2008), with many more showing elevated depressive symptoms (Barefoot et al. 2000; Carney and Freedland 2003; Frasure-Smith and Lesperance 2003).

Relatively few studies have reported prevalence rates for in-hospital anxiety. In studies of CABGS patients, both presurgical and postsurgical anxiety rates tend to be reported. In some cases, anxiety is shown to remit after surgery. For example, in a German study of 142 CABGS patients, with anxiety classified as Hospital Anxiety and Depression Scale – Anxiety (HADS-A) scores ≥8, the presurgical rate was 34 % (Krannich et al. 2007). By 10 days postsurgery, the prevalence of anxiety had reduced, albeit nonsignificantly, to 25 % (Krannich et al. 2007). Symptom remission was more likely in younger than in older patients (Krannich et al. 2007). However, in other studies, anxiety rates increase after surgery. For example, in an Australian study of 147 CABGS patients, with anxiety classified using the Depression, Anxiety and Stress Scale (DASS), the preoperative prevalence of mild to severe anxiety was 27 %, whereas the postoperative prevalence was significantly higher at 45 % (Andrew et al. 2000). The inclusion of patients with “mild” symptoms (DASS anxiety scores 8–9) may have inflated these rates: excluding these patients, the presurgical and postsurgical prevalence of moderate to severe anxiety (DASS anxiety ≥10) was 20 % and 33 %, respectively (Andrew et al. 2000). In addition, some patients awaiting surgery have either generalized anxiety disorder (GAD) or panic disorder, as assessed by structured diagnostic interview. A recent review indicated prevalence rates varying from 2 % to 10.2 % for GAD and 10.8 % for panic disorder presurgery (Tully and Baker 2012). The review confirmed that many more patients have subclinical anxiety symptoms both pre- and postsurgery (Tully and Baker 2012).

These rates of in-hospital post-event anxiety and depression are considerably higher than seen in the general community. For example, approximately 5 % of Australian adults report a depressive illness and around 4 % anxiety-related problems (AIHW 2012). Similarly, the prevalence of major depression in American adults is approximately 5 % (American Psychiatric Association 2013; Egede 2007). In a study comparing AMI and CABGS patients with healthy adults, rates of anxiety and depression were significantly higher in both patient groups (Moser et al. 2010). It appears that rates of anxiety and depression among cardiac patients are up to four times that seen in the general population.

Impacts of Anxiety and Depression on Health Behaviors, Morbidity, and Mortality

Modifiable risk factors account for up to 90 % of the overall risk of acute myocardial infarction (AMI) (Yusuf et al. 2004). In patients with established coronary heart disease, modifiable risk factors affect the progression of the disease and the likelihood of a future event, while lifestyle changes improve risk factor profiles and prognosis (Euroaspire II Study Group 2001). In particular, smoking cessation reduces cardiac patients’ mortality risk by 36 % after 5 years (Critchley and Capewell 2003) and by 50 % after 10 years (Cavender et al. 1992). Increasing physical activity also reduces the risk of further events and death (Iestra et al. 2005; Moholdt et al. 2008), as does reducing dietary fat intake (Iestra et al. 2005; Mead et al. 2006). Nonetheless, the prevalence of unhealthy lifestyles and modifiable risk factors remains high in cardiac populations (Euroaspire II Study Group 2001; Murphy et al. 2011).

Post-event anxiety and depression put cardiac patients at a distinct disadvantage in terms of engagement in activities that promote health and well-being. Compared with their nondepressed counterparts, depressed patients are more likely to smoke (Gravely-Witte et al. 2009; Kronish et al. 2006; Murphy et al. 2012) and to relapse after quitting (Perez et al. 2008). They consume higher levels of dietary fat (Murphy et al. 2012; Ziegelstein et al. 2000) and engage in less physical activity (Allan et al. 2007; Kronish et al. 2006; Murphy et al. 2012; Ziegelstein et al. 2000) than those who are not depressed. Similarly, anxious patients have higher smoking rates (Kuhl et al. 2009; Murphy et al. 2012; Perez et al. 2008) and dietary fat intake (Murphy et al. 2012), although, once sociodemographic factors are taken into account, their physical activity levels tend to be similar to those of non-anxious patients (Kuhl et al. 2009; Murphy et al. 2012).

