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BMC Cardiovascular Disorders

, 19:143 | Cite as

Patients with ST segment elevation myocardial infarction: moderating effect of perceived control on the relationship between depression and in-hospital complications

  • Mohannad Eid AbuRuzEmail author
Open Access
Research article
  • 106 Downloads
Part of the following topical collections:
  1. Coronary artery disease

Abstract

Background

Cardiovascular diseases remain the top global killer, with nearly 80% of related mortalities occurring in developing countries. Over half of cardiovascular diseases’ mortality is due to coronary heart disease, which is commonly linked to acute myocardial infarction. Psychological factors (i.e., depression and anxiety) after acute myocardial infarction are associated with higher levels of complications and mortality. Perceived control moderated the effect of anxiety on complications in different cardiac populations, but impacts on depression and complications after acute myocardial infarction are not well studied. This study explores the moderating effect of perceived control on the relationship between depression and complications after ST segment elevation myocardial infarction.

Methods

Three hundred patients with a confirmed diagnosis of ST segment elevation myocardial infarction participated in this prospective observational study. Patients answered socio-demographic data, the depression subscale of the Hospital Anxiety and Depression Scale (HADS), and the Control Attitude Scale-Revised (CAS-R) questionnaires. In-hospital complications and all other necessary data were extracted from medical records after discharge. Data were analyzed using logistic regression.

Results

24% developed at least one complication. Patients with high depression scores (8–21) were more likely to develop complications (χ2 = 34.15, p < .001) than those with low depression scores (0–7). Patients with high levels of perceived control had lower levels of depression than those with low perceived control (mean [SD], 9.47 [6.43] vs. 12.31 [6.66], p < .001). The results of logistic regression showed that perceived control moderated the association between depression and complications, since depression scores, perceived control scores, and the interaction between depression and perceived control were significant predictors of complications. Participants with high depression and low perceived control had the highest rate of complications (31.5% vs. 15.4%, P < .001).

Conclusions

Depression increased complications after ST segment elevation myocardial infarction. Perceived control moderated this relationship. Assessment of depression and enhancement of perceived control in patients with acute myocardial infarction can decrease complications and improve outcomes.

Keywords

Acute myocardial infarction Depression Perceived control Complications 

Abbreviations

AMI

Acute myocardial infarction

CAS-R

Control attitude scale revised

CHD

Coronary heart disease

CVDs

Cardiovascular diseases

HADS

Hospital anxiety and depression scale

IRB

Institutional review board

LVEF

Left ventricular ejection fraction

PC

Perceived control

RA

Research assistant

STEMI

ST-segment elevation myocardial infarction

Background

Cardiovascular diseases (CVDs) are the most common cause of death worldwide [1]. In the US alone, there is more than 90 million diagnosed with at least one type of CVD [1]. Approximately 80% of all deaths nationwide due to CVDs occur in developing (low and middle income) countries [1]. In the developing countries of the Middle East, mortality rates due to CVDs are increasing [2]; in Jordan, 35% of all deaths occur as a result of CVDs [3].

More than half of all CVDs are due to coronary heart disease (CHD) [1]. Every 40 s an American will have an acute myocardial infarction (AMI) due to CHD. In 2019, it is estimated that 720,000 Americans will have a new AMI, and 335,000 will have a recurrent event [1]. Nearly 35% of patients who experience a CHD event yearly will die from it, and ≈15% who develop AMI will die of it [1]. In Jordan, 131 deaths per 100,000 are due to CHD, accounting for nearly 20% of all deaths [3].

In the US, during the period from 2001 and 2011, in-hospital mortality after ST segment elevation myocardial infarction (STEMI) increased for patients without any intervention, did not change for patients who received percutanous coronary intervention, and decreased for patients who had coronary artery bypass surgery [1]. Therefore, determining physiological and psychological factors affecting mortality and morbidity for patients with STEMI is warranted.

