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J Behav Med (2011) 34:351359 DOI 10.


Causal attributions among patients undergoing coronary artery bypass surgery: gender aspects and relation to depressive symptomatology
Anne Dunkel Friederike Kendel Elke Lehmkuhl Roland Hetzer Vera Regitz-Zagrosek

Received: July 29, 2010 / Accepted: January 27, 2011 / Published online: February 9, 2011 Springer Science+Business Media, LLC 2011

Abstract Causal attributions made by patients for their coronary heart disease may contribute to gender differences in emotional adjustment. The purpose of this study was to determine gender differences in causal attributions and to analyze the associations between causal attributions and depressive symptomatology in patients undergoing coronary artery bypass graft (CABG) surgery. Nine hundred and seventy-nine patients (mean age 66.8 years, 19.9% women) completed a modied version of the Illness Perception Questionnaire (IPQ) and the depression module of the Patient Health Questionnaire (PHQ-9) 13 days before CABG-surgery and 1 year after surgery. Men were more likely to name their health behavior (men: 40.2%, women: 26.9%, P \ .001) as a cause of disease, whereas women were more likely to cite destiny (women: 34.7%, men: 25.7%, P = .012). Regression analyses showed cross-sectional and longitudinal associations of attributions with depressive symptomatology which were independent of gender, sociodemographic and clinical variables. Attribution to personality and stress were associated with an increase in depressive symptomatology. Causal attributions may present a valuable approach for identifying patients at

risk for depression and the implementation of targeted interventions. Keywords Causal attributions CABG Gender differences Depression

Introduction Coronary artery bypass graft (CABG) surgery is a frequently performed surgical procedure in patients suffering coronary heart disease. Women display less benecial outcomes following CABG (Regitz-Zagrosek et al. 2004; Vaccarino et al. 2003b) characterized by higher early mortality rates (Kim et al. 2007) and poorer psychological and physical functioning (Vaccarino 2003a). Studies identied multiple factors contributing to this gender disparity, including womens increased age, referral bias, comorbid diseases or procedural differences (Blankstein et al. 2005; Hussain et al. 1998; Vaccarino et al. 2003a). Previous research has highlighted the role of depression for surgery outcome (Blumenthal et al. 2003; Burg et al. 2003; Mallik et al. 2005). Depression is highly prevalent in patients undergoing CABG (Pirraglia et al. 1999) with considerably higher estimates in females compared to males. Moreover, depression is an established risk factor for cardiovascular morbidity and mortality in patients suffering coronary artery disease (Lett et al. 2008; Weidner and Kendel 2010). In patients undergoing CABG, depression has been shown to relate to elevated mortality rates (Baker et al. 2001; Blumenthal et al. 2003; Burg et al. 2003; Mallik et al. 2005), higher risk of cardiac-related readmissions (Oxlad et al. 2006a), increased post-operative length of hospital stay (Oxlad et al. 2006b), and worse quality of life (Mallik et al. 2005).

A. Dunkel (&) E. Lehmkuhl V. Regitz-Zagrosek Berlin Institute of Gender in Medicine (GiM), - Universita tsmedizin Berlin, Luisenstr. 65, Charite 10117 Berlin, Germany e-mail: F. Kendel - Universita tsmedizin Institute for Medical Psychology, Charite Berlin, Luisenstr. 57, 10117 Berlin, Germany E. Lehmkuhl R. Hetzer V. Regitz-Zagrosek Deutsches Herzzentrum Berlin, Brunnenhof 2-4, 13353 Berlin, Germany