In addition to their poor health behaviors, depressed patients are less adherent to recommended treatments (DiMatteo et al. 2000). First, they show poorer medication adherence than nondepressed patients, being more likely to forget to take their medications and to skip doses and less likely to take medication as prescribed (Gehi et al. 2005; Kronish et al. 2006). Second, they are disinclined to attend cardiac rehabilitation programs (Frasure-Smith et al. 1993; Kronish et al. 2006; Whitmarsh et al. 2003; Blumenthal et al. 1999; Lane et al. 2001) and, if they do attend, are more likely to discontinue (Blumenthal et al. 1999; Kronish et al. 2006). Both medication adherence (Ho et al. 2006) and attendance at cardiac rehabilitation (Beauchamp et al. 2013; Denollet and Brutsaert 2001) have been shown to impact positively on survival.

It is not surprising then that cardiac patients who are anxious or depressed after an acute cardiac event have poorer morbidity and mortality outcomes than their non-anxious and nondepressed counterparts (van Melle et al. 2004; Barth et al. 2004). For example, anxious patients are at increased risk of hospital readmission within 30 days of discharge after CABGS (Murphy et al. 2008b) and of reinfarction following a first AMI (Strik et al. 2003). In terms of mortality outcomes, presurgical anxiety has been shown to predict all-cause mortality, independent of age and comorbid disease (Tully et al. 2008a). Post-event anxiety has also been shown to predict cardiac mortality up to 3 years after a first event, independent of other risk factors (Strik et al. 2003). A recent review included four studies reporting associations between generalized anxiety disorder (GAD) and cardiac morbidity and mortality among CHD patients (Tully et al. 2013). The earliest study, involving 804 acute coronary syndrome (ACS) patients, reported a 2.29 increased risk of re-event or death at 2 years in patients shown to have GAD at 2 months post-event (Frasure-Smith and Lesperance 2008). The largest study, involving over 1,000 CHD patients, demonstrated a 74 % increased risk of re-event or death, with adjustment for confounders, among patients with GAD (Martens et al. 2010). An Australian study of 158 CABGS patients showed that GAD conferred a threefold increased risk of in-hospital re-events and death, after adjustment for confounders (Tully et al. 2011). Contrary to other findings, a 2011 study of 436 ACS patients found that GAD was associated with a reduced risk of death over 5 years post-event, suggesting that GAD may have a protective effect (Parker et al. 2011). Likewise, a study of over 2,000 cardiac patients referred for exercise testing found that elevated anxiety as assessed by the HADS-A was associated with lower 5-year mortality (Herrmann et al. 2000). While it increases risks via physiological mechanisms (Olafiranye et al. 2011), anxiety may simultaneously encourage help-seeking behaviors that reduce risk (Herrmann et al. 2000). Consistent with this view, it has been suggested that some forms of anxiety, particularly generalized anxiety about health, might actually improve cardiac medication adherence (DiMatteo et al. 2000).

Depressed patients are similarly at risk of reinfarction after AMI (Frasure-Smith et al. 1993; Strik et al. 2003) and of a recurrent cardiac event and hospital readmission in the first 12 months after bypass (Connerney et al. 2001; Tully et al. 2008b). Likewise, numerous studies conducted in the late 1990s and early 2000s demonstrated that post-event depression predicts mortality up to 10 years later (Barefoot et al. 2000; Frasure-Smith et al. 1999; Welin et al. 2000). Two meta-analyses published in 2004 confirmed the earlier findings, demonstrating that depression more than doubles the risk of mortality after a cardiac event (Barth et al. 2004; van Melle et al. 2004). One meta-analysis included 20 studies of patients with a range of CHD diagnoses, with the length of follow-up varying from 3 months to 10 years (Barth et al. 2004). The authors reported an unadjusted odds ratio of 2.24 between depression and all-cause mortality (Barth et al. 2004). The other meta-analysis was restricted to studies of post-AMI patients, involved 6,367 patients across 16 cohorts, and endpoints within 2 years (van Melle et al. 2004). The authors reported odds ratios for all-cause and cardiac mortality of 2.38 and 2.59, respectively (van Melle et al. 2004). Of note was the finding that the association between depression and mortality was more pronounced in studies undertaken prior to 1992, possibly due to improved treatments for CHD which may simultaneously reduce the negative physiological impact of depression (Carney et al. 2004; van Melle et al. 2004).