Psychological manifestations after AMI are very common, with the most common being depression and anxiety. The incidence of depression after AMI might be as high as 80% [4, 5]. Previous studies have found evidence that depression is associated with short- and long-term complications after AMI. In the short term, starting as early as the first 20 min after AMI [6, 7, 8, 9], depression was an independent predictor of complications such as acute recurrent ischemia, re-infarction, ventricular tachycardia, ventricular fibrillation, cardiogenic shock, pulmonary edema, inflammation (i.e., endocarditis), left ventricular mural thrombus, and in-hospital death [3, 4, 6, 7, 10]. Moreover, high levels of depression were associated with higher levels of fatigue and longer hospitalization, especially in critical care units [4], and lower levels of left ventricular ejection fraction (LVEF) [11].

Over the long term, depression is a more significant predictor than traditional risk factors such as smoking and hyperlipidemia for adverse outcomes after AMI [12, 13]. Depression was associated with increased risk of re-infarction, readmissions [14, 15], and ischemic cardiac events [16, 17, 18]. Moreover, in longitudinal studies (up to 10 years post-event) depression increased morbidity and mortality after AMI [19, 20]. In addition, depression played a significant role of incomplete recovery [21], poor quality of life [22, 23], postponing return to work [24], lack of adherence to medication and health care team instructions [25], and not following the rehabilitation protocols after AMI [26].

The effect of depression on cardiac mortality after AMI was assessed in a scientific statement from the American Heart Association based on their analysis of 11 studies. A significant relationship was reported in 8 studies [27]. Based on the results of their analysis, the American Heart Association reinforced their appraisal of depression as a risk factor for complications and mortality after AMI [27]. Patients’ coping, psychosocial repossession, and quality of life after AMI depends on psychological (i.e., depression) instead of physiological factors [3, 28]. It has been shown that personal control and social support have protective effects against depression, and improve quality of life in different cardiac populations [29, 30]. Therefore, if depression is assessed and managed well for patients with AMI, this might improve their outcomes and decrease complications.

Perceived control (PC) is a new strategy under investigation that might have a protective effect against depression in patients with AMI. It has been defined as “an individual’s belief that he or she has the resources required to cope with negative events in a way that positively influences their adversive nature” [28]. To our knowledge, no studies were specifically designed to check the effect of PC on depression and in-hospital complications in patients with AMI. However, different studies investigated the relationship between PC and anxiety, finding that PC was negatively associated with anxiety in AMI, cardiac surgery, and heart failure [28]; moreover, it was an independent predictor of anxiety in these populations, and moderated the relationship between anxiety and in-hospital complications [3, 31]. Therefore, the major purpose of this study was to check if there is a moderating effect of PC on the relationship between depression and in-hospital complications after STEMI.

Methods

Research design, sample, and setting

This study employed a prospective, non-experimental, observational design, recruiting participants from one governmental and two private hospitals in Amman. Inclusion criteria comprised: (1) cardiology STEMI diagnosis (confirmed), with increased enzyme and cardiac changes (indicated by ECG); (2) adult patients (aged over 18 years); (3) not in unusual pain and stable hemodynamically at the time of interview; (4) able to give (and sign) informed consent and to participate by answering questionnaire items; and (5) not suffering from critical comorbidities and serious non-cardiac conditions (e.g. stroke, sepsis, and shock). Exclusion criteria included those who prior to PC or depression manifested in-hospital complications, in order to explore the longitudinal, cause-and-effect dimension of the clinical problem.

A logistic regression sample-size calculator was used a priori to ensure that the findings would have significance statistically. Criteria included estimated event rate (occurrence of complications) of 27% [31], two-tailed test with power of 0.8, and alpha of 0.05. Regression analysis was conducted with 13 independent variables. The consequent requirement was 238 participants, thus 300 participants were included to account for dropout and attrition etc. (Fig. 1).
Fig. 1

Patient flow diagram. A total of 300 patients were included in the final analyses PC: Perceived control.

Ethical considerations

The Applied Science Private University Amman’s Institutional Review Board (IRB) Committee analyzed this study and accorded it their ethical approval (IRB#: Faculty 024). Consequently, the University President formally requested that the hospital directors enable and assist the fieldwork. Subsequently, the medical directors in the studied settings were met by the principal investigator to ensure their acknowledgement and cooperation with the approval letter, and they issued their own permission to begin data collection and to apply the study fieldwork.