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In order to identify high risk patients and to improve surgery outcomes, recent research has focussed on the correlates of depression, how they may differ between the sexes and how to mitigate its effects on outcome (Burker et al. 1995; Dunkel et al. 2009; Pirraglia et al. 1999). In addition to sociodemographic variables (Dunkel et al. 2009; Pirraglia et al. 1999), low social support (Burker et al. 1995; Pirraglia et al. 1999) and clinical factors (Dunkel et al. 2009; Pirraglia et al. 1999), patients personal beliefs about their illness seem to be an important factor contributing to depressive symptomatology. One such belief involves the perceived causes of disease, the causal attributions, which are dened as post-hoc interpretations or redenitions of what caused the illness (Roesch and Weiner 2001). In the context of uncertain, unexpected or threatening events such as life-threatening illness or surgery, causal attributions are commonly generated (Turnquist et al. 1988). A systematic review identied stress and lifestyle factors as the most important causal attributions in heart disease patients (French et al. 2001). In addition, heredity, overweight, hypertension, workload, and fate are cited frequently. Increasing evidence shows marked gender differences in causal attributions, with women formulating fewer attributions to health behavior than men (Aalto et al. 2005; Astin and Jones 2004; Grace et al. 2005; Martin et al. 2005). In particular, men more often attribute their illness to diet, overwork and alcohol, whereas women are more likely to blame heredity (Grace et al. 2005). According to self-regulation theory (Leventhal et al. 1984), patients personal beliefs about their illness present an important factor contributing to coping, psychological adjustment, and health outcomes (Petrie et al. 1996). Among patients with coronary heart disease, causal attributions have been investigated in relation to their impact on health behavior change, such as smoking cessation, stress reduction, or exercise (Darr et al. 2008; French et al. 2005a, 2005b; Gump et al. 2001; Martin et al. 2005). In addition, illness perceptions have been discussed as predictors of rehabilitation attendance (French et al. 2005b). Recent studies investigating subjective illness perceptions in relation to emotional adjustment did not include causal attributions (Dickens et al. 2008; Hermele et al. 2007; Stafford et al. 2009). So far, few studies have systematically explored the impact of causal attributions on depressive symptomatology. In a cross-sectional study, Grace et al. (2005) found stress, mental attitude, family problems, emotions, and personality to be related to the degree of depressive symptomatology. However, prospective studies are needed to investigate the role that illness perceptions may play in the course of depressive symptomatology (Grace et al. 2005).

Therefore, the objective of this study were to (1) analyse gender differences in causal attributions; and (2) to examine associations between causal attributions and depressive symptomatology in a cross-sectional and longitudinal study design.

Methods Study participants and procedure Participants for this study were enrolled in the context of a large prospective clinical study, which was part of the Competence Network of Heart Failure. From January 2005 to July 2008 1,917 patients, scheduled for bypass surgery at the Deutsches Herzzentrum, Department of Cardiothoracic and Vascular Surgery, Berlin, were approached 1-3 days before surgery. Exclusion criteria were: (1) inability to read or to answer the study questionnaires (e.g. dementia, difculties with the language), and (2) age below 18 years. Of the 1,587 CABG-patients who fullled inclusion criteria and provided written consent, 53 patients did not provide data on causal attributions and were thus excluded from the analyses. The follow-up assessment took place 1 year after surgery and was not completed by 563 (36.7%) participants due to death (112 patients, 7.3%), worsening of health status, or termination of study participation without specic reasons. This resulted in a nal study sample of 971 patients (19.9% women) with 99.2% Caucasian ethnicity. Patients contributing at both time points did not differ from those who did not participate at both time points across age and causal attributions except for a more frequent attribution to genes in continuers (v2(1) = 7.14, P = .008). However, non-continuers were more likely to be male (v2(1) = 14.68, P \ .001), to display higher depression scores (T(1039) = 3.11, P = .002), and lower left ventricular ejection fraction (LVEF) (T(1063) = -5.451, P \ .001) at baseline. The institutional review board approved the study protocol. Measures Self-reported sociodemographic data included age, sex, education and partner status. Clinical data, including disease severity (measured with LVEF), history of myocardial infarction (MI) and risk factors such as smoking, body mass index (BMI), and family history of MI before 60 years were obtained from case report forms. Social support was measured using a German adaption of the ENRICHD Social Support Inventory (ESSI) (ENRICHDInvestigators 2000) German Adaption (Kendel et al. in press).


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Causal attributions Six specic causal attributions which have been shown to be relevant in heart disease (French et al. 2001; French et al. 2005a; Grace et al. 2005) were assessed 13 days before surgery: (a) stress and mental load (e.g. workload, family stress, stressful life events, emotional turbulences), (b) heredity factors (genes, family history of heart disease), (c) health behavior such as smoking, unhealthy nutrition, excessive alcohol consumption, (d) personality factors (e.g. ambitious, impatient, short-tempered personality) (e) destiny (fate), and (f) environmental factors such as pollution or noise. Additionally, an item assessing other attributions was included. Accordingly, the self-report measure of causal attributions consisted of 7 items which were adopted from the Illness perception Questionnaire (IPQ) (Weinman et al. rster and Taubert 2006). An 1996), German adaption: (Fo opening statement was given: Diseases might have diverse causes. What do you think contributed to your disease? Following this patients were asked to indicate an explanation for their disease: The cause for my disease might be (a) stress/mental load, (b) my genes, (c) health behavior (smoking, nutrition, alcohol), (d) my personality, (e) destiny or fate, (f) environment (noise, pollution) or (g) other causes. Items were completed on a 4-point scale with response options ranging from not true to exactly true. Because of a marked non-normality of the distribution, these scales were dichotomized clustering patients that indicated not true/scarcely true vs patients indicating almost true/exactly true. Patients that believed in other causes were asked to provide a narrative response. Missing items on single causal attributions were considered not true if any other causal attribution was answered.

