Heart disease accounts for 1 in 3 deaths worldwide.1 There is a well-established link in the clinical literature between heart disease and mental health problems, most notably depression, anxiety, and posttraumatic stress. Rates of major depressive disorder, anxiety disorders, and posttraumatic stress disorder (PTSD) in cardiac patients have been reported to be as high as 20%, 15.52%, and 15% across both genders, respectively.2–4 The presence of mental health problems such as these can have dire consequences for cardiac patients: Those who become depressed, anxious, or afflicted with posttraumatic stress reactions are more likely to die from further cardiac complications than are those who do not.3,5–9 There is an extensive literature on the impact of depression, anxiety,10,11 and PTSD12 on the course of heart disease. However, the vast majority of studies conducted to date have dealt with the ways in which mental health conditions, particularly depression, contribute to the onset of heart disease. Much less is known at the present time about what triggers the development of these afflictions after a cardiac event and how they might be identified or prevented. Most of the extant literature does not address this issue specifically.
Objective of the Present Scoping Review
In light of this state of affairs, the principal aim of this scoping review of the medical and psychological literatures was to identify the potential risk and protective factors for the development of depression, anxiety, and PTSD in patients with heart disease. This information will serve to inform the preparation and dissemination of prevention and treatment programs. It may also prove useful in the identification of those at a particular risk for these mental health problems.
To achieve this objective, we sought to answer 2 main research questions:
- What are the risk factors for the onset of depression, anxiety, and PTSD in people with heart disease?
- What are the factors that prevent the onset of depression, anxiety, and PTSD in people with heart disease?
For the purposes of this review, “depression,” “anxiety,” and “posttraumatic stress” were defined according to the diagnostic criteria set forth in the version of the Diagnostic and Statistical Manual of Mental Disorders (DSM) that was current at the time of data collection in the articles under review (DSM [Third Edition] [APA, 1980]; DSM [Fourth Edition] or DSM-IV [APA, 1994], or DSM [Fifth Edition] or DSM-5 [APA, 2013]). The reason for using older DSM criteria to define our research terms is that a large majority of the longitudinal studies of risk and protective factors for psychological disorders among patients with heart disease published between the years 1996 and 2016 are based on DSM-IV classifications. Any substantive review of the literature published during that period must therefore include results derived from the penultimate version of the DSM. However, given that the DSM-5 was published in 2013, we were open to the possibility that there might be a few studies based on the more recent diagnostic criteria. The most striking difference between the 2 editions of this nomenclature as far as depression, anxiety, and posttraumatic stress are concerned is the creation of a new diagnostic category for PTSD and traumatic stressor-related disorders.13 Before the publication of the DSM-5, PTSD was considered an anxiety disorder.
We wanted to glean the maximum amount of information from the literature on the onset and prevention of depression, anxiety, and posttraumatic stress in patients with heart disease. However, because of the relative paucity of studies in which participants met criteria for specific psychiatric disorders, we also included studies in which participants were not necessarily classified into a particular diagnostic category but whose symptoms of depression, anxiety, and posttraumatic stress were measured by psychometrically sound instruments.
“Heart disease” was defined as any of the 4 major types of cardiovascular conditions: coronary heart disease (CHD) with or without dysrhythmia, cardiomyopathy, valvular dysfunction, or electrical disorders of the heart (eg, dysrhythmia). It is noteworthy that most research on the psychosocial risk factors for and consequences of heart disease, including the studies examined in the present review, has been conducted with people who have CHD.14
For this scoping review, we followed the method of Arksey and O’Malley15 for summarizing and propagating research findings and for identifying gaps in the research literature. As per their recommendations, we selected a research question (ie, “What are the risk and protective factors for depression, anxiety, and posttraumatic stress in cardiac patients?”), identified relevant studies, selected relevant studies, and charted the data.
Studies were retained if they met the following criteria: (1) symptoms of depression, anxiety, and posttraumatic stress were examined within the context of heart disease; (2) depression, anxiety, and posttraumatic stress either were defined according to DSM criteria or were measured using psychometrically valid and reliable instruments; and (3) the researchers tracked either risk or protective factors for the development of depression, anxiety, or posttraumatic stress.