Procedure

Research assistants (RAs) were engaged to collect data from hospitals, with critical care nursing master’s degrees, and training in cardiovascular care. Each potential participant in the studied settings who met the inclusion criteria was approached by the RAs, who explained the study to them in depth, along with all pertinent ethical information (e.g. voluntary participation and right to withdraw etc.), and those who subsequently wished to take part were asked to sign a form indicating their informed consent. Participants were interviewed while hemodynamically stable during their initial 3 days following admission (mean ± SD; 35 ± 16 h). Socio-demographic information was recorded by the RAs, who also delivered the Control Attitude Scale-Revised (CAS-R) and the depression subscale of the Hospital Anxiety and Depression Scale (HADS). Upon discharge, RAs noted from participants’ medical records their in-hospital complications (if applicable) along with any other pertinent comorbidities.

Measurement of variables

  • Clinical and Socio-Demographic Characteristics

As mentioned previously, following participants’ discharge from hospital (i.e. upon completion of their in-patient treatment), the RAs extracted socio-demographic and clinical data from their medical records, including gender, age, smoking profile, vital signs upon admission and chest pain severity, and experience of diabetes mellitus, emergency and ICU medications, hypertension, LVEF, and myocardial infarction.
  • Depression

Arabic HADS was used to assess depression. Numerous cardiac studies affirm its psychometric proprieties (Cronbach’s α 0.87) [6, 32, 33, 34, 35]. The seven items are rated on a four-point Likert scale, ranging from 0 to 3, where 3 refers to the maximum severity and frequency of symptoms. The values assigned for each item add up to a net score ranging from 0 to 21, which are then classified according to depression severity as normal (0–7), mild (8–10), moderate (11–14), and severe (15–21) [6, 32].
  • In-Hospital Complications

STEMI frequently results in in-hospital complications [3, 4, 7, 8, 31], of which the following are common: (a) ventricular fibrillation; (b) ventricular tachycardia warranting care, particularly ≥30 s (attributable to hemodynamic instability); (c) acute recurrent ischemia; (d) cardiogenic shock; (e) reinfarction; (f) acute pulmonary edema; and (g) mortality.
  • Perceived Control

Arabic CAS-R was deployed to measure PC, having displayed acceptable psychometric proprieties among cardiac populations. Hypothesis testing has displayed its construct validity for known associations, and its reliability and validity have been demonstrated among 500 STEMI participants (Cronbach’s α 0.85) [3]. The tool comprises eight items answerable with Likert-type scales, with responses descending from 5 “totally agree” to 1 “totally disagree”. Net scores are in the range of 8–40, with lower scores denoting lower PC levels. Due to the lack of mean norms, other researchers deployed median values as delimitation points [3, 31]; following this method, the resultant median in this study was set as the cut-off point (29), whereby participants with higher scores for PC had high PC, and vice-versa.

Data analysis

Data analysis was conducted with recourse to SPSS (version 24). Statistical significance was denoted by p value < .05. Clinical and socio-demographic characteristics related to depression changes at baseline were described by frequencies, percentages, and Mean ± SD. Continuous and categorical variables were analyzed using Student’s t-test or χ2, respectively, to ensure that the studied variables were pertinent to the research. Variables differing between the high and low depression groups could thus be controlled for the purposes of subsequent analyses.

To control for the other variables and to determine the impacts of PC, depression, and interaction term (moderating effect), multiple hierarchal logistic regression was deployed, yielding results as odds ratios and 95% confidence intervals. Three blocks were applied for regression: (1) age and gender; (2) history of diabetes, emergency department medication (e.g. beta block, aspirin, or anti-depressant), hypertension, LVEF, previous myocardial infarction, and smoking; and (3) PC and depression scores, and depression*PC interaction. Multicollinearity between variables was absent, as indicated by variance inflation factor (less than 3).