Analysis Prior to analysis all data was screened for normality. To reduce skewness and improve the normality, homoscedasticity, and linearity of residuals, a square root transformation was performed on the PHQ-9. Baseline characteristics of male and female study participants were compared using independent sample t test if continuous and v2-tests for categorical data. Longitudinal change in depression was analysed using repeated measures ANOVA including gender as a between-subject factor. Gender differences in causal attributions were analysed using v2-tests. The openended causal item asking for other attributions was coded by a group of experts. Therefore, an inductive approach was used and subsequently, a descriptive analysis was performed. To evaluate intercorrelations between causal attributions as well as associations between attributions and conceptual related variables Pearsons correlations were calculated. Gender differences in strength of associations were analysed using Fishers Z transformation. In addition, logistic regression models were tted to examine whether gender constituted an independent predictor for causal attributions after adjusting for relevant conceptual related variables. To examine the second study objective hierarchical multiple regression analyses of causal attributions on (a) depressive symptomatology at baseline and (b) depressive symptomatology 1 year post surgery were performed. Therefore, sociodemographics (age, gender, education), clinical variables (LVEF, history of MI, family history of MI \ 60 years, body mass index, smoking) and social support were included as control variables. Subsequently, the six causal attributions (excluding the non-specic other causes item) were entered into regression equation. To assess the change in depressive symptomatology from baseline to 1 year post surgery, the baseline score was entered in a rst step (Cohen and Cohen 1983). Gender specic effects were explored by applying the moderator approach described by Baron and Kenny (1986). Data were analysed using SPSS for Windows, version 16.0. All tests were two tailed with an a level of .05.

Depressive symptomatology The depression module of the Patient Health Questionnaire we et al. (PHQ-9) (Spitzer et al. 1999) German version (Lo 2002) is a self-report measure to assess the severity of depressive symptoms within the past 2 weeks. The 9 items directly display diagnostic criteria from the DSM-IV for major depression. The German version has shown excellent we et al. 2004). Items are reliability and validity (Lo endorsed on a 4-point scale with the response options not at all, several days, more than half the days, and nearly every day. The score ranges from 0 to 27, with higher scores indicating higher levels of depression. Cronbachs alpha was a = .791. Cutpoints of 5, 10, 15, and 20 represent the thresholds for mild, moderate, moderately severe, and severe depression (Kroenke et al. 2001).

Results Characteristics of the sample Baseline characteristics are shown in Table 1. Women were older, less educated, and more often living alone than men. However, they were less likely to smoke and had a better LVEF. Women also displayed higher levels of depressive symptomatology before surgery and perceived less social support.


354 Table 1 Baseline sample characteristics Total sample (N = 971) Sociodemographics Age, mean (SD) Education [ 9 years, % Living alone, % Clinical variables LVEF, mean (SD) History of MI, % Family history of MI before 60 years, % Smoking (former and current), % BMI, mean (SD) Psychological scales Depressive symptomatology, mean (SD) Low social support, %

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Men (n = 778)

Women (n = 193)

66.81 (9.03) 51.2 23.2 55.91 (13.49) 42.8 19.9 69.4 27.83 (4.33) 5.61 (4.31) 12.7

65.85 (8.1) 54.3 16.0 55.33 (13.82) 43.6 19.5 74.8 27.83 (4.15) 5.24 (4.11) 11.6

70.02 (9.38) 38.5 52.3 58.29 (11.79) 39.9 21.2 47.4 27.82 (5.00) 7.08 (4.77) 17.0

\.001 \.001 \.001 .003 .355 .595 \.001 .989 \.001a .045

LVEF left ventricular ejection fraction, MI myocardial infarction, BMI body mass index t test was performed on square root transformed data; to facilitate interpretation cells display untransfomed data