In an effort to identify as many studies as possible, we did not specify an age range for study participants, and we did not stipulate that a particular type of study design was necessary to be retained in this scoping review. We recognize that longitudinal studies are the most appropriate for identifying risk and protective factors, but we included cross-sectional studies in the interest of generating a comprehensive collection of studies. We excluded articles whose focus was on psychosocial factors (eg, depression, anxiety, quality of life before the cardiac event) as predictors of heart disease.
The search was limited to articles published in English or French (as English and French are the 2 official languages of Canada) since 1996. After consulting with a librarian at the Université du Québec en Outaouais, we searched the following databases: Scopus, PsycARTICLES, Psychology and Behavioral Sciences Collection, Sage Journals, and MEDLINE. Our initial search generated only a handful of articles that met our inclusion criteria (N = 27), so we expanded the search terms of keywords to include: [(“heart disease” OR “myocardial infarction” OR “coronary heart disease”) AND (“anxiety disorder” OR “anxiety” OR “depression” OR “depressive disorder” OR “posttraumatic stress” OR “PTSD”) AND (“prevention” OR “predictive factors” OR “predictor” OR “risk factors”)] as illustrated in the Figure.
Once they generated the first list of studies, 2 independent reviewers (P.V. and F.M.) screened the titles of all articles and excluded those that did not meet inclusion criteria (see above). These reviewers then repeated this procedure as they examined the abstracts of the articles retained after the screening of titles, followed by the careful reading of full-text articles. Finally, the reviewers searched the lists of citations within the retained articles in pursuit of additional articles that might meet inclusion criteria, as per the suggestions of Hepplestone and colleagues.16 Questions about whether or not to include an article were resolved upon consultation with the first author (P.G.).
Our search initially generated 484 articles with potential relevance. After screening the titles, 271 of them were retained for abstract screening. Of those, careful reading of the abstracts led to the exclusion of an additional 243 articles. Full-text revisions of the remaining 28 articles led to the exclusion of an additional 10 articles because either they did not define depression, anxiety, or posttraumatic stress according to DSM criteria or they did not use psychometrically established instruments to measure these constructs. Hand searches of the reference sections of the articles we retained generated an additional 23 articles that met inclusion criteria. Thus, a total of 41 articles were included in this review.
Fourteen studies of risk factors for depression in people with heart disease emerged from our review. The risk factors that appeared on a consistent basis in the literature were (1) symptoms of depression at or before baseline, (2) psychosocial vulnerabilities, (3) gender, and (4) age.
Symptoms of Depression at or Before Baseline
The results of 8 studies indicate that patients’ levels of depressive symptoms at or before baseline can be significant predictors of its progression over time. One of these was a longitudinal study of 200 patients undergoing diagnostic evaluations for CHD in the midwestern United States in the late 1990s. In it, Hance et al17 found that 17% of patients met DSM-IV criteria for “minor depression” (ie, the presence of at least 2 depressive symptoms on a persistent basis for at least 2 weeks) and another 17% of them met diagnostic criteria for a major depressive episode. The investigators determined the presence and severity of symptoms of depression using the National Institute of Mental Health Diagnostic Interview Schedule.18 Forty-two percent of patients with minor depression at baseline and 50% of patients with major depression at baseline met diagnostic criteria for a major depressive episode at a 12-month follow-up. Only 6 of these patients received any kind of treatment of depression during the follow-up period, which suggests that the condition tends to worsen without any intervention. The authors concluded that it is important to detect the presence of symptoms of depression and to treat patients with heart disease with subthreshold depression early on, given its likelihood of developing into a major depressive episode.17
Similarly, Lespérance et al19 studied depression using the Beck Depression Inventory-II (BDI-II)20 in 222 patients hospitalized after a myocardial infarction (MI) in Eastern Canada and noted that 27.5% of them reported having had at least 1 episode of major depression in their life before the MI. They also discovered that those with a history of depression were more likely to be depressed upon hospitalization for MI than were those without a history of depression.