Results

Socio-demographic and clinical characteristics

The sample consisted of a total 300 participants, including 231 men and 69 women. During hospitalization, 72 participants (24%) developed at least one complication (Table 1). Patients with high depression scores (8–21) were more likely to develop complications (χ2 = 34.15, p < .001) than those with low depression scores (0–7). Moreover, they have lower levels of LVEF (M [SD], 44.60 [7.31] vs. 53.05 [7.12], p < .001). Patients with high levels of PC had lower levels of depression than those with low PC (M [SD], 9.47 [6.43] vs. 12.31 [6.66], p < .001). Socio-demographic and clinical characteristics relative to depression levels are presented in Table 2. Only one clinical variable differed between low and high depression groups: patients in the high depression group received anti-depressant medication more frequently than those in the low depression group Table 3. There were no differences in any socio-demographic or clinical variables between those who continued the study and those who dropped out.
Table 1

Specific complications developed and their percentages

Complication developed

aNumber of patients (%)

Acute recurrent ischemia

30 (41.7)

Pulmonary edema

10 (13.9)

Sustained ventricular tachycardia

9 (12.5)

Re-infarction

8 (11.1)

Cardiogenic shock

7 (9.7)

In-hospital death.

3 (4.2)

Ventricular fibrillation

2 (2.8)

aMore than one patient developed more than one complication

Table 2

Sociodemographic and clinical characteristics of the sample based on depression levels (N = 300)

Characteristic

High Depression (n = 195)

Low Depression (n = 105)

Age

69.5 ± 9.0

69.02 ± 10.0

Gender

 Male

149 (76.4)

82 (78.1)

 Female

46 (23.6)

23 (21.9)

History of DM

80 (41.0)

49 (46.7)

History of HTN

155 (79.5)

86 (81.9)

History of previous AMI

122 (62.6)

75 (71.4)

History of smoking

146 (74.9)

83 (79.0)

Severity of chest pain

5.17 ± 2.2

5.26 ± 2.2

Ejection fraction

44.6 ± 7.3

53.05 ± 7.1**

Development of complications

59 (30.3)

48 (18.8)**

Values are presented as M ± SD or n (%), DM Diabetes Miletus, HTN Hypertension, AMI Acute myocardial infarction, ** significant at P < .001

Table 3

Treatment received during hospitalization (N = 300)

Treatment

High Depression (n = 195)

Low Depression (n = 105)

Thrombolytic agents

80 (41.0)

37 (35.2)

Beta blocker

98 (50.3)

50 (47.6)

Aspirin

175 (89.7)

90 (85.7)

Anti-depressant

113 (58.0)

42 (40.0)*

Coronary artery bypass graft

20 (10.3)

12 (11.4)

Angioplasty

119 (61.0)

67 (63.8)

Values are presented as n (%).* significant at P < .05

Checking the moderating effect

The results of the logistic regression are presented in Table 4. The model shows five significant predictors: history of previous AMI, depression scores, PC scores, LVEF, and the interaction between depression and PC. Perceived control moderated the association between depression and complications since depression scores, PC scores, and the interaction between depression and PC were significant predictors of complications. Participants with high depression and low PC have the highest rate of complications (31.5% vs. 15.4%, p < .001) (Fig. 2).
Table 4

Logistic regression analysis for predictors of in-hospital complications

Predictor

Odds ratio

Wald

95% CI

p value

History of previous AMI

2.21

8.61

1.51–4.31

.005

Depression scores

1.51

7.70

1.11–2.01

.007

Perceived control

0.81

7.01

0.75–0.99

.008

LVEF

0.83

6.22

0.71–0.96

.030

Depression scores * Perceived control

1.61

8.31

1.22–2.21

.006

AMI Acute myocardial infarction, CI Confidence interval, LVEF Left ventricular ejection fraction. Variables used in the model (age, gender, history of diabetes, history of hypertension, history of smoking, history of previous AMI,, beta blocker use, anti-depressant use, aspirin use, left ventricular ejection fraction, depression scores, perceived control scores, and the interaction between depression and perceived control)

Fig. 2

Comparison of percentage of patients who developed complications based on depression levels and PC. Patients with high depression and low PC had the highest complication rate indicating the moderating level of PC on the relationship between depression and complications. ***p < .001. Abbreviation: PC, perceived control.

