The reciprocal relationship between depression and acute coronary syndrome (ACS) is well known. On the one hand, depression is an independent risk factor for the onset of ACS; on the other hand, patients with ACS are prone to concurrent depression.1 The incidence of depression among patients with ACS is reported to be 11% to 37% depending on different diagnostic criteria. Nearly 20% of patients with ACS experience major depression, most of whom have subclinical symptoms; however, fewer than one-third of patients are diagnosed.2 Depression after the occurrence of ACS has adverse effects on the patient, aggravates ACS severity, prolongs hospital stay, and increases the incidence of cardiovascular event recurrence, as well as mortality.3 For example, Myers et al4 reported that patients with coronary heart disease living with comorbid depression have a 1.3 times longer hospital stay, that the possibility of noncompliance with the treatment plan increases by 3 times, and that these patients are more reluctant to quit smoking, participate in sports activities, and undergo cardiac rehabilitation. Indeed, it is reported that, compared with a nondepressed state, depression increases the risk of cardiac adverse outcomes by 1.6- to 2.7-fold and the risk of cardiac mortality increases by 2.4-fold.5,6
The causes of concurrent depression among patients with ACS are diverse and complex, and the etiology and mechanism of depression concurrent with ACS remain unclear. Previous studies have found that depression among patients with ACS is associated with gender, disease severity, complications, history of depression, marital status, living alone, and the individual's personality.7–9 Nonetheless, the conclusions of these studies are not entirely consistent because of the different regions from which the research populations were recruited, the small sample sizes, and the different research designs and methods. For instance, there are 2 conflicting reports of whether the incidence of depression is associated with the severity of ACS.9,10 Unfortunately, there is no evidence-based medical research to confirm the conclusions. Accordingly, the authors of this study adopted the evidence-based medical approach, incorporated homogenous literature, expanded previous sample sizes, and performed a meta-analysis for factors such as demographics, living habits, and critical factors of the disease to identify risk factors for depression in patients with ACS. The results will help to guide clinicians in implementing drug and psychological interventions in the early stages of high-risk depression, as well as to prevent and ameliorate the occurrence of depression, thereby improving prognosis.
Materials and Methods
Articles published during January 1996 to March 2018 were retrieved from the PubMed, Web of Science, EMBASE, and EBSCO databases according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement. The search was a combination of mesh terms and free words of “acute coronary syndromes,” “ST elevation myocardial infarction,” “non-ST-elevation myocardial infarction,” “anginas, unstable,” “depressions,” and “factor, risk”; the search details are provided in the supplementary search list (Supplemental Digital Content, available at http://links.lww.com/JCN/A64). The reference lists of the identified trials and review articles were also manually screened to identify any additional relevant studies. The language was limited to English literature.
The inclusion criteria were as follows: (1) patients older than 18 years; (2) patients meeting the diagnostic criteria for ACS: ST-segment elevation myocardial infarction (MI), which was defined as typical chest pain with a new ST-segment elevation of 2 mm or greater on at least 2 contiguous electrocardiographic leads and a more than 3-fold increase in creatine kinase–MB level compared with normal; non–ST-segment elevation MI, which was defined as chest pain and positive cardiac biochemical marker detection without new ST-segment elevation; and unstable angina, which was determined by the presence of typical chest pain with or without ST-T wave changes or positive cardiac biochemical marker detection; (3) depression diagnosis based on patient disease history, clinical symptoms, physical examination, and laboratory examination or by using different widely accepted scales such as the Beck Depression Inventory; International Classification of Diseases, Tenth Revision; Hospital Anxiety and Depression Scale-Depression; Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition; Hamilton Depression Scale; and Beck Depression Inventory-II; and (4) the full text published in English.
The exclusion criteria were as follows: (1) patients with severe physical illness, such as multiple organ failure, and/or with severe mental illness, such as schizophrenia, or cognitive dysfunction, such as Alzheimer's disease; (2) non-ACS patients; and (3) review articles. For repeat studies, we included only the most recent study.
The following information was independently extracted and recorded by 2 investigators (M.Z.Y. and Q.F.): the first author's name, article title, date of publication, type of study, duration of study, diagnostic criteria for ACS and depression, sample size (case group/control group), country and region, incidence of depression, odds ratio (OR) values, and 95% confidence interval (CI).