Next, Strik and colleagues21 in the Netherlands found in a longitudinal study of 70 cardiac patients that those with greater than the cutoff points for depression on the Symptom Checklist-9022 or the Zung Depression Scale23 at baseline were more likely to receive a diagnosis of major depression 1, 3, and 6 months after an MI, as determined by a clinical interview with a psychiatrist using a DSM (Third Edition) checklist.21 Also in the Netherlands, Spijkerman and collaborators discovered that history of depression, as indicated by the Composite International Diagnostic Interview (CIDI),24 was one of a number of significant predictors of symptoms of depression at 3, 6, and 12 months post-MI in 528 patients.25 Others were female gender, longer hospital stay for cardiac care, symptoms of exhaustion before the MI, and poor ejection fraction.
In another study, Dickens et al26 examined risk factors for depression in a sample of 315 patients in the United Kingdom. Their results revealed that psychiatric history as indicated in a baseline interview post-MI made an independent contribution to the prediction of scores in the clinical range on the Hospital Anxiety and Depression Scale (HADS)27 1 year later.26 They also uncovered a link between a number of psychosocial variables and depression (see below).
Other studies have yielded similar findings. For example, Schrader et al28 conducted a longitudinal study of 785 people with heart disease in Australia. Patients were admitted for MI, unstable angina, dysrhythmia, coronary artery bypass grafting, or congestive heart failure. The researchers examined a variety of variables at baseline to determine which ones would predict the onset of depression at 3- and 12-month follow-ups. These included participants’ depression level upon admission (measured using the Center for Epidemiologic Studies Depression Scale (CED-S),29 demographic variables (eg, gender, age, socioeconomic status), history of cardiac or emotional problems, length of current hospital stay, previous hospitalizations, and risk factors for heart disease such as tobacco use.28 Findings indicated that depression in the moderate to severe range on the CED-S at baseline; a previous diagnosis of depression, anxiety, or stress; and smoking were significant predictors of moderate to severe depression at 12-month follow-up. In addition, 73% of patients classified as moderately or severely depressed at baseline were mildly, moderately, or severely depressed after 12 months.28 As did Hance et al,17 these investigators made sure not to include patients who had received treatment of depression in their sample to have an accurate picture of its natural course. They concluded that clinicians ought to assess the psychiatric history of cardiac patients and to reassess them 3 months after their initial hospitalization to determine whether or not symptoms of depression have remitted.
More recently, a team of investigators in Australia looked into the trajectories of anxiety and depression of 160 cardiac patients over 6 months.30 They measured depression and anxiety using the HADS. They also took into account patients’ mental health history, tobacco use, financial strain, comorbidities with other diseases, and perceptions of available social support. Results of this investigation revealed that, in 29% of the patients (n = 47), depressive symptoms tended to increase over the 6 months after admission to hospital for acute MI, acute coronary syndrome (ACS), or coronary artery bypass grafting.30 A history of depression was among the most powerful predictors of worsening depression over time, as were the lack of a close confidant, poor self-reported health, and a history of anxiety.30 This finding reflects one uncovered earlier by researchers in the Netherlands who also discovered that history of depression, as determined by a structured clinical interview (CIDI),24 along with cardiac history and the negative affect and social inhibition typical of what is known as “type D personality,” predicted the onset and course of depression in the year after an MI in 287 patients.31
Finally, Rothenbacher and associates32 conducted a longitudinal study of 996 patients with CHD in 2 cardiac rehabilitation clinics in Germany. Similar to the other findings reported here, these investigators found that nearly 63% of those with scores in the clinical range on the HADS at baseline continued to demonstrate significant symptoms at 1-year follow-up.
We found 2 studies in which psychosocial vulnerabilities predicted depression in cardiac patients. In one, reviewed in the previous section, social isolation and lack of a close confidant were significant predictors of depression 12 months post-MI.26 In another, which was a study of 339 patients in Ireland with ACS (defined as MI or unstable angina), Doyle and colleagues33 discovered that the presence of 1 or more psychosocial vulnerabilities explained a significantly greater proportion of the variance in symptoms of depression in their sample (as measured by the HADS) than did demographic variables (eg, age), risk factors for heart disease, and heart disease severity by themselves.33 The psychosocial vulnerabilities that they measured were stressful life occurrences, lack of pleasant events, belief in a just world (“bad things happen to bad people”), and the tendency to experience but actively stifle negative emotions (ie, type D personality).33 They also found that psychosocial vulnerabilities were independent predictors of the presence of depression. Taken together, these results led Doyle and associates33 to conclude that psychosocial vulnerabilities were actually better predictors of depression in cardiac patients than were demographic and disease-related variables. This is critical because it highlights the need to attend to intrapersonal and interpersonal aspects of cardiac patients’ experience when assessing and treating them for depression.