Other important findings

Previous myocardial infarction and high levels of depression increased the occurrence of complications by 121 and 51%, respectively. High levels of PC have a protective effect against complications by 19%. Moreover, high levels of LVEF have a protective effect against complication by 17%.

Discussion

This pioneering investigation demonstrates that PC moderates depression related to post-STEMI complications in in-hospital settings in a developing country. In other words, the results demonstrate that PC moderates post-STEMI in-hospital complications in relation to psychological symptoms (i.e. depression and anxiety) [3, 31]. Depression and PC were both independent predictors of these complications, affirming the findings of previous studies on the former predictor [4, 5, 6, 36]: PC militates against depression, while the latter predisposes patients to such complications, the most prolific of which was acute recurrent ischemia [3, 4, 7, 8, 31]. Approximately one-quarter (24%) of participants in this study developed some form of complication.

This study thus affirms previous investigations finding relatively high prevalence of in-hospital complications following STEMI, contrary to research that found no significant link between in-hospital complications and depression [37, 38, 39, 40, 41]. Numerous potential reasons for these divergent findings can be postulated, including differing operational definitions of depression itself, different data collection techniques (e.g. timing of depression evaluation), different sample sizes, and a lack of regard for depression moderators. Depression-measuring tools may have wide indications spanning numerous forms of illness, including subclinical CHD. In this study, HADS was used to measure depression, to differentiate depression among physically ill patients, which removes somatic indications that can obscure factors of heart disease but which may blunt depression detection [3, 6, 35]. As a result, this study is conservative in its estimation of the significance of the relationship between in-hospital complications and depression.

There are numerous possible causes of the link between complications and depression. For instance, physiologically, the experience of depression inhibits para-sympathetic neuronal activity, and activates sympathetic nervous activity, which gives a fillip to activities conducive to complications (e.g. inflammation, fibrillation threshold changes, decreased variability in heart rate, and increased aggregation of platelets) [2, 6, 8, 31]. Initial proliferation of such physiological variables immediately after AMI is highly linked to the development of complications [2, 6, 8, 31]. In terms of behavior, depression is linked to reduced enthusiasm, exercise, and healthy eating, and increased smoking and other unhealthy behaviors [3, 28, 31], albeit these usually play a minimal role in the experience of acute clinical/ health events [3, 28, 31].

Depression experienced during or in the wake of dangerous or critical events and experiences can be moderated by PC to reduce in-hospital complications, particularly in terms of improving coping skills [31, 42], and reducing anxiety, whose mechanisms are similar to depression [31, 42]. This entails that the association between in-hospital complications and anxiety is strong when PC is low, and vice-versa. Consequently, increased PC reduces in-hospital complications and creates a protective cardiac impact: it reduces anxiety and stimulation of the sympathetic nervous system, supporting parasympathetic nervous activity [31, 42], thus guarding from complications.

The empirical results of this study support general conclusions reached by previous researchers, and are of potential clinical importance with regard to depression being associated with lower LVEF [11]; every increase in LVEF units increases by 17% the protective effect against in-hospital complications [3, 28, 31]. Improved quality of life among STEMI patients is also linked to higher LVEF, thus enhancing the latter may improve the former, which may also control depression, high levels of which correspond to low prevalence of LVEF. The results of this investigation thus affirm the moderating role of PC on depression and improved LVEF.

Conclusions

In patients with STEMI, depression is associated with increased risk of complications in the early phase. Perceived control has a protective and moderating effect on this relationship. Assessment of depression and enhancement of PC in this group might decrease complications, morbidity, and mortality.

Limitations

The major limitation of this study was the exclusion of hemodynamically unstable patients, which might decrease the incidence of in-hospital complications. Moreover, data were collected from one major city in Jordan, which might limit the generalizability of the results.

Notes

Acknowledgements

I wish to thank research assistants who helped in the data collection for this research project.

Authors’ contributions

This is a single author manuscript. The author read and approved the final manuscript.

Funding

This is a personal research without any type of funding.