In both, female and male patients, depression improved over the rst year following surgery (F(1, 969) = 7.54, P = .006). At both measurement points, women displayed higher depression levels than men (F(1, 969) = 25.8, P \ .001). There were no signicant interaction effects. Causal attributions in male and female patients The most common attributions for both men and women were stress/mental load (47.8%) followed by genes (42.5%) (Fig. 1). Men were more likely to name their health behavior (men: 40.2%, women: 26.9%, P \ .001) as a cause of disease, whereas women were more likely to

endorse destiny (women: 34.7%, men: 25.7%, P = .012). In addition to the pre-dened attributions, 12.4% of patients specied other causes accounting for their disease. The most frequent other causes were diabetes (16 patients) and old age (21 patients). Furthermore, patients indicated attributions classiable to stress/mental load such as death of a loved one (n = 3), stress at work (n = 6) and physically strenuous work for many years (n = 11). Intercorrelations between causal attributions ranged from r = .009 to r = .199 (Table 2), and can thus be classied as small (Cohen 1992). Pearsons correlations were inspected to explore associations between causal attributions and sociodemographic as well as clinical

Fig. 1 Causal attributions in female and male patients. ***P \ .001, *P \ .05



Percentage of patients

*** *
males females





0 Stress/ mental load

Genes Health behaviour Destiny Environment Personality Others

Causal attribution


J Behav Med (2011) 34:351359 Table 2 Intercorrelations between causal attributions Stress/mental load Stress/mental load Genes Health behavior Personality Destiny Environment Genes .063* Health behavior .134** -.016 Personality .199** .132** .089** Destiny .009 .059 -.076* .111**


Environment .175** .045 .020 .067* .127**

Bold values indicate signicant gender differences in strength of association: r (environment, genes)men = .014, r (environment, genes)women = .170, P = .05 ** P \ .01, * P \ .05 Table 3 Pearsons correlations between causal attributions and sociodemographic/clinical variables at baseline Age Stress/mental load Genes Health behavior Personality Destiny Environment 2.201** -.16** -.345** -.056 .043 -.050 Education [ 9 years .004 .086** .073* .042 -.091** -.038 Low support .147** -.017 .052** -.016 .012 .023 LVEF -.041 .037 -.079* -.049 -.017 .033 History of MI .101** -.004 .041 -.01 -.002 .004 MI in family -.006 .219** .050 .036 -.024 -.037 BMI .058 -.029 .123** -.005 -.024 .033 Smoking .039 -.058 .313** -.006 2.016 .042

Bold values indicate signicant gender differences in strength of association: r (stress, age)men = -.18, r (stress, age)women = -.335, P = .04; r (stress, BMI)men = .003, r (stress, BMI)women = .256, P = .003; r (destiny, smoking)men = .058, r (destiny, smoking)women = -.117, P = .03 LVEF left ventricular ejection fraction, MI myocardial infarction, BMI body mass index ** P \ .01, * P \ .05

variables (Table 3). Attribution to stress and mental load were related to younger age, low social support, and previous MI. Attribution to genes was associated with younger age, higher education and family history of MI before 60 years. Attribution to health behavior correlated with higher education, BMI, and smoking as well as with lower social support, age and LVEF. Attribution to destiny was associated with a lower educational status. Associations between attribution to stress and age as well as association between attribution to stress and BMI were signicantly stronger in women compared to men. Moreover smoking correlated only in women negatively with attribution to destiny. Logistic regression analysis was conducted to examine whether the described gender differences in causal attributions might be accounted by sociodemographic or clinical variables. Following adjustment for the sociodemographic and clinical variables displayed in Table 3, including the interaction between gender and smoking, female gender (OR = 1.67, P = .009, 95% CI [1.142.46]) remained an independent predictor for attribution to destiny. With respect to health behavior female gender reached only marginal signicance (OR = 0.676, P = .064, 95% CI [0.4471.023]) after adjustment for clinical and sociodemographic variables.

Relationship between causal attributions and depressive symptomatology Cross-sectional regression analyses showed associations of stress/mental load, personality, and destiny with higher levels of depression after controlling for confounding variables (Table 4). None of the gender X attribution interaction terms reached signicance. A second set of regression analyses was conducted to demonstrate potential effects of causal attributions on the change in depression. Causal attributions to stress and personality were predictive of an increase in depression scores independent of sociodemographic and other relevant confounders (Table 5). Again, the inclusion of interaction terms (gender X attribution) did not improve the regression models.

Discussion Our results indicate interesting gender differences in causal attributions of patients undergoing CABG: Men were more likely to name their health behavior as a cause of their heart disease, whereas women were more likely to cite destiny.