Our search revealed a link between female gender and risk for depression in cardiac patients. As previously mentioned, Dickens and colleagues26 found in one of the studies cited previously that female gender was a significant predictor of depression at follow-up with patients with MI. In a similar vein, Gottlieb and colleagues34 found women with heart failure to be more likely to exhibit symptoms of depression than men in their cross-sectional sample of 155 cardiac patients in the United States.34 They found that race predicted depression among men, with white men more likely than black men with heart failure to exhibit depression on the BDI-II. Spijkerman et al25 also found women to be at a particular risk for becoming depressed in the months after an MI, whereas Mallik and colleagues35 found in their study of 2498 patients post-MI in 19 centers across the United States using the 9-question Brief Patient Health Questionnaire36 that women exhibited higher levels of depression than did men upon hospitalization, particularly women younger than 60 years.35 Finally, in a study of 944 patients with unstable angina or MI in the United States, Naqvi and associates37 determined that female gender was a strong predictor of depressive symptoms post-MI, whereas male gender in combination with a history of cardiac illness (ie, previous MI) also predicted the presence of symptoms of depression, as measured by the Zung Self-Assessment Depression Scale.23
The risk factors for depression in cardiac patients reported in the previous paragraphs all emerged on a consistent basis from the literature. There was, however, another that was only reported in 3 studies but that is noteworthy nonetheless: younger age. For instance, Dickens and colleagues26 found that the younger cardiac patients were, the more likely they were to become depressed. van Melle et al38 found in their analyses of data from 2177 patients in the Netherlands who had had an MI that younger age and more severe left ventricular dysfunction reliably predicted the presence of a major depressive disorder 1 year after the cardiac event, as indicated by the CIDI. These findings echo those of Mallik et al,35 who noted that women younger than 60 years had the highest levels of depression in their sample of any demographic group. This suggests that relative youth and organic, physical factors might play a role in developing depression.
We identified 4 studies of factors that might protect people with heart disease from developing depression. These included 2 studies of (1) social support39,40 and 2 studies of (2) preventive treatments.41,42 Of the preventive treatments proposed, one was pharmacological41 and the other was nonpharmacological.42
An early study of 2810 people with various chronic diseases in the Netherlands yielded evidence of the impact of social support on symptoms of depression in those with heart disease (N = 537).40 The investigators measured both structural (ie, marital status and the number of close relationships reported) and functional (ie, practical and emotional support) social support. They found in their cross-sectional sample that self-reports of being married or in a committed partner relationship, higher numbers of close relationships, and greater emotional support predicted fewer symptoms of depression in cardiac patients, as measured by the CED-S.
A longitudinal study conducted in the Eastern United States recently generated similar findings and also revealed some of the dangers of a lack of social support. Specifically, Friedmann and colleagues39 discovered in their sample of 108 patients with heart failure that those with higher levels of social support at baseline were significantly less depressed than were those with lower levels of social support, as indicated by the Social Support Questionnaire-643 and the BDI-II.20 Another notable finding from this study was that lower social support at baseline predicted significant increases in symptoms of depression in the 2 years that followed. These results testify both to the protective effects of perceived social support and to the deleterious impact of a lack of social support as far as depression is concerned. Finally, it should be pointed out that 80% of the participants in Friedmann and colleagues’ study were male. This is important because it suggests that meaningful social connections seem to be just as crucial for men with heart failure as they are for women, if not more so.