Ethics approval and consent to participate

Approval was granted by the IRB committee at the Applied Science Private University. All participants signed a written informed consent.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

References

  1. 1.
    Benjamin EJ, Virani SS, Callaway CW, Chamberlain AM, Chang AR, Cheng S, Chiuve SE, Cushman M, Delling FN, Deo R, et al. Heart disease and stroke Statistics-2018 update: a report from the American Heart Association. Circulation. 2018;137(12):e67–e492.PubMedCrossRefGoogle Scholar
  2. 2.
    AbuRuz ME, Masa'Deh R. Gender differences in anxiety and complications early after acute myocardial infarction. J Cardiovasc Nurs. 2017;32(6):538–43.PubMedCrossRefGoogle Scholar
  3. 3.
    AbuRuz ME. Perceived control moderates the relationship between anxiety and in-hospital complications after ST segment elevation myocardial infarction. J Multidiscip Healthc. 2018;11:359–65.PubMedPubMedCentralCrossRefGoogle Scholar
  4. 4.
    AbuRuz ME, Alaloul F, Al-Dweik G. Depressive symptoms are associated with in-hospital complications following acute myocardial infarction. In: Applied nursing research : ANR 2018, vol. 39. p. 65–70.PubMedCrossRefGoogle Scholar
  5. 5.
    Thombs BD, Bass EB, Ford DE, Stewart KJ, Tsilidis KK, Patel U, Fauerbach JA, Bush DE, Ziegelstein RC. Prevalence of depression in survivors of acute myocardial infarction. J Gen Intern Med. 2006;21(1):30–8.PubMedPubMedCentralCrossRefGoogle Scholar
  6. 6.
    AbuRuz ME, Al-Dweik G. Depressive symptoms and complications early after acute myocardial infarction: gender differences. Open Nurs J. 2018;12:205–14.PubMedPubMedCentralCrossRefGoogle Scholar
  7. 7.
    Abed MA, Frazier S, Hall LA, Moser DK. Anxiolytic medication use is not associated with anxiety level and does not reduce complications after acute myocardial infarction. J Clin Nurs. 2013;22(11–12):1559–68.PubMedCrossRefGoogle Scholar
  8. 8.
    Abu Ruz ME, Lennie TA, Moser DK. Effects of beta-blockers and anxiety on complication rates after acute myocardial infarction. Am J Crit Care. 2011;20(1):67–73 quiz 74.PubMedCrossRefGoogle Scholar
  9. 9.
    Moser DK, Dracup K. Is anxiety early after myocardial infarction associated with subsequent ischemic and arrhythmic events. Psychosom Med. 1996;58(5):395–401.PubMedCrossRefGoogle Scholar
  10. 10.
    Grewal K, Stewart DE, Abbey SE, Leung YW, Irvine J, Grace SL. Timing of depressive symptom onset and in-hospital complications among acute coronary syndrome inpatients. Psychosomatics. 2010;51(4):283–8.PubMedPubMedCentralCrossRefGoogle Scholar
  11. 11.
    Bagherian-Sararoudi R, Gilani B, Ehsan HB, Sanei H. Relationship between left ventricular ejection fraction and depression following myocardial infarction: An original article. Arya Atheroscler ARYA Atherosclerosis. 2013;9(1).Google Scholar
  12. 12.
    Goldston K, Baillie AJ. Depression and coronary heart disease: a review of the epidemiological evidence, explanatory mechanisms and management approaches. Clin Psychol Rev. 2008;28(2):288–306.PubMedCrossRefGoogle Scholar
  13. 13.
    Steptoe A, Brydon L. Emotional triggering of cardiac events. Neurosci Biobehav Rev. 2009;33(2):63–70.PubMedCrossRefGoogle Scholar
  14. 14.
    Reese RL, Freedland KE, Steinmeyer BC, Rich MW, Rackley JW, Carney RM. Depression and rehospitalization following acute myocardial infarction. Circ Cardiovasc Qual Outcomes. 2011;4(6):626–33.PubMedPubMedCentralCrossRefGoogle Scholar
  15. 15.