356 Table 4 Hierarchical regression analyses for baseline depressive symptomatology DR2 Control variablesa Causal attributions Stress/mental load Genes Health behavior Personality Destiny Environment R2/R2adjusted

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.107* .055* .181 -.037 .052 .067 .067 .051 .162/.148 \.001 .251 .123 .032 .031 .102

* P \ .001 Control variables include: gender, age, education, LVEF, History of MI, family history of MI \ 60 years, BMI, smoking, low social support

Table 5 Hierarchical regression analyses for change in depressive symptomatology from baseline to 1 year after CABG DR2 Baseline depression Control variablesa Causal attributions Stress/mental load Genes Health behavior Personality Destiny Environment R2/R2adjusted

.277* .019** .013** .066 .013 .008 .071 .046 -.029 .310/.296 .029 .664 .784 .013 .105 .302

* P \ .001, ** P \ .01 Control variables include: gender, age, education, LVEF, History of MI, family history of MI \ 60 years, BMI, smoking, low social support

Moreover, attributions to stress/mental load and personality were associated with depressive symptomatology before CABG-surgery and 1 year after surgery. Gender differences in causal attributions The observed attributional gender difference with men more frequently naming their health behavior as a cause of their disease was previously also found in patients after MI (King 2002; Martin et al. 2005), patients undergoing percutaneous coronary angioplasty (Astin and Jones 2004), patients with acute coronary syndrome (Grace et al. 2005; Perkins-Porras et al. 2008), and other coronary heart disease patients (Aalto et al. 2005). Martin et al. (2005) argue that this attributional difference seems unlikely to reect a healthier lifestyle of the female patient, because male and

female patients were comparable in their baseline health status. However, our baseline assessment revealed that female patients were less likely to be current smokers compared to male patients. Moreover, it is important to note that there were signicant preoperative gender differences with respect to LVEF and sociodemographic variables. As reported in previous studies, sociodemographic variables and risk factors are related to patients causal attributions (Cameron et al. 2005; French et al. 2005a; Perkins-Porras et al. 2008). In line with this nding our results demonstrated a medium-sized concordance between certain risk factors such as smoking or family history of MI and corresponding causal attributions. Moreover, we showed that the associations between baseline variables and causal attributions may differ depending on the patients gender. For example, the negative association between age and attribution to stress appeared more pronounced in women than in men. In both men and women, older age was associated with attribution to health behaviour, proposing an explanation for the above described gender difference. Indeed, once the older age of women and other sociodemographic and clinical variables had been taken into account, differences in attribution to health behaviour reached only borderline signicance. Gump et al. (2001), highlight the role of age with respect to causal attributions. The authors argue that individuals generate their illness perceptions based on the covariation of their own behavior and the onset of illness. Therefore, patients who have smoked for many years and developed coronary heart disease later in life might be less likely to attribute the disease to health behaviour and more likely to attribute it to age. It is also important to keep in mind that coronary heart disease is often considered as a male disease, with women not seeing themselves at particular risk (Robertson 2001). As a consequence coronary heart disease self schemas of women should be less well developed than those of men (Martin et al. 2005) and it might be more difcult for women to integrate coronary heart disease -related information on health behaviors into their self-concept. As a result women might be more likely to refer to chance, bad luck or destiny as causes of their disease, as has been reported in a previous studies (PerkinsPorras et al. 2008). This is supported by the present results. The fact that women in our study were more likely to blame destiny as a cause of their disease might be reective of a female tendency to blame uncontrollable causes (Astin and Jones 2004). Indeed, womens limited perception of control has been discussed as a factor contributing to gender differences in depression (Nolen-Hoeksema et al. 1999). However, in contrast to previous studies (Astin and Jones 2004; Grace et al. 2005) attribution to genes, another uncontrollable attribution, was not cited more frequently in females.