In an effort to reduce the incidence of depression in people with heart disease, Hansen and colleagues41 conducted a study on the effects of the antidepressant escitalopram on 120 patients with ACS in Denmark.41 They found that, compared with 120 patients who received a placebo in the year after the diagnosis of their heart condition, the patients who took an antidepressant (escitalopram) were significantly less likely to develop depression, as indicated by meeting International Classification of Diseases, Tenth Revision, criteria for a depressive disorder. Despite these findings, the notion of prescribing antidepressants to people who do not have depression, along with the shortcomings of Hansen and colleagues’ design and conclusions, has faced heavy criticism.44
An alternative to pharmacological prevention involves the use of psychologically oriented, nonpharmacological therapies. An example of such an intervention is the “Beating Hearts Programme” designed by Turner and associates42 in Australia. In their randomized controlled trial, they found that their 8-week group program, which combined cognitive-behavioral and motivational interviewing techniques, led to significantly greater reductions of symptoms of depression as measured on the BDI-II in the treatment group than in the control group. There were 272 patients with heart disease in their study. This finding suggests that an emphasis on realistic thinking and behavioral adjustment might stave off the onset of or diminish the severity of symptoms of depression in people with heart disease.
Our search generated 3 studies in which investigators examined risk factors for anxiety in individuals with heart disease. We did not come across studies of protective factors per se.
The results of a cross-cultural study of anxiety conducted in the early 2000s revealed a gender effect on the presence of anxiety in the 72 hours after an acute MI. Women demonstrated significantly more numerous symptoms of anxiety than did men, as measured by the Brief Symptom Inventory,22 in a sample of 912 cardiac patients from Australia, the United States, Japan, South Korea, and the United Kingdom.45 Thus, as with depression, female gender seems to be more closely associated with symptoms of anxiety in cardiac patients.
Type D Personality
Type D personality was a significant predictor of anxiety, as measured by the HADS,27 after 12 months of postpercutaneous coronary intervention in a sample of 416 patients in the Netherlands followed over the course of a year after their admission to the hospital.46 This suggests that people who tend to stifle or inhibit their strong emotions are more at risk for becoming anxious as their heart disease progresses.
In the study conducted by Murphy et al30 (see the previous section on depression), significant predictors of persistent anxiety included a history of anxiety, a history of depression, lack of health insurance, smoking, diabetes, and being single. As is the case with depression, the presence of anxiety before the diagnosis of heart disease seems to put patients at risk for developing more serious symptoms of anxiety afterward.
Our search generated 21 studies of risk factors for PTSD in cardiac patients. We did not uncover any studies that addressed protective factors specifically for this population, although it is generally accepted that social support attenuates the effects of posttraumatic stressors.47 Various psychosocial vulnerabilities emerged as significant risk factors for the development of PTSD in cardiac patients.
Psychosocial Vulnerabilities and Personality Traits
Bennett and Brooke48 conducted a study of 69 patients in the United Kingdom who had had an MI in the 6 to 12 months before their investigation. They measured symptoms of PTSD using the Impact of Event Scale (IES)49 and examined the effects of a number of variables including alexithymia (ie, impairment in the ability to identify and process emotions), negative affect, awareness of having a heart attack, and social support. They found in their cross-sectional investigation that higher levels of alexithymia, negative affect, and awareness of having a heart attack while it was happening; lower levels of perceived social support (ie, availability of confidants and the emotional presence of others); and age predicted more severe PTSD symptoms.48 Two years later, Bennett and colleagues50 discovered that the intensity of patients’ self-reported fright at the time of the cardiac event and the presence of negative affect predicted intrusive thoughts on the IES 3 months after their first MI.50 In a similar vein, Roberge et al51 discovered in their study of 477 patients with MI in French Canada that the intensity of patients’ perceptions of the severity of their MI and the danger it posed, the presence of intense symptoms of depression or acute stress disorder in the days after the MI, psychiatric history, and female gender were significant predictors of PTSD as assessed by the Structured Clinical Interview for DSM-IV 52 in the month after the MI.
A few years later, in Denmark, Pedersen et al53 compared the prevalence of PTSD in 112 patients who had had an MI in the 4 to 6 weeks leading up to their study with the prevalence of PTSD in 116 matched controls. They measured PTSD with the Posttraumatic Diagnostic Scale.54 Results indicated that patients with MI were 3 times as likely as controls to meet diagnostic criteria for PTSD and that depression, anxiety, and the personality trait known as neuroticism (defined in this context as elevated levels of negative affect) predicted the presence of PTSD. It is noteworthy that, in this sample, the clinical severity of the cardiac event was not a significant predictor of PTSD.55 This group of researchers also discovered that the presence of depression, anxiety, and neurotic (ie, negative emotionality, anxiety) and type D personality traits predicted PTSD in the aftermath of an MI.55,56 Similarly, Whitehead et al57 found that negative affect, hostility, and the presence of pain, depression, and acute stress upon hospital admission were independent predictors of participants’ scores on the PTSD Symptom Scale–Self-Report Version.58 They conducted their investigation on 135 patients with ACS in the United Kingdom.