Literature Quality Evaluation
In this study, we used the Newcastle-Ottawa Scale to evaluate the quality of each study. It is a nonrandomized controlled trial quality evaluation instrument composed of 3 parts: object selection, comparability of cases and controls, and results. The full score is 9 points; 0 to 4 and 5 to 9 points refer to low- and high-quality articles, respectively.11 Two investigators (M.Z.Y. and Q.F.) independently carried out the quality assessment; when there was an inconsistent conclusion, it was decided by a third investigator (G.W.L.).
The meta-analysis was performed using Review Manager 5.2 and STATA 12.0 software. Review Manager 5.2 was used to calculate the OR values and 95% CIs of the various risk factors for post-ACS depression. A CI of the OR value not equal to 1 and P < .05 indicated statistical significance.
Sensitivity analysis is an important method for assessing heterogeneity; thus, only the conclusions of homogenous literature included in the study are reliable. The I 2 test can identify the extent of heterogeneity, with I 2 = 0%, 25%, and 75% representing low, medium, and high heterogeneity, respectively. Sensitivity analysis is used to determine the sensitivity of a study result for meta-analysis. In this study, results for factors with high heterogeneity were removed sequentially, and the OR before and after the removal of the literature was then compared to determine the effect of that study literature on the overall results and to determine whether it is the source of any observed heterogeneity. The causes of heterogeneity were then analyzed, including differences in research objects and designs and statistical methods. When the effect on the results is large, it can be removed.
With regard to published bias, systematic errors exist between the reported results and the measured but unreported results. For example, research factors involving privacy can result in selective reporting of the results. Although this situation cannot be avoided, we can identify the existence of publication bias by applying Begg and Egger's tests (P < .05 indicates the presence of publication bias). If publication bias is found among the included studies, we should be cautious when evaluating the results of those studies.
Literature Search and Quality Evaluation Results
The literature search process is shown in the Figure.
We retrieved 6056 articles (PubMed, 1533; EMBASE, 2275; Web of Science, 975; EBSCO, 1272; and other sources, 1). We used endnoteX7 software to remove 1749 duplicate articles, and after reading the title and abstract, we excluded another 4180 articles. The full text of the remaining 127 articles was read, and 30 articles were found to meet the inclusion criteria. This meta-analysis encompasses 3 159 764 patients, 1 961 612 of whom were male and 1 198 152 were female. The incidence of post-ACS depression was 5% to 69.3%. Basic information regarding the 30 articles is shown in Table 1. They were all high-quality articles, and the quality evaluation scores are also shown in Table 1.
Risk Factors for Depression
We indicated that post-ACS depression was significantly related to the following risk factors: social demographic factors (female gender, low education level, and living alone), marriage status (never married and widowed), work status (unemployed and housewife), unhealthy lifestyle (obesity and current smoker), comorbidities (dyslipidemia, hypertension, diabetes, previous myocardial infarction, history of depressive disorder, family history of depression, history of chronic obstructive pulmonary disease, history of angina, and congestive heart failure), severity of ACS (Killip > 1, Killip > 2, left ventricular ejection fraction < 35%), treatment-related factors (use of calcium channel blockers, antidepression treatment, previous percutaneous transluminal coronary angioplasty, and previous coronary artery bypass graft. These results are listed in Table 2.
Conversely, marriage, high education level, and employment were protective factors. In addition, there were no significant differences between the 2 groups for the following factors: medium education level, hypercholesterolemia, family history of coronary artery disease, left ventricular ejection fraction less than 40%, anterior site of myocardial infarction, Q wave myocardial infarction, β-blocker use, angioplasty, antiplatelet use, lipid-lowering drug use, thrombolysis, angiotensin-converting enzyme inhibitor use, digoxin use, revascularization, diuretic use, recent percutaneous transluminal coronary angioplasty treatment, recent oronary artery bypass graft treatment, and statin use (P > .05). Please see Table 2 for details.