Indeed, the mechanisms whereby depression might adversely affect patients’ outcomes have been well documented and debated. In particular, depression and CHD share several biological mechanisms. Depressed patients have higher levels of biomarkers that promote atherosclerosis, reduced heart rate variability suggesting increased sympathetic activity, increased C-reactive protein, an indicator of increased inflammatory response, altered serotonergic pathways, and altered platelet aggregability (Carney et al. 1988; Lichtman et al. 2008; Sheps and Rozanski 2005; Soufer et al. 2002; Taylor 2010). It has also been postulated that CHD and depression have common genetic patterns related to serotonin and inflammatory responses (McCaffery et al. 2006). Together with their behavioral disadvantage, depressed patients are also socioeconomically disadvantaged through their lower income and education, manual occupations, and social isolation (Cheok et al. 2003), all of which are associated with increased mortality risk (Brummet et al. 2003; Case et al. 1992). Importantly though, it has been suggested that more research is needed on possible mechanisms underlying the relationship between depression and mortality (Carney et al. 2004).

So what of the role of cardiac disease severity in explaining the association between post-event depression and mortality? Is it possible that depressed patients are at increased risk of re-events and earlier death largely because of their advanced atherosclerosis? Unfortunately, some studies have not adequately controlled for disease severity in investigating the causal relationship between depression and death. Only six of the studies included in the meta-analysis by Barth and colleagues controlled for disease severity, using either ejection fraction (Carney et al. 2003; Connerney et al. 2001; Welin et al. 2000), Killip class (Frasure-Smith et al. 1993, 1995), or a combined hazard score including ejection fraction and other indicators of myocardial damage (Barefoot et al. 2000). A further two controlled for previous AMI (Herrmann et al. 2000; Irvine et al. 1999). Six also controlled variously for other potential confounders, including age (Barefoot et al. 2000; Carney et al. 2003; Herrmann et al. 2000; Ladwig et al. 1994), smoking status (Carney et al. 2003; Frasure-Smith et al. 1993, 1995; Welin et al. 2000), diabetes (Carney et al. 2003), hypertension (Herrmann et al. 2000; Welin et al. 2000), and hypercholesterolemia (Welin et al. 2000). In the meta-analysis, the adjusted odds ratio remained significant but dropped to 1.76 indicating that depression conferred a 75 % increased risk of death rather than the doubling of risk seen prior to adjustment (Barth et al. 2004). Nonetheless, depression remained predictive independent of disease severity. The meta-analysis by van Melle and colleagues involved only bivariate analyses and thus did not take into account the effects of possible confounders such as disease severity, diabetes, smoking, and other elevated risk factors. Several authors have noted the importance of adjusting for confounders, particularly disease severity (Lane et al. 2005; Murphy et al. 2013). The postulated physiological and biochemical mechanisms for the link between post-event depression and mortality suggest that it is imperative that disease severity is accounted for in such studies.

Identification of Depression in Cardiac Patients

Given their poorer prognosis, it is important to identify and support patients who are anxious or depressed after their cardiac event. This section focuses on strategies for identifying depressed cardiac patients in particular and discusses the inherent difficulties in ensuring accurate identification. The treatment of anxious and depressed patients is discussed in other chapters.

Current Depression Screening Guidelines

In light of the high prevalence and prognostic importance of post-event depression, it has been proposed that all cardiac patients should be screened for depression around the time of their cardiac event. Specifically, in 2008, the American Heart Association recommended that all cardiac patients be screened for depression “in various settings, including the hospital, physician’s office, clinic, and cardiac rehabilitation centre” (Lichtman et al. 2008). Australian guidelines, released in 2013, similarly recommend routine depression assessments “at first presentation and again at the next follow-up appointment,” with repeat assessments recommended on a yearly basis (Colquhoun et al. 2013). The Australian guidelines specifically recommend a screen 2–3 months after the cardiac event (Colquhoun et al. 2013).