Psychosocial vulnerabilities and personality traits also seemed to play a role in the development of PTSD in a different sample of 120 patients who had had an MI in the United Kingdom. Chung et al59,60 found, for instance, that somatic problems, anxiety, social dysfunction, and depression, as measured by the General Health Questionnaire,61 were significantly more prevalent in patients with PTSD than they were in those with partial or no PTSD or in matched controls. They also found that patients who had PTSD demonstrated elevated levels of neuroticism and displayed more antagonistic tendencies than did participants without PTSD or matched controls. Patients with PTSD also tended to engage in more emotion-focused (ie, trying to change how one feels about one’s illness) than problem-focused (ie, making changes to alleviate their illness) coping with heart disease.
In a smaller sample of 31 patients recovering from an MI in the United States, Rocha and colleagues62 found that youth, the presence of depressive symptoms, self-reported anxiety during the MI, and membership in the black community were significant predictors of PTSD, as assessed by the Structured Clinical Interview for DSM-IV.62 These results resemble those of Guler et al63 in Switzerland, who discovered that youth, self-reported fear of dying, and feelings of helplessness predicted the presence of a diagnosis of PTSD.63 These researchers used the Clinical Administered PTSD Scale64 in a sample of 394 patients who had had an MI. In addition to these psychosocial factors, stressful life events post-MI (eg, death of a significant other, diagnosis of a serious illness, car accident, war) also seemed to contribute to the onset of PTSD in 116 patients with MI in Israel.65
More recently, Deng and colleagues66 conducted an investigation of PTSD in 134 people with adult congenital heart disease in Pennsylvania.66 As is typical of samples of individuals with adult congenital heart disease, participants in this study were relatively young (mean age, 34.6 years). Psychosocial variables were measured using the IES-Revised,67 the PTSD Checklist-Civilian Version,68 and the HADS.27 Results indicated that the presence of depressive symptoms and the year of their most recent cardiac surgery predicted the presence of PTSD, which the researchers detected in 11% of their sample on the IES-Revised and 21% of their sample using the PTSD Checklist.68 Higher levels of depression and more recent cardiac surgery were thus related to more prevalent PTSD. The finding that an illness a person is born with, such as congenital heart disease, is related to posttraumatic reactions later in life is significant and eye-opening. The idea that more subtle types of heart disease might trigger posttraumatic reactions suggests a personal, subjective component to the way in which an individual perceives and reacts to his/her condition. Thus, the actual severity of the disease might not be as important as how one experiences it.
This is precisely what Ginzburg et al69 found in their study of 112 patients with MI in Israel. In their sample, they developed a 5-item self-report measure of patients’ perception of the severity of their cardiac disease, which was a more powerful predictor of the onset of symptoms of acute stress disorder and PTSD than was the actual severity of the cardiac event itself. A prospective study published in 2003 revealed similar findings: patients who perceived the severity of their MI to be elevated were more likely to be diagnosed with PTSD 7 months after the event than were those who did not perceive their illness to be as severe.70
Ginzburg and Ein-Dor71 generated analogous findings several years later, when their investigation of 173 patients with MI demonstrated that those who experienced their heart attack as more life threatening at the time of the event, regardless of its actual severity, were more likely to exhibit signs of acute stress at an 8-year follow-up than were those who perceived their MI as less dangerous.
Subjective interpretations of MI severity were also significant predictors of PTSD (as measured by the Clinical Administered PTSD Scale) in Wiedemar and colleagues’72 study of 400 patients in the United Kingdom, as was patients’ perceived control over their illness in a small correlational study of 52 patients with MI in the Eastern United States.73 Finally, Oflaz and colleagues analyzed data from 76 patients diagnosed with MI in Turkey and noted that patients who were diagnosed with PTSD indicated on the Brief Illness Perception Questionnaire74 that they were significantly more affected physically and emotionally by their illness than were patients without PTSD, irrespective of the severity of their MI.