Sensitivity analysis was conducted by sequentially removing the articles and comparing the OR values before and after. For the factor of family history of depression, after removing the heterogeneous study of Carney et al (2009), I 2 changed from 60% to 23% and OR changed from 1.79 (95% CI, 1.03–3.08) to 1.38 (95% CI, 0.85–2.25). The reason for this difference may be the study period (October 1996 to October 1999), which was different from that of the other articles (May 2006 to March 2013); according to previous reports, the incidence of depression was higher during the period of October 1996 to October 1999. Similarly, after excluding Carney et al (2009), I 2 for thrombolysis changed from 63% to 21% and OR changed from 0.87 (95% CI, 0.68–1.11) to 0.79 (95% CI, 0.65–0.96). This may be due to the fact that the diagnostic criteria for depression (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition) and the geographical origin of the study (United States) were different from other literature. Regarding the risk factor of Q wave myocardial infarction, removing Myers et al (2012) changed I 2 from 58% to 28% and OR from 0.86 (95% CI, 0.67–1.11) to 0.81 (95% CI, 0.69–0.94); the reason may be that the periods between this study (February 1992 to February 1993) and others (October 1996 to November 2001) differed. For revascularization, removing De Jonge et al (2006) caused I 2 to change from 59% to 0%, with OR changing from 0.92 (95% CI, 0.55–1.54) to 0.68 (95% CI, 0.47–0.98). In the study, patients with myocardial infarction were involved, whereas in the other literature, patients with ACS were involved. The scope of patients of the two was not the same. Removing Frasure-Smith et al (2007) changed the I 2 for statin use from 54% to 0% and OR from 1.26 (95% CI, 0.89–1.78) to 1.49 (95% CI, 1.12–1.99). In that study, the diagnostic criterion for depression was Beck Depression Inventory-II, but other studies used International Classification of Diseases, Tenth Revision.
In contrast, other factors, such as female gender, widow status, obesity, current smoking, hypercholesterolemia, hypertension, diabetes, history of depressive disorders, congestive heart failure, antiplatelet, diuretics, and percutaneous transluminal coronary angioplasty, were not affected by removal of any of the articles, suggesting that these results are stable.
Begg and Egger's values for all risk factors are listed in Table 2. Egger's values for risk factors of never married, living alone, and diabetes and Begg's values for antidepressant use were significant (P < .05), suggesting published bias for these factors. Therefore, the conclusions should be considered with caution. Begg and Egger's values for other risk factors were not significant (P > .05), suggesting no published bias for these factors and that these conclusions are credible.
On the basis of the results of this meta-analysis, the incidence of post-ACS depression was 5% to 69.3%. The large gap among the articles may be that the incidences of depression in Schulman-Marcus et al (2016), Sørensen et al (2005), and Joergensen et al (2016), with a low incidence of self-depression, were 0.05, 0.1, and 0.11, respectively; the diagnostic criteria used were International Classification of Diseases Ninth Revision and International Classification of Diseases, Tenth Revision, with a study duration of 1999 to 2012 and involving patients with ACS and non-ST-elevation myocardial infarction. Meanwhile, the incidences of Carney et al (2009) and Lesperance et al (1996) were 0.693 and 0.519, respectively; the diagnostic criteria were Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition and Diagnostic and Statistical Manual of Mental Disorders Third Edition; and the study duration was 1991 to 1999 and involving patients with myocardial infarction. Therefore, because of the inconsistency between many small–sample-size studies and the different approaches of defining “depression,” the scope of inclusion was different and the length of the study varied. These disorders led to the large gap in incidence of depression among the articles.
Depression has a large impact on the prognosis of ACS; therefore, depression should be detected early to enable early intervention. In this study, the authors found the occurrence of depression to be associated with sociodemographic factors, unhealthy lifestyle, comorbidities, ACS disease severity, and treatment-related factors.
Social and Demographic Factors
Social and demographic factors such as female gender, low education level, marriage status (never married and widow), work status (unemployed and housewife), and living alone were risk factors for depression, whereas married status, high education level, and employment were protective factors.
Compared with men, women are more prone to depression; the risk of depression among women was 1.79 times that among men, which is consistent with a recent study.10 This may be related to 2 factors. The first is the change in estrogen level; endocrine changes after menopause increase a woman's susceptibility to post-ACS depression.37 The second reason is likely social psychological factors. Most women have multiple roles in both the family and society, bear intense competition and work pressure, participate in fewer social activities, and have less social support.20 These factors contribute to negative feelings, which can easily cause depression.