Both guidelines recommend using the Patient Health Questionnaire (PHQ) for screening, with endorsement of either or both of the PHQ-2 items warranting administration of the full PHQ-9. The PHQ-9 has been shown to have good sensitivity and specificity when used with cardiac patients (Gilbody et al. 2008). It can be completed in less than 5 min and yields both a provisional depression diagnosis and a severity score (Lichtman et al. 2008). The items correspond with the nine features of depression used in determining a diagnosis of major depressive disorder (MDD), as outlined in the Diagnostic and Statistical Manual of Mental Disorders (DSM) (American Psychiatric Association 2013).

A positive screen requires specific action, depending on the severity of depression indicated. For patients with mild symptoms (PHQ < 10), a “wait and watch” protocol applies, with rescreening during a subsequent medical appointment recommended (Colquhoun et al. 2013; Lichtman et al. 2008). For patients with high scores (PHQ ≥ 10), referral for more comprehensive clinical evaluation by a professional qualified in the diagnosis and management of depression is advised (Colquhoun et al. 2013; Lichtman et al. 2008).

Problems with Depression Screening in Cardiac Patients

Since the release of the depression screening guidelines, there has been some debate as to the appropriateness of depression screening recommendations. Some authors have noted that there is insufficient evidence that routine depression screening is beneficial, with no clear evidence of positive patient outcomes (Ski and Thompson 2011; Thombs et al. 2009; Tully and Baker 2012). Indeed, shortly after the American guidelines were released, a systematic review reported that no trials had tested the impacts of depression screening on either depression or CHD outcomes (Thombs et al. 2008). A systematic review of five trials of “screen and refer” protocols undertaken in the primary care setting concluded that while screening improves detection and increases treatment, it does not improve depression symptoms or patient outcomes (Gilbody et al. 2008). As noted by Thombs and colleagues, screening protocols “cannot be advocated until a thorough evaluation of risk and benefit is completed” (Thombs et al. 2009). Clearly more research on the impact of depression screening is required.

In addition, it has been noted that there would be significant costs if screening and referral guidelines were strictly followed, both in terms of burden on the service system and negative impacts on the patient. In particular, Thombs and Ziegelstein highlight the perils of false-positive assessment, including “unnecessary diagnostic testing, adverse effects and costs of inappropriate treatment, and the sequelae of being incorrectly labeled” (Thombs and Ziegelstein 2010). Thombs and colleagues also note that such a practice “would be unduly resource intensive” and, to be effective, would require significant changes in current models of care (Thombs et al. 2008).

While the hospital stay may represent an opportune time for depression screening from a practical standpoint, the risks of misclassification are particularly high at this time (Hasnain et al. 2011; Murphy et al. 2013; Ski and Thompson 2011; Tully and Higgins 2014). As noted above, there is a possibility of “false-positive” classification of patients with transient in-hospital distress symptoms. Hasnain and colleagues state that “screening too close to the cardiac event would likely categorize a larger number of patients as depressed than it might if it was done later” (Hasnain et al. 2011). In addition, there is a possibility of “false-negative” classification of patients who have delayed depressive symptoms which appear during convalescence, in the period after hospital discharge. In a recent review, Hare and colleagues argue that “reported depression is often repressed or suppressed in hospital because of initial denial of affect” (Hare et al. 2013).

Two issues are at work in regard to early misclassification: first, whether the presenting symptoms are actually depression or, instead, a normal bereavement response to the life-threatening event, which would more accurately be described as “mourning” (Freud 1917), “normal sadness” (Horwitz and Wakefield 2005, 2007), or “adjustment disorder” (Goble et al. 1989; Hare et al. 2013), and, second, the course of the depressive symptoms in the period after hospital discharge, that is, whether the symptoms are transient, chronic, or persistent (Murphy et al. 2008a, 2013; Tully and Higgins 2014). Both these issues are discussed in the following section.