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Association between attributions and depressive symptomatology Consistent with previous research (Vaccarino et al. 2003a), women in our sample displayed substantially higher emotional distress in terms of depression than men. These gender differences were found before surgery as well as 1 year after CABG, evidencing similar trajectories in men and women. Our results demonstrate that attributions relate to depressive symptomatology. In both men and women, attributions to stress, personality, and destiny were crosssectionally associated with higher depression scores. These associations persisted when controlling for potential confounders. Similarly, Grace et al. (2005) described associations between a cardiac patients belief in psychological causes, such as stress or worry, mental attitude, family problems, emotions, and personality and the degree of depressive symptomatology. In order to identify the inuence of causal attributions on depressive symptomatology over time, we investigated longitudinal associations. Two attributional factors predicted depression 1 year post-surgery: patients ascribing their disease to personality and patients ascribing their disease to stress/mental load both experienced deterioration in depressive symptomatology. At rst sight this result seems little surprising. We know that certain personality traits and stressful life events are related to depressive symptoms in various populations. However, the present study focuses on the patients subjective perception of illness causation, whichin contrast to complex aetiological disease modelsreect naive constructions of illness causation. In this, intercorrelations between different causal attributions were generally low, showing that our patients do not agree on a general pattern of illness causation. According to the Common Sense Model of Self Regulation (Leventhal et al. 1984), the causal attributions are part of mental illness representations which form the basis for patient coping responses and will inuence emotional outcome such as depression. In their review, Roesch and Weiner (2001) propose that attributions function as mediating variables in the stressillness relationship. In this model, causal attributions may either increase or decrease the effects of patients stress due to the upcoming CABG-surgery. Two approaches may provide a useful framework to explain the present associations between causal attributions and depressive symptomatology. First, Weiners attributional theory (Weiner 1985) suggests that particular dimensions of causal attributionslocus, stability and controllabilityare associated to emotional and behavioral adjustment. For negative events, internal, stable and uncontrollable attributions, such as the belief that ones personality caused coronary heart

disease, should lead to decrements in self-esteem (consequence of locus dimension), to decreased expectancies of future recovery (consequence of stability dimension) and the belief that nothing can be done (consequence of controllability dimension). Hence personality attributions might result in helplessness and resignation and ultimately lead to more depressive symptomatology. In the same way, patients attribution of coronary heart disease to stress/ mental load might also result in elevated depressive symptoms when patients experience stress as self-made (internal), expect little improvement of stress sources (global) and believe that stress is not subject to volitional control (uncontrollability). However, to support this hypothesis it would be necessary to gather more detailed information on what patients mean when reporting stress as a cause of their disease. In contrast to Weiners broad dimensions of causal attributions, others suggested that specic attributional categories such as self blame might be associated to emotional adjustment (Hall et al. 2003; Tennen and Afeck 1990). In particular, characterological self-blame such as personality attribution, has been viewed as maladaptive in the context of negative events (Hall et al. 2003; Janoff-Bulman 1979), because it refers to enduring aspects of the individual. As a result, characterological self-blame offers limited possibilities for patients to control and change the course of disease and therefore may relate to depressive symptomatology. Although the results do not explain gender differences in depressive symptoms (non- signicant interaction between gender and causal attributions), the present nding suggests that the early identication of maladaptive attributions might be clinically important. Therefore cardiologists should ask patients prior CABG-surgery about their subjective beliefs of illness causation, in order to identify patients at depressive risk and therefore at risk for worse surgery outcome. These patients might benet from extra information and communication strategies that facilitate adaptive causal attributions that empower them and preserve their self esteem. Moreover, recent research suggests benecial effects of specic illness perception interventions (Broadbent et al. 2009). We are aware of several limitations to this study. First, our assessment of depression relied on self-report assessment (PHQ-9). However, the depression module of the PHQ-9 directly assesses diagnostic criteria for major depression according to DSM-IV and has shown excellent we et al. 2004). Second, the single item meavalidity (Lo sure for causal attributions is problematic due to a lack of reliability (Epstein 1983). Nonetheless, a lack of reliability appears less dangerous for hypotheses testing because it underestimates the true association between attributions and depressive symptomatology. Third, the study is monocentric, limiting generalizability of study results.



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Fourth, the drop-out rate of study participants 1 year after surgery was confounded with central study variables such as depression and gender. Post hoc survival analyses revealed that this attrition bias is partly ascribable to higher mortality rates of female and depressive patients. However, causal attributions were both cross-sectionally and longitudinally associated with depressive symptomatology, which strengthens the studys results. The fact that causal attributions do not account for a great deal of variance afrms that cognitive beliefs are not the sole determinants of depressive symptomatology in patients undergoing CABG, but rather present one potential mechanism contributing to emotional distress. Therefore, future research might incorporate the role of disease severity including duration of disease, perioperative complications or major cardiac events that may confound the described relationships. In conclusion, our results suggest gender differences in causal attributions, with men more often reporting health behavior and women more often blaming destiny. These gender differences are partly ascribable to underlying sociodemographic differences, such as womens older age when undergoing CABG. Moreover, causal attributions account for a variation in depressive symptomatology before surgery and 1 year following CABG-surgery. Considering this, the identication of maladaptive causal attributions before surgery appears valuable. Subsequently, targeted communication strategies and interventions to reframe these attributions may improve depressive symptoms in men and women and thereby enhance recovery.

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