The level of education affects a patient's awareness of disease-related knowledge and thus affects behavior.38 The authors found that the risk of depression was 1.33 times higher for patients with primary school and lower education levels than for patients with higher education levels. The reason may be that patients with lower education levels have reduced awareness about ACS, and thus the body cannot effectively address the discomfort caused by negative emotions. In contrast, patients with a higher education level may have a relatively rich knowledge of coronary heart disease prevention and treatment.
Compared with unmarried people, married individuals have a lower risk of depression. As marriage can provide better social, economic, and emotional support to patients with ACS, as well as make patients feel safe and comfortable, those patients may have more confidence in facing the disease and the anxiety caused by the disease may decrease.39 The authors found that marriage was a protective factor, which is consistent with the findings of Mallik et al.40
Widows represent a special female population that usually lacks social support, are under poor economic conditions, and live alone.9 These are risk factors for depression. The authors found that the risk of depression in widows was 2.34 times that in nonwidowed patients and that widow status was a risk factor for depression among patients with ACS, which is consistent with previous findings.
Larsen et al41 reported that patients who live alone are prone to depression, and we also found that the risk of depression among patients who live alone was increased by 1.17 times. Patients who live alone are often introverted and divorced or widowed, lack social support, and feel loneliness and a lack of security.10,15 They are more likely to have psychological problems. Overall, living alone was a risk factor for depression.
An unemployed or housewife status was closely related to the occurrence of depression. Employed workers have a stable economic income and a stable interpersonal circle; moreover, work can bring self-satisfaction, which can resolve anxiety and other negative emotions. In this study, employment was a protective factor for depression. Therefore, reentering the workforce may help reduce the risk of depression.
Unhealthy Lifestyle: Current Smoker
Healthy behavior is a controllable risk factor in many diseases. In addition, an unhealthy lifestyle increases the risk for concurrent ACS and depression. Acute coronary syndrome is associated with smoking, alcoholism, lack of exercise, and poor diet.42 At the same time, patients with depression often adopt unhealthy lifestyles, such as smoking, alcoholism, and overeating, to relieve depressed emotions, which will induce and aggravate ACS. The authors found that current smokers were at a 1.37 times greater risk for depression than nonsmokers. Busch et al43 conducted relevant studies showing that depression is significantly correlated with smoking and that it can be used as an independent predictor of death from coronary heart disease.
Comorbidities: Hypertension, Dyslipidemia, Diabetes, Pre–Myocardial Infarction, Chronic Obstructive Pulmonary Disease, Angina, Congestive Heart Failure, History of Depressive Disorders, and Family History of Depression
Hypertension, diabetes, and dyslipidemia are cardiovascular risk factors classified as “metabolic syndrome”; they have been shown to be closely related to the development and progression of coronary heart disease.44 Cardiovascular risk factors and depression scale scores are positively correlated, and depression can enhance the role of these risk factors in cardiovascular disease. The authors found that patients with comorbidities such as hypertension, dyslipidemia, and diabetes were at a 1.38-, 1.31-, and 1.50-fold greater risk for depression, respectively.
Patients with comorbidities such as pre-myocardial infarction, COPD, angina, and congestive heart failure are more likely to develop depression. Indeed, we found that patients with pre-myocardial infarction, chronic obstructive pulmonary disease, angina, and congestive heart failure comorbidities had a 1.35-, 1.39-, 1.60-, and 2.03-fold greater risk of depression, respectively, than patients without such complications. The levels of relevant inflammatory mediators are increased in those with heart disease, especially myocardial infarction or coronary heart disease, which can activate depression symptoms.45 Therefore, these patients exhibit a high incidence of severe depression. Dickens et al13 confirmed that frequent angina was the only predictor of depression at 12 months after myocardial infarction. Moreover, myocardial infarction, chronic obstructive pulmonary disease, angina, and congestive heart failure are incurable chronic diseases that are usually accompanied by recurrence of chest pain, difficulty breathing, and other symptoms. Patients with these afflictions have restricted lifestyles (unable to participate in certain intense or stimulating exercises, have to adopt special diets, and/or have sleep disorders), their capacity for daily activity is reduced (cannot work as usual, physical strength has declined, and/or cannot take care of others), they are on long-term medication, they have great economic burden, and they can easily feel nervous, anxious, or a lack of enthusiasm for life or experience depression.