    Wu Q, Kling JM. Depression and the risk of myocardial infarction and coronary death: a meta-analysis of prospective cohort studies. Medicine (Baltimore). 2016;95(6):e2815.CrossRefGoogle Scholar
  16. 16.
    Meijer A, Conradi HJ, Bos EH, Thombs BD, van Melle JP, de Jonge P. Prognostic association of depression following myocardial infarction with mortality and cardiovascular events: a meta-analysis of 25 years of research. Gen Hosp Psychiatry. 2011;33(3):203–16.PubMedCrossRefGoogle Scholar
  17. 17.
    Bekke-Hansen S, Trockel M, Burg MM, Taylor CB. Depressive symptom dimensions and cardiac prognosis following myocardial infarction: results from the ENRICHD clinical trial. Psychol Med. 2012;42(1):51–60.PubMedCrossRefGoogle Scholar
  18. 18.
    Denollet J, Martens EJ, Smith OR, Burg MM. Efficient assessment of depressive symptoms and their prognostic value in myocardial infarction patients. J Affect Disord. 2010;120(1–3):105–11.PubMedCrossRefGoogle Scholar
  19. 19.
    van Dijk MR, Utens EM, Dulfer K, Al-Qezweny MN, van Geuns RJ, Daemen J, van Domburg RT. Depression and anxiety symptoms as predictors of mortality in PCI patients at 10 years of follow-up. Eur J Prev Cardiol. 2016;23(5):552–8.PubMedCrossRefGoogle Scholar
  20. 20.
    Du J, Zhang D, Yin Y, Zhang X, Li J, Liu D, Pan F, Chen W. The personality and psychological stress predict major adverse cardiovascular events in patients with coronary heart disease after percutaneous coronary intervention for five years. Medicine (Baltimore). 2016;95(15):e3364.CrossRefGoogle Scholar
  21. 21.
    Lesperance F, Frasure-Smith N, Juneau M, Theroux P. Depression and 1-year prognosis in unstable angina. Arch Intern Med. 2000;160(9):1354–60.PubMedCrossRefGoogle Scholar
  22. 22.
    Beck CA, Joseph L, Belisle P, Pilote L. Predictors of quality of life 6 months and 1 year after acute myocardial infarction. Am Heart J. 2001;142(2):271–9.PubMedCrossRefGoogle Scholar
  23. 23.
    de Jonge P, Spijkerman TA, van den Brink RH, Ormel J. Depression after myocardial infarction is a risk factor for declining health related quality of life and increased disability and cardiac complaints at 12 months. Heart. 2006;92(1):32–9.PubMedCrossRefGoogle Scholar
  24. 24.
    Soderman E, Lisspers J, Sundin O. Depression as a predictor of return to work in patients with coronary artery disease. Soc Sci Med. 2003;56(1):193–202.PubMedCrossRefGoogle Scholar
  25. 25.
    Lin EH, Katon W, Von Korff M, Rutter C, Simon GE, Oliver M, Ciechanowski P, Ludman EJ, Bush T, Young B. Relationship of depression and diabetes self-care, medication adherence, and preventive care. Diabetes Care. 2004;27(9):2154–60.PubMedCrossRefGoogle Scholar
  26. 26.
    Leifheit-Limson EC, Kasl SV, Lin H, Buchanan DM, Peterson PN, Spertus JA, Lichtman JH. Adherence to risk factor management instructions after acute myocardial infarction: the role of emotional support and depressive symptoms. Ann Behav Med. 2012;43(2):198–207.PubMedPubMedCentralCrossRefGoogle Scholar
  27. 27.
    Lichtman JH, Froelicher ES, Blumenthal JA, Carney RM, Doering LV, Frasure-Smith N, Freedland KE, Jaffe AS, Leifheit-Limson EC, Sheps DS, 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. 2014;129(12):1350–69.PubMedCrossRefGoogle Scholar
  28. 28.
    Moser DK, Riegel B, McKinley S, Doering LV, Meischke H, Heo S, Lennie TA, Dracup K. The control attitudes scale-revised: psychometric evaluation in three groups of patients with cardiac illness. Nurs Res. 2009;58(1):42–51.PubMedPubMedCentralCrossRefGoogle Scholar
  29. 29.