High Incidence of Transient “Normal” Distress

Many patients experience a strong emotional reaction at the time of or soon after an acute cardiac event. Common emotional responses include shock, low or fluctuating mood, sadness, worry, guilt, and anger (Goble et al. 1989; Hare et al. 2013; Higgins et al. 2007). Mood change is displayed by tiredness, irritability, tearfulness, loss of pleasure in usual activities, withdrawal from others, early waking and other sleep disturbances, and changes in appetite and sex drive (Goble et al. 1989; Hare et al. 2013; Higgins et al. 2007). Cognitive changes that typically co-occur include confusion and forgetfulness, inability to concentrate, nightmares, reduced self-esteem, concerns about role changes, particularly regarding paid work, physical health and independence, and pessimism about the future (Goble et al. 1989; Hare et al. 2013; Higgins et al. 2007).

These mood changes and associated symptoms can be considered part of the normal emotional reaction to the cardiac event. It has been noted that “after acute cardiac illness, depression is a normal response to loss, threat of other losses, and awareness of mortality” (Goble et al. 1989). Indeed, Goble and colleagues argue that “after acute AMI, depression is to be expected… is not an abnormal reaction and is not an illness” (Goble et al. 1989). More recent authors have similarly agreed that symptoms characteristically associated with depression – fatigue, loss of appetite, reduced activity, insomnia, and difficulty concentrating – may occur as a normal reaction to illness, hospitalization, or significant loss (Hare et al. 2013; Horwitz and Wakefield 2005, 2007; Thombs et al. 2006; Tully and Baker 2012; Tully and Higgins 2014).

Indeed, many of the symptoms of common distress or bereavement that typically follow the acute event closely mirror the criteria for a diagnosis of depression. This overlap underscores the difficulties of accurate diagnosis close to the cardiac event. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM) (American Psychiatric Association 2013), for a diagnosis of major depressive disorder (MDD), at least five of the nine symptoms listed in Box 1 need to be present nearly every day for the previous 2 weeks. These symptoms are very similar to the “normal emotional reactions” outlined earlier. Several authors have noted the conceptual overlap between “normal sadness or distress” and depression (Goble et al. 1989; Hare et al. 2013; Horwitz and Wakefield 2007; Murphy et al. 2014; Thombs et al. 2006; Tully and Baker 2012). In their book The Loss of Sadness, Horwitz and Wakefield argue that the “recent explosion of putative depressive disorder… is largely a product of classifying many instances of normal sadness as mental disorders” (Horwitz and Wakefield 2007).

Given the similarity between the diagnostic criteria and the emotional reactions that commonly accompany a cardiac event, the challenge for health professionals is to differentiate a “normal common reaction” from “depression,” particularly when patients are assessed during hospitalization or soon after discharge. It has been noted that “the separation of normal sadness and depressive disorder is a sensible and legitimate, indeed a crucial one” (Horwitz and Wakefield 2007). Understanding the course of symptoms can assist health professionals in distinguishing between the two conditions.

Box 1: DSM Criteria for Major Depression

  • Depressed mood or irritable (feels sad or empty or appears tearful)

  • Decreased interest of pleasure

  • Change in weight or appetite

  • Change in sleep

  • Change in activity

  • Fatigue of loss of energy

  • Guilt/worthlessness

  • Diminished concentration

  • Thoughts of death or suicide

The Course of Depression: Persistence, Resolution, and Delay

Many studies have investigated the course of depression after a cardiac event, tracking patients at various points during the first 12 months after hospital discharge. These studies point to the transient nature of depressive symptoms for many patients, reinforcing the notion of a normal emotional reaction that passes with time. When patients are reassessed within the first 2 months of their cardiac event, persistence of depression is quite prevalent: typically, around 60 % (Davis and Jensen 1988) to 70 % (Lauzon et al. 2003) of patients who are depressed in hospital remain so at 2 months. However, when patients are reassessed at later timepoints, depression persistence is less likely. For example, of 30 patients with in-hospital major depression in Schleifer and colleagues’ study of 190 AMI patients, major depression persisted in only 11 (36 %) by 3–4 months post-event (Schleifer et al. 1989). This constitutes less than 6 % of the full baseline sample, a rate similar to that seen in the general population. In a Norwegian study of 288 AMI patients, rates of both anxiety and depression at 3, 6, 12, and 18 months post-event were no higher than seen in the general population (Hanssen et al. 2009). Indeed, in regard to depressive symptoms, AMI patients showed significantly lower HADS-D scores than the reference group at the 3- and 12-month assessments (Hanssen et al. 2009).