History of Depressive Disorders and a Family History of Depression
The authors confirmed that patients with a history of depression are more likely to develop depression again, with an OR value of 3.52. Depression is associated with a variety of factors. In addition to cardiac surgery-related factors, multivariate logistic regression analysis confirms the link with biological genetic factors (family history of mental disorders). In this study, patients with a family history of depression had a 1.79 times greater risk for depression than did other patients. In addition, behavioral factors (medication compliance) and social and familial environmental factors (negative life events) are important risk factors for the recurrence of depression.46 Spijkerman et al12 reported neuroticism as a risk factor for recurrent depression. Patients with pre-depression likely have little psychological preparation for treatment, an incomplete understanding of the disease, and great psychological stress. These factors may lead to mania or depression and other symptoms, such as insomnia, anxiety, a poor appetite, and other performance-related symptoms, resulting in a significantly reduced ability to adapt to life situations. As a result, patients experience increased sensitivity to stress factors, which exacerbates the stress response and makes them more prone to mental disorders. Moreover, authors of a recent meta-analysis showed that antidepressants did not improve heart rate variability among these patients47; thus, even if depression was cured, the incidence of adverse cardiac events was not reduced.
Severity of Acute Coronary Syndrome Disease: Killip > 1, Killip ≥ 2, and Ejection Fraction < 35%
Many studies have found that patients with severe depression also exhibit a low ejection fraction and a high Killip level.21 We found that Killip greater than 1 and greater than or equal to 2 are risk factors for depression among patients with ACS. The Killip level is used to correlate ACS with heart failure. The OR value of Killip greater than or equal to 2 is 1.71, higher than that of Killip greater than 1 (OR, 1.39), indicating that a greater risk of heart failure is associated with a greater risk of depression. Patients with heart failure frequently relapse, have a poor quality of life, have a heavy economic burden, and exhibit delayed healing, which are major causes of depression among patients with ACS.
Ejection fraction is an index that represents left ventricular function; a lower value indicates a lower left ventricular ejection rate and thus a heavier burden on the patient's heart. Frasure-Smith et al found that the risk of depression in patients with myocardial infarction having an ejection fraction of less than 35% was increased by 1.5 times. In this study, the risk of depression in patients with an ejection fraction less than 35% was 1.61-fold that of patients with ejection fraction of 35% or greater. However, other studies have found that the severity of the disease, as reflected by ejection fraction or Killip, is not associated with depression.12,23,25 Therefore, plausible causes need to be confirmed by additional studies in the future.
Treatment Factors: the Use of Calcium Channel Blockers and Antidepressants, Percutaneous Transluminal Coronary Angioplasty, and Coronary Artery Bypass Graft
Because of the side effects of drugs, patients who use calcium channel blockers and antidepressant drugs exhibit a high incidence of depression. Calcium channel blockers can lead to orthostatic hypotension, facial flushing, and other symptoms, resulting in depression.48 In addition, it has been previously reported that the treatment effect of antidepressants on patients with ACS living with depression is reduced compared with that of non-ACS patients with depression.
Percutaneous transluminal coronary angioplasty and coronary artery bypass graft are commonly used means of treating coronary heart disease; by increasing myocardial perfusion, the ischemic myocardium may be saved and heart function may improve. Coronary artery bypass graft is an invasive treatment with high costs, and patients who undergo coronary artery bypass graft require long-term medication; it may also cause negative psychological activity in patients with ACS.49 Authors of a prospective study published in The Lancet showed that, among 309 patients undergoing coronary artery bypass graft, the rate of severe depression was 20% and the incidence of adverse cardiac events was 27% after 1 year, significantly higher than those among patients without depression.50 Studies have also shown that serum levels of inflammatory markers, such as IL-6 and IL-1, are significantly increased in patients with coronary heart disease after treatment. Thus, depression among this patient population may be related to activation of the immune system and inflammatory factors in the body after treatment.51
In addition to the factors discussed and analyzed previously, a large number of studies have confirmed that sleep disturbance is a risk factor for depression in the general population52; there are also reports that sleep disorders are also closely related to the occurrence of depression in patients with ACS.53 However, there were no reports of sleep problems in the 30 articles included in the meta-analysis. The reason is that Preferred Reporting Items for Systematic Reviews and Meta-Analyses system report specifications are mainly used in randomized controlled and interventional studies and have wide applications. In contrast, the literature included in this study was case-control and cohort studies. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses system report specification was poorly targeted. For example, there were no specific search methods, searcher qualifications, manual search content, and unpublished literature processing and reporting. There are limitations to the risk factors detected.