Ethnic Minority Status
In another intriguing study conducted in the United Kingdom, Wikman and colleagues75 discovered in their longitudinal study of posttraumatic symptoms in 213 patients with ACS that ethnic minority status and social deprivation, in addition to risk factors detected in other studies (eg, depressed mood, type D personality traits), predicted a diagnosis of PTSD 12 months after the cardiac event.
Attachment and Alexithymia
Finally, other socio-affective variables also seem to be related to the onset of PTSD in people with heart disease. These include attachment anxiety (ie, the tendency to fear emotional abandonment by significant others) and alexithymia. For example, a group of Chinese researchers76 noted in a sample of 97 patients recovering from an MI that those with elevated levels of attachment anxiety and alexithymia also endorsed symptoms of PTSD on the PTSD Checklist–Civilian Version.77 This suggests that personal relationships and the ability to identify and regulate emotions might play a role in the onset of PTSD in cardiac patients.
One of the striking findings from this review is the relative paucity of data available on risk and protective factors for depression, anxiety, and posttraumatic stress in cardiac patients. This is especially true for anxiety and anxiety disorders. In addition, most of the research we found was on risk rather than resilience vis-à-vis their mental health in patients with heart disease. Another problem we encountered was that most studies we came across focused on mental health problems as risk factors for heart disease and the recurrence of heart disease, not vice versa,3,53,78 whereas we sought to answer the question, “What might contribute to or protect from mental health problems in heart patients?” We discuss the answers to this question in the following paragraphs.
Depression and Anxiety
We did uncover some consistencies in the literature on risk factors for depression, anxiety, and posttraumatic stress in cardiac patients that provide valuable insight into the potential causes and progression of mental health problems related to heart disease. First, vulnerability to depression or anxiety before the onset of heart disease and the presence of symptoms at baseline seem to increase the chances of compounding or developing depression and anxiety after the diagnosis of heart disease.28,30,32 Stressful life events and the presence of type D personality traits (ie, the stifling of negative emotional experiences) also seem to predict depression,33 anxiety,45,46 and posttraumatic stress56 in people with heart disease, as does female gender25,26,34,37 and relative youth.26,38
The risk factors for PTSD in cardiac patients are similar to those detected for depression and anxiety. According to the results in this review, high levels of negative affect or difficulty identifying and expressing negative affect48,50,55 seem to predict PTSD in cardiac patients. As is true of depression and anxiety, the presence of mental health problems before the onset of heart disease also seems to predict PTSD in cardiac patients.55,66 Low perceived social support also emerged as an important predictor of PTSD symptoms in people with heart disease.48 This reflects the general trend in the psychological literature that highlights the importance of social support, and the couple relationship in particular, in preventing and coping with PTSD.79–81 Social support even seems to be related to relapse and to the recurrence of cardiac events, such that decreases in perceived socioemotional support over time increase patients’ risk of having another heart attack by 10%.53 Loneliness and isolation thus seem strongly related to vulnerability to develop PTSD in cardiac patients and to the exacerbation of the heart pathology itself.
Other noteworthy risk factors for PTSD in patients with heart disease to emerge in our review were the subjective perceptions and experiences of the disease and its impact, irrespective of the actual severity or danger of the affliction.69,71 This is an important finding because it suggests that clinicians ought to attend to what the constraints imposed by heart disease mean to their patients, to their sense of identity, and to their self-esteem. We recall the case of a patient who developed PTSD after an angioplasty. Although this procedure is relatively painless, this person felt completely at the mercy of the hospital staff and medical professionals who conducted it. This ran counter to his sense of independence and autonomy, of which he was quite proud. This subjective sense of powerlessness was terrifying for him and triggered a posttraumatic stress reaction.