Some studies have used statistical modeling techniques to track the possible trajectories of depression in patients after AMI and CABGS. These studies have similarly shown considerable resolution of in-hospital depressive symptoms. For example, in an Australian cohort of 184 CABGS patients, all 26 (14 %) patients who were above threshold for depression in hospital followed a trajectory of symptom resolution, mostly in the first 2–3 months, and were under threshold by the 6-month mark (Murphy et al. 2008a). Similarly, in a cohort of 160 AMI and CABGS patients, all 27 (17 %) who were above threshold in hospital showed resolution by 6 months (Murphy et al. 2014). In a Netherlands study of 475 AMI patients, where five depression trajectories were identified, a lower but still substantial 26 % of patients who were depressed in hospital showed remission of symptoms over the 12 months after their event (Kaptein et al. 2006). These findings suggest that, for many patients, in-hospital depressive symptoms resolve during convalescence. Several authors have agreed that early depressive symptoms remit spontaneously for many cardiac patients (Hare et al. 2013; Tully and Baker 2012).

At the same time, other patients who are not depressed in hospital go on to become depressed in the months that follow. For example, in a cohort of 555 CABGS patients, 36 (6.5 %) developed depression in 6 months after discharge, representing 9 % of initially nondepressed patients (Blumenthal et al. 2003). Similarly, in a cohort of 123 CABGS patients who were nondepressed at baseline, 22 (10 %) had developed depression by 6 months (Peterson et al. 2002). Likewise, in the cohort of 184 CABGS patients, 26 (14 %) who were not depressed in hospital had become depressed by the 6-month mark, representing 16 % of the initially nondepressed patients (Murphy et al. 2008a). These findings suggest that between 10 % and 16 % of initially nondepressed CABGS patients go on to develop depression by 6 months after surgery.

It is useful to overlay a trauma framework when considering trajectories of depressive symptoms after an acute cardiac event. While much of the early trauma research focused on responses to external events such as war, terrorism, accident, assault, and natural disasters, more recent studies have considered acute health crises as “traumatic” events (Tedstone and Tarrier 2003). Traumatic events are defined as events that are out of the ordinary, leave people with a perceived lack of control or sense of powerlessness, and create long-lasting problems leading to a sense of hopelessness (Cavalcanti-Ribeiro et al. 2012). Some of the common psychological problems associated with traumatic events are intrusive thoughts and memories, flashbacks, hypervigilance, mental and behavioral avoidance, sadness, and sleep problems (Joseph 2011). Depending upon the nature of the stressor, its intensity, severity, and duration of suffering or threat, psychological responses such as anxiety, fear, guilt, anger, and irritability may be present for a long time after the threat has receded (Tedeschi and Calhoun 2004). Thoughts and feelings are affected, especially if the event was sudden (such as an AMI), with initial reactions of shock, psychological numbness, disbelief, anger, fear, and worry. Anxiety is one of the most commonly reported responses and tends to be associated with a perception of significant threat to life or health (Tedeschi and Calhoun 1995). Depressive symptoms – including sadness, low energy, and decreased interest in life – are also common and tend to be associated with the perception of significant loss (Hodgkinson and Stewart 1991). It is not necessarily the type of event but rather an individual’s perception of it and response to it in the aftermath that renders it as stressful or traumatic.