This article has several limitations. First, the diagnostic criteria for depression were different from those in most articles, which include Beck Depression Inventory, International Classification of Diseases, Tenth Revision, Hospital Anxiety and Depression Scale-Depression, Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, and Hamilton Depression Scale, and thus the incidence of depression was different. Second, because of the limited number of articles, publication bias was associated with several risk factors, such as never married, living alone, diabetes, and treatment with antidepressants. Therefore, we should be cautious when considering the conclusions. Third, authors in only 3 articles reported the characteristics of primary depression and recurrent depression, and therefore their differences were only described in this study. The authors found that women, patients with a low level of education, patients taking antidepressant drug treatment, patients with a family history of depression, and smokers were more likely to develop recurrent depression. In addition, as few studies investigated the effect of social and family support, economic levels, cardiovascular disease severity, and other factors on depression, further studies should be conducted to address the lapse in knowledge.
Although it is well known that sleep and depression are very closely related, the evidence in the published literature on this relationship is mostly descriptive. The relationship between them cannot be analyzed because of the lack of data, and this should be addressed in the future in control or prospective randomized controlled trials.
The authors of this meta-analysis investigated many risk factors for post-ACS depression. Individuals who have a good marriage, receive higher education, engage in stable work, practice a healthy lifestyle (smoking cessation, low-fat diet, and weight control), and do not have comorbidities such as hypertension, dyslipidemia, diabetes, pre-myocardial infarction, chronic obstructive pulmonary disease, angina, congestive heart failure, history of depressive disorders, and family history of depression have a lower risk of post-ACS depression. However, among patients with ACS, it is important to distinguish whether it is the first occurrence of depression or recurrent depression; therefore, additional studies should be conducted regarding this matter.
What's New and Important?
- On the basis of the different diagnostic criteria for depression, the incidence of depression among patients with ACS is 5% to 69.3%.
- The top 5 risk factors for post-ACS depression are antidepression treatment, housewife status, history of depressive disorders, widow status, and history of congestive heart failure. Conversely, a married status, high education, and employment are protective factors.
- Regardless of nonintervention factors such as gender, people who have a good marriage, receive higher education, engage in stable work, and practice a healthy lifestyle (smoking cessation, low-fat diet, and control weight) have a reduced risk of post-ACS depression.
1. Osler M, Mårtensson S, Wium-Andersen IK, et al. Depression
after first hospital admission for acute coronary syndrome
: a study of time of onset and impact on survival. Am J Epidemiol
2. Smolderen KG, Spertus JA, Reid KJ, et al. The association of cognitive and somatic depressive symptoms with depression
recognition and outcomes after myocardial infarction. Circ Cardiovasc Qual Outcomes
3. Nicholson A, Kuper H, Hemingway H. Depression
as an aetiologic and prognostic factor in coronary heart disease: a meta-analysis of 6362 events among 146 538 participants in 54 observational studies. Eur Heart J
4. Myers V, Gerber Y, Benyamini Y, et al. Post-myocardial infarction depression
: increased hospital admissions and reduced adoption of secondary prevention measures—a longitudinal study. J Psychosom Res
5. Lichtman JH, Froelicher ES, Blumenthal JA, et al. Depression
as a risk factor for poor prognosis among patients with acute coronary syndrome