    Kidd T, Poole L, Leigh E, Ronaldson A, Jahangiri M, Steptoe A. Health-related personal control predicts depression symptoms and quality of life but not health behaviour following coronary artery bypass graft surgery. J Behav Med. 2016;39(1):120–7.PubMedCrossRefGoogle Scholar
  30. 30.
    Alaloul F, AbuRuz ME, Moser DK, Hall LA, Al-Sadi A. Factors associated with quality of life in Arab patients with heart failure. Scand J Caring Sci. 2017;31(1):104–11.PubMedCrossRefGoogle Scholar
  31. 31.
    Moser DK, Riegel B, McKinley S, Doering LV, An K, Sheahan S. Impact of anxiety and perceived control on in-hospital complications after acute myocardial infarction. Psychosom Med. 2007;69(1):10–6.PubMedCrossRefGoogle Scholar
  32. 32.
    Bjelland I, Dahl AA, Haug TT, Neckelmann D. The validity of the hospital anxiety and depression scale. An updated literature review. J Psychosom Res. 2002;52(2):69–77.PubMedPubMedCentralCrossRefGoogle Scholar
  33. 33.
    el-Rufaie OE, Absood G. Validity study of the hospital anxiety and depression scale among a group of Saudi patients. Br J Psychiatry. 1987;151:687–8.PubMedCrossRefGoogle Scholar
  34. 34.
    el-Rufaie OE, Albar AA, Al-Dabal BK. Identifying anxiety and depressive disorders among primary care patients: a pilot study. Acta Psychiatr Scand. 1988;77(3):280–2.PubMedCrossRefGoogle Scholar
  35. 35.
    el-Rufaie OE, Absood GH. Retesting the validity of the Arabic version of the hospital anxiety and depression (HAD) scale in primary health care. Soc Psychiatry Psychiatr Epidemiol. 1995;30(1):26–31.PubMedCrossRefGoogle Scholar
  36. 36.
    Shang YX, Ding WQ, Qiu HY, Zhu FP, Yan SZ, Wang XL. Association of depression with inflammation in hospitalized patients of myocardial infarction. Pak J Med Sci. 2014;30(4):692–7.PubMedPubMedCentralCrossRefGoogle Scholar
  37. 37.
    McKinley S, Fien M, Riegel B, Meischke H, Aburuz ME, Lennie TA, Moser DK. Complications after acute coronary syndrome are reduced by perceived control of cardiac illness. J Adv Nurs. 2012;68(10):2320–30.PubMedCrossRefGoogle Scholar
  38. 38.
    Lane D, Carroll D, Ring C, Beevers DG, Lip GY. Effects of depression and anxiety on mortality and quality-of-life 4 months after myocardial infarction. J Psychosom Res. 2000;49(4):229–38.PubMedCrossRefGoogle Scholar
  39. 39.
    Mayou RA, Gill D, Thompson DR, Day A, Hicks N, Volmink J, Neil A. Depression and anxiety as predictors of outcome after myocardial infarction. Psychosom Med. 2000;62(2):212–9.PubMedCrossRefGoogle Scholar
  40. 40.
    Nakamura S, Kato K, Yoshida A, Fukuma N, Okumura Y, Ito H, Mizuno K. Prognostic value of depression, anxiety, and anger in hospitalized cardiovascular disease patients for predicting adverse cardiac outcomes. Am J Cardiol. 2013;111(10):1432–6.PubMedCrossRefGoogle Scholar
  41. 41.
    Welin C, Lappas G, Wilhelmsen L. Independent importance of psychosocial factors for prognosis after myocardial infarction. J Intern Med. 2000;247(6):629–39.PubMedCrossRefGoogle Scholar
  42. 42.
    Moser DK, Dracup K. Impact of cardiopulmonary resuscitation training on perceived control in spouses of recovering cardiac patients. Res Nurs Health. 2000;23(4):270–8.PubMedCrossRefGoogle Scholar

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© The Author(s). 2019

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Authors and Affiliations

  1. 1.Clinical Nursing DepartmentFaculty of Nursing, Applied Science Private UniversityAmmanJordan

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