According to trauma theory, there are four typical responses to a traumatic event such as an acute cardiac event or, indeed, other life-threatening illnesses or unexpected diagnosis of disease. First, there are those – such as the patients described earlier – “who recover.” Second, there are those with “chronic” symptoms, whose early depression symptoms persist beyond the period of physical recovery. Third, there are those with “delayed” symptoms, as outlined above, which do not appear until further into the convalescence period. And finally, there are “resilient” patients who do not experience depressive symptoms after their acute event. These four typical responses to trauma are depicted in Fig. 1.
Fig. 1

Four typical trajectories of depressive symptoms after an acute cardiac event

There is some evidence in the cardiac literature that only patients whose symptoms are present beyond initial convalescence after the acute event – those with either chronic or delayed symptoms – are at increased mortality risk (Blumenthal et al. 2003; Murphy et al. 2008a, b; Tully and Baker 2012). In the US study of CABGS patients, those whose in-hospital depression resolved in the first 6 months had a 5-year mortality risk of 10 %, identical to that of nondepressed patients, whereas those whose in-hospital depression persisted had almost twice that mortality risk (Blumenthal et al. 2003). Patients with “new” depression had an intermediate mortality risk of 14 % (Blumenthal et al. 2003). In a 3-year follow-up of 124 CABGS patients, the rates of re-events and death were significantly higher in those with “new” depression at 6 months: the 3-year re-event/mortality rate was 14 % in those who developed “new” depression compared to 3 % in those who remained nondepressed over the 6-month post-event period (Peterson et al. 2002). In a 12-year follow-up of 180 Australian AMI and CABGS patients, there was a high 64 % mortality among those whose in-hospital depression persisted or worsened and a low 14 % mortality rate among those whose in-hospital symptoms resolved (Murphy et al. 2013). Indeed, the death rate among those with remitted depression was lower than that among patients who were nondepressed in hospital and remained so during convalescence (Murphy et al. 2013). These findings suggest that in-hospital depressive symptoms do not necessitate a poor prognosis and further point to the probability of misclassification of “at-risk” patients if identification is based purely on an in-hospital assessment.

Indications for Risk Stratification

Given the risks of and problems associated with misclassification, it is important that strategies are adopted to ensure accurate identification of depressed patients. First and foremost, it has been recommended that systems be established for repeat screening of cardiac patients further into convalescence, so that identification is not based purely on a single, in-hospital screen (Colquhoun et al. 2013; Hare et al. 2013; Murphy et al. 2013; Ski and Thompson 2011). Ideal opportunities for repeat screening include during patients’ attendance at cardiac rehabilitation programs and regular visits to the general practitioner, family physician, and cardiologist (Hare et al. 2013; Murphy et al. 2013). It has also been suggested that psychologists undertake opportune depression screening in presenting cardiac patients (Tully and Higgins 2014).

Second, it would seem prudent that health professionals be alert to patients at higher risk of depression, using sociodemographic and medical characteristics as identifiers or “red flags.” It has been noted that “risk stratification of patients who screen positive for depression soon after an acute cardiac event is essential to prevent unnecessary intervention” (Hasnain et al. 2011). Patients who are at higher risk of developing depression after a cardiac event could potentially be flagged upon admission to or discharge from hospital and at later points during convalescence.

Several sociodemographic and medical characteristics have been identified as risk factors for anxiety and depression after an acute cardiac event. Female cardiac patients (Burker et al. 1995; Cheok et al. 2003; Duits et al. 1998; Keresztes et al. 2003; Mallik et al. 2005; Strik et al. 2004) and those who are younger (Cheok et al. 2003; Gallagher et al. 2003; Mallik et al. 2005; Strik et al. 2004) consistently show higher rates of depression than males and older patients, respectively. Social isolation, lack of social support, and living alone also increase the risk of post-event depression (Burker et al. 1995; Cheok et al. 2003; Frasure-Smith et al. 2000). Unemployment also confers increased risk (Cheok et al. 2003; Gallagher et al. 2003), as does poor physical health and lower physical functioning (Cheok et al. 2003; Mallik et al. 2005), the presence of comorbidities (Mallik et al. 2005; Watkins et al. 2003), and other associated conditions such as diabetes (Frasure-Smith et al. 1999, 2000). While relatively few studies have identified predictors of post-event anxiety, female gender (Duits et al. 1998; Moser et al. 2010) and low education (Moser et al. 2010) have been identified as significant risk factors. There is some evidence that AMI patients experience more anxiety and depression than CABGS patients in early convalescence (Westin et al. 1997), although there is no evidence that this difference is sustained (Moser et al. 2010; Westin et al. 1997).