: systematic review and recommendations: a scientific statement from the American Heart Association. Circulation
6. van Melle JP, de Jonge P, Spijkerman TA, et al. Prognostic association of depression
following myocardial infarction with mortality and cardiovascular events: a meta-analysis. Psychosom Med
7. Pelletier R, Lavoie KL, Bacon SL, et al. Depression
and disease severity in patients with premature acute coronary syndrome
. Am J Med
8. Strik JJ, Lousberg R, Cheriex EC, Honig A. One year cumulative incidence of depression
following myocardial infarction and impact on cardiac outcome. J Psychosom Res
9. Ossola P, Paglia F, Pelosi A, et al. Risk factors for incident depression
in patients at first acute coronary syndrome
. Psychiatry Res
10. Joergensen TS, Maartensson S, Ibfelt EH, et al. Depression
following acute coronary syndrome
: a Danish nationwide study of potential risk factors. Soc Psychiatry Psychiatr Epidemiol
11. Stang A. Critical evaluation of the Newcastle-Ottawa scale for the assessment of the quality of nonrandomized studies in meta-analyses. Eur J Epidemiol
12. Spijkerman TA, van den Brink RH, Jansen JH, Crijns HJ, Ormel J. Who is at risk of post-MI depressive symptoms? J Psychosom Res
13. Dickens CM, Percival C, McGowan L, et al. The risk factors for depression
in first myocardial infarction patients. Psychol Med
14. Doyle F, McGee HM, Conroy RM, et al. What predicts depression
in cardiac patients: sociodemographic factors, disease severity or theoretical vulnerabilities? Psychol Health
15. Agarwal M, Trivedi JK, Sinh PK, Dalal PK, Saran RK. Depression
in patients of myocardial infarction—a cross-sectional study in northern India. J Assoc Physicians India
16. Rieckmann N, Burg MM, Gerin W, et al. Depression
vulnerabilities in patients with different levels of depressive symptoms after acute coronary syndromes. Psychother Psychosom
17. van Melle JP, de Jonge P, Kuyper AM, et al. Prediction of depressive disorder following myocardial infarction data from the Myocardial infarction and Depression
-Intervention Trial (MIND-IT). Int J Cardiol
18. Kang HJ, Stewart R, Bae KY, et al. Predictors of depressive disorder following acute coronary syndrome
: results from K-DEPACS and EsDEPACS. J Affect Disord
19. Romanelli J, Fauerbach JA, Bush DE, Ziegelstein RC. The significance of depression
in older patients after myocardial infarction. J Am Geriatr Soc
20. Naqvi TZ, Rafique AM, Andreas V, et al. Predictors of depressive symptoms post-acute coronary syndrome
. Gend Med
21. Carney RM, Freedland KE, Steinmeyer B, et al. History of depression
and survival after acute myocardial infarction. Psychosom Med
22. Dias CC, Mateus PS, Mateus C, et al. Acute coronary syndrome
. Rev Port Cardiol
23. De Jonge P, van den Brink RH, Spijkerman TA, et al. Only incident depressive episodes after myocardial infarction are associated with new cardiovascular events. J Am Coll Cardiol
24. Lauzon C, Beck CA, Huynh T, et al. Depression
and prognosis following hospital admission because of acute myocardial infarction. CMAJ
25. Lesperance F, Frasure-Smith N, Talajic M. Major depression
before and after myocardial infarction: its nature and consequences. Psychosom Med
26. Sørensen C, Brandes A, Hendricks O, et al. Psychosocial predictors of depression
in patients with acute coronary syndrome
. Acta Psychiatr Scand
27. Marchesi C, Ossola P, Scagnelli F, et al. Type D personality in never-depressed patients and the development of major and minor depression
after acute coronary syndrome
. J Affect Disord
28. Whang W, Davidson KW, Palmeri NO, et al. Relations among depressive symptoms, electrocardiographic hypertrophy, and cardiac events in non-ST elevation acute coronary syndrome
patients. Eur Heart J Acute Cardiovasc Care
29. Figueiredo JHC, Silva NASE, Pereira BB, Oliveira GMM. Major depression
and acute coronary syndrome
-related factors. Arq Bras Cardiol
30. Kronish IM, Rieckmann N, Schwartz JE, Schwartz DR, Davidson KW. Is depression
after an acute coronary syndrome