As much as a lack of social support predicts the onset of PTSD and the worsening of physical symptoms in cardiac patients, the presence of social support seems to provide a buffer against mental health problems. In this review, being married, having close friends, and experiencing emotional support emerged as important protective factors against depression.39,40 This corroborates mounting evidence of the power of interpersonal relationships characterized by close emotional ties to protect against depression, anxiety, and PTSD in healthy populations.82,83 There is also some support for the usefulness of treating cardiac patients with antidepressants or psychotherapy once they receive a diagnosis of heart disease to stave off major depression.41,42
A number of studies cited in this review indicate a greater risk for depression and anxiety for women than for men.26,34 Indeed, some research suggests that women with heart disease are more likely to become depressed than men and to remain depressed over the course of the year after their cardiac event.84,85 Others37 have found that both men and women with heart disease can be prone to developing depression, depending on their history of cardiac illness. Men who have had cardiac events in the past seem in some cases to be more at risk for depression than those who experience one for the first time. This was not the case for women in Naqvi et al’s37 study.
However, certain mental health problems manifest themselves differently in men and women. This is particularly true of depression. Men who are depressed tend to feel irritable and frustrated, to lose interest in once-pleasurable activities, and to turn to alcohol. These symptoms are often more salient than are reports of prolonged feelings of sadness or crying spells with unidentified causes, which reflect current diagnostic criteria for a major depressive disorder.86 This has led to the suggestion that diagnostic criteria and assessment instruments ought to be adjusted to reflect the behavioral and emotional manifestations of depression in men that might differ from those that are more typically detected in women.86 The results of a recent investigation in Canada revealed that men are open to seeking help for depression if they are properly informed about its symptoms and treatment,87 which is less likely if their symptoms go undetected. A more thorough understanding of the differential risk and protective factors for depression and other mental health problems in men and women with heart disease would most likely help reach a larger portion of the at-risk population. Unfortunately, we identified virtually no studies that dealt with the issue of potentially gender-specific manifestations of depression, anxiety, or posttraumatic stress or of risk factors for these problems that might be specific to men and women.
In addition to greater attention to gender differences in the etiology and course of depression, anxiety, and posttraumatic stress, it will also be necessary to gain a better understanding of factors that protect against these mental health problems in people with heart disease. We uncovered very few studies of what might prevent patients with heart disease from becoming depressed or anxious or from developing posttraumatic stress reactions. Although it is extremely important to identify and screen for risk factors, more information on protective factors would enable the development of prevention programs and perhaps decrease the incidence of mental health problems in this population.
There is also a pressing need for much more data on anxiety and anxiety disorders as a consequence of heart disease. Clinical experience and a few studies have indicated that people diagnosed with heart disease tend to become more anxious and worried about physiological sensations than they were before the onset of heart disease. However, there is insufficient information now about what puts men and women at risk for, or what might protect them from, developing an anxiety disorder after a diagnosis of heart disease.
There are some limitations to the present review. First, although we followed a systematic series of steps to generate as many articles as possible, there is a chance that other pertinent articles on risk and protective factors for depression, anxiety, and posttraumatic stress in the wake of heart disease do exist. We endeavored to minimize this possibility by revising our search string and including more synonyms for keywords, but this does not guarantee that this review is exhaustive.
Next, it is important to interpret the findings of this review with caution because of the lack of information on certain variables (see above). Some findings seem to be robust (eg, a history of mental health problems as a predictor of mental health problems after cardiac diagnosis), but others have been the object of very little investigation. This is especially true of variables related to ethnic minority status, attachment, and alexithymia.
This scoping review highlights the gaps of research on risk and protective factors in the development of depression, anxiety, and posttraumatic stress after a cardiac event. This has major implications for the early identification and prevention of these conditions in practice. It is important to attend to the mental health history, the potential stifling of negative emotional experiences, and the presence and quality of social support in patients with heart disease because these factors seem to be relatively consistent predictors of depression, anxiety, and posttraumatic stress in this population. Much more research into prevention and on gender differences is necessary to hone the detection and treatment of these problems in people with heart disease.
What’s New and Important?
- To correctly identify and respond to symptoms of depression, anxiety, and posttraumatic stress in patients with heart disease, our results suggest that it is important to pay particular attention to the mental health history, tendency to stifle negative emotional experiences (known as “type D personality”), and social support in patients with heart disease. These factors, along with gender and younger age, seem to be relatively consistent predictors of mental health problems in this population.
- There are noteworthy gender differences in the manifestation of mental health problems, particularly depression. These need to be taken into account when assessing the mental health of cardiac patients.
The authors would like to acknowledge the generous financial support of the Movember Foundation of Canada.
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