Some studies have specifically focused on the identification of red flags for persistent, worsening, or new depressive symptoms in the post-event period, as a means of identifying patients at high risk of chronic or delayed depression (Murphy et al. 2008a, 2014). Key red flags include having a history of depression or anxiety, younger age (aged <55), living alone or other indicators of social isolation, poorer self-rated health, financial difficulties, diabetes and other comorbid conditions, smoking, and compounded loss (Murphy et al. 2008a, c, 2014). Key red flags for increased depression risk are shown in Box 2. Several authors have similarly emphasized the importance of the patients’ mental health history as a strong indicator of depression risk post-event (Martens et al. 2008; Spijkerman et al. 2005). Rather than relying on depression screen results in isolation, health practitioners could be guided by the presence or absence of these red flags as to whether a particular patient is at heightened risk of a poor depression trajectory. Patients who screen positive and also present with specific red flags could be stratified for more rigorous follow-up, rescreening, referral, and treatment. Simultaneously patients who initially screen negative but who present with red flags for increased depression risk could be targeted for repeat screening.

Box 2: Red Flags for Increased Depression Risk

  • History of anxiety or depression

  • Age ≤55 years

  • Living alone or lack of social support

  • Poor self-rated health

  • Financial difficulty

  • Diabetes

  • Other comorbid conditions

  • Smoking

  • Recent bereavement or compounded loss

Implications for Clinical Practice

What are the implications of these findings in terms of clinical practice? Given that early distress resolves for many patients, patients who present with early symptoms can be reassured that their distress, worry, and other changes in mood and behaviors are likely to be transient and can be considered part of a “ normal adjustment response.” Normalizing common emotional reactions to a cardiac event may well enhance psychological recovery and warrant empirical investigation. Already there is some evidence that it is desired by patients. A study of 160 Australian cardiac patients demonstrated that over 80 % want to be told about what to expect emotionally after they leave hospital (Murphy et al. 2015). The symptoms commonly experienced by patients after the event – low or fluctuating mood, tearfulness, loss of pleasure in usual activities, sleep disturbance, reduced self-esteem, changes in appetite and sex drive, concerns about role changes, and worries about the future (Goble et al. 1989; Higgins et al. 2007) – are typical of a normal grief response to an experience of loss or trauma (Goble et al. 1989). “Prevention and management depend on the patient’s learning that a depressed mood is a normal temporary response to the illness… and that recovery is the rule” (Goble et al. 1989).

Nonetheless, identification of depressed patients is essential. Given that one in five patients goes on to experience serious depression and is thereby at increased morbidity and mortality risk, patients also need to be alerted that depression is possible. If patients are alerted to this risk early on, before hospital discharge, they may be better placed to identify depressive symptoms if and when they arise. Again this hypothesis warrants empirical investigation.

Health professionals can be guided by both the trajectories of the symptoms, based on repeat screens, and the presence of other risk indicators or red flags as to whether a particular patient is likely to be experiencing a normal emotional reaction or is, indeed, likely to be depressed. Stratification of high-risk patients toward more rigorous follow-up, referral, and treatment may improve patient outcomes without unduly burdening the health system and warrants further investigation.

The importance of repeat screening cannot be overemphasized. Health professionals across a range of healthcare settings need to be equipped to undertake depression assessment. These include cardiologists, who see the patient on multiple occasions from the time of the event, physicians and practice nurses working in general practice, and nurses and other health professionals working both on the hospital ward and in cardiac rehabilitation. Approaches might include routine screening for all presenting patients or, in some settings, targeted screening of high-risk patients.


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Copyright information

© Springer Science+Business Media Singapore 2015

Authors and Affiliations

  • Barbara M. Murphy
    • 1
    • 2
    • 5
    Email author
  • Rosemary O. Higgins
    • 1
    • 3
  • Alun C. Jackson
    • 1
    • 4
  1. 1.Heart Research CentreMelbourneAustralia
  2. 2.Department of PsychologyUniversity of MelbourneMelbourneAustralia
  3. 3.Department of PhysiotherapyUniversity of MelbourneMelbourneAustralia
  4. 4.Centre on Behavioral HealthUniversity of Hong KongPokfulamHong Kong
  5. 5.Faculty of HealthUniversity of NewcastleNSWAustralia

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