simply a marker of known prognostic factors for mortality? Psychosom Med
31. Lafitte M, Tastet S, Perez P, et al. High sensitivity C reactive protein, Fibrinogen levels and the onset of major depressive disorder in post-acute coronary syndrome
. BMC Cardiovasc Disord
32. Grace SL, Abbey SE, Kapral MK, et al. Effect of depression
on five-year mortality after an acute coronary syndrome
. Am J Cardiol
33. Frasure-Smith N, Lespérance F, Irwin MR, Sauvé C, Lespérance J, Théroux P. Depression
, C-reactive protein and two-year major adverse cardiac events in men after acute coronary syndromes. Biol Psychiatry
34. Di Benedetto M, Lindner H, Hare DL, et al. Depression
following acute coronary syndromes: a comparison between the Cardiac Depression
Scale and the Beck Depression
Inventory II. J Psychosom Res
35. Lespérance F, Frasure-Smith N, Juneau M, et al. Depression
and 1-year prognosis in unstable angina
. Arch Intern Med
36. Schulman-Marcus J, Shah T, Swaminathan RV, et al. Comparison of recent trends in patients with and without major depression
and acute ST-elevation myocardial infarction. Am J Cardiol
37. Doyle F, McGee H, Conroy R, et al. Systematic review and individual patient data meta-analysis of sex differences in depression
and prognosis in persons with myocardial infarction: a MINDMAPS study. Psychosom Med
38. O'Brien F, O'Donnell S, McKee G, Mooney M, Moser D. Knowledge, attitudes, and beliefs about acute coronary syndrome
in patients diagnosed with ACS: an Irish cross-sectional study. Eur J Cardiovasc Nurs
39. Horn EE, Xu Y, Beam CR, Turkheimer E, Emery RE. Accounting for the physical and mental health benefits of entry into marriage: a genetically informed study of selection and causation. J Fam Psychol
40. Mallik S, Spertus JA, Reid KJ, et al. Depressive symptoms after acute myocardial infarction: evidence for highest rates in younger women. Arch Intern Med
41. Larsen KK, Christensen B, Søndergaard J, Vestergaard M. Depressive symptoms and risk of new cardiovascular events or death in patients with myocardial infarction: a population-based longitudinal study examining health behaviors and health care interventions. PLoS One
42. Dalen JE, Alpert JS, Goldberg RJ, Weinstein RS. The epidemic of the 20(th) century: coronary heart disease. Am J Med
43. Busch AM, Borrelli B, Leventhal AM. The relationship between smoking and depression
post-acute coronary syndrome
. Curr Cardiovasc Risk Rep
44. Wang Q, Chair SY, Wong EM, et al. Comparing the predictive abilities of different metabolic syndrome definitions for acute coronary syndrome
: a case-control study in Chinese adults. Metab Syndr Relat Disord
45. Liu H, Luiten PG, Eisel UL, Dejongste MJ, Schoemaker RG. Depression
after myocardial infarction: TNF-α-induced alterations of the blood-brain barrier and its putative therapeutic implications. Neurosci Biobehav Rev
46. Burcusa SL, Iacono WG. Risk for recurrence in depression
. Clin Psychol Rev
47. Zuidersma M, Conradi HJ, van Melle JP, Ormel J, de Jonge P. Depression
treatment after myocardial infarction and long-term risk of subsequent cardiovascular events and mortality: a randomized controlled trial. J Psychosom Res
48. Hallas J. Evidence of depression
provoked by cardiovascular medication: a prescription sequence symmetry analysis. Epidemiology
49. Teixeira R, Vieira MJ, Ribeiro MA, et al. Prognosis following acute coronary syndromes according to prior coronary artery bypass grafting: meta-analysis. Eur Heart J Acute Cardiovasc Care
50. Connerney I, Shapiro PA, McLaughlin JS, et al. Relation between depression
after coronary artery bypass surgery and 12-month outcome: a prospective study. Lancet
51. Dinan TG. Inflammatory markers in depression
. Curr Opin Psychiatry
52. Kim JM, Stewart R, Kim SW, Yang SJ, Shin IS, Yoon JS. Insomnia, depression
, and physical disorders in late life: a 2-year longitudinal community study in Koreans. Sleep
53. Kim JM, Stewart R, Bae KY, et al. Correlates and escitalopram treatment effects on sleep disturbance in patients with acute coronary syndrome
: K-DEPACS and EsDEPACS. Sleep