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Psychosomatics 46:355-361, August 2005
© 2005 The Academy of Psychosomatic Medicine

Depression Following Acute Myocardial Infarction: A Prospective Relationship With Ongoing Health and Function

James A. Fauerbach, Ph.D., David E. Bush, M.D., Brett D. Thombs, Ph.D., Una D. McCann, M.D., Joshua Fogel, Ph.D., and Roy C. Ziegelstein, M.D.

Received Oct. 23, 2003; revision received Nov. 13, 2004; accepted Dec. 16, 2004. From the Department of Psychiatry & Behavioral Sciences, Department of Physical Medicine & Rehabilitation, and Department of Medicine, Division of Cardiology, The Johns Hopkins University School of Medicine; and the Department of Economics, Brooklyn College of the City University of New York, Brooklyn, N.Y. Address correspondence and reprint requests to Dr. Fauerbach, c/o Baltimore Regional Burn Center, Johns Hopkins Bayview Medical Center, 4940 Eastern Ave. Baltimore, MD 21224; JFAUERBA{at}JHMI.edu (e-mail).


  ABSTRACT

 
 TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 REFERENCES
 
The relationship between baseline depression and health-related quality of life were examined in a cohort of patients after hospitalization due to acute myocardial infarction (N=196). Patients were assessed for presence of mood disturbance, anxiety, and quality of life at the time of hospitalization and again 4 months later. Baseline assessment was used to assign subjects to a depressed or a nondepressed group. Adjusting for preinfarction quality of life, in-hospital anxiety, and demographic variables, depression was prospectively and independently related to reduced global health at 4 months as well as reduced overall mental health—including vitality, psychological health, and social function—and increased role interference from psychological problems.

Key Words: myocardial infarction • depression • quality-of-life • comorbidity


  INTRODUCTION

 
 TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 REFERENCES
 
Depressive symptoms during hospitalization for acute myocardial infarction occur in as many as 45% of patients1 and significantly increase the short-term risk for morbidity and mortality, even after established risk factors, including left ventricular ejection fraction, Killip class, age, and history of prior infarction,2,3 are controlled. Depression following myocardial infarction also predicts long-term mortality.4 Behavioral (especially nonadherence to risk-reduction recommendations), neuroendocrine, and thrombotic mechanisms have been proposed as pathways through which depression affects health after myocardial infarction.57 Depression has been associated with poor treatment adherence in patients with8,9 and without10,11 cardiac disease.

Similarly, perceived quality of life has been related to mortality and has been found to be a better predictor of mortality than objective health indices (e.g., left ventricular ejection fraction and exercise treadmill testing) among elderly patients with chronic diseases.12 Quality-of-life variables have also been found to be predictive of poor treatment adherence among myocardial infarction patients, even after adjustment for depression.13

Thus, both depression and quality of life have been found to relate to health outcomes in myocardial infarction patients. In addition, there appears to be a meaningful relationship between depression and quality of life. Depression has been found to relate to reduced quality of life to a degree equal to or greater than that of other chronic health problems (e.g., advanced coronary artery disease, angina)14 and traditional measures of cardiac function (e.g., ejection fraction, ischemia).15 A 6-year, population-based, longitudinal study of community-dwelling elderly adults found baseline symptoms of depression to increase the likelihood of becoming disabled, decrease the likelihood of recovering from a disabling condition among those who developed impairment, and decrease quality of life.16

Among postmyocardial infarction patients, cross-sectional results after 5 months show depression associated with both physical and mental health domain scores of the SF-36, a quality-of-life measure.17 Depression and anxiety were both associated with quality of life 4 months after myocardial infarction,18 and emotional distress predicted poor SF-36 scores on all eight subscales 3 and 12 months after myocardial infarction, while subthreshold distress did not.19 At both 4 months20 and 12 months21 after myocardial infarction, baseline depression was the best predictor of quality of life. In addition to postmyocardial infarction patients, poor quality of life has been found to predict a poorer long-term outcome among those with chronic cardiac disease.22,23

These studies relating depression to subsequent quality of life have important limitations. First, design and sampling issues, as well as patient and treatment characteristics particular to these studies, suggest the need for replication. Second, insufficient attention has been paid to identifying specific functional domains that are negatively impacted by the presence of depression. Third, while poor quality of life predicts a poorer long-term outcome, to our knowledge, no studies have addressed the possibility that poor quality of life prior to the myocardial infarction may account for this relationship. The present study addresses these gaps in the scientific literature. Specifically, the objectives of the study include 1) replicating the relationship between depression following myocardial infarction and quality of life, both at baseline and after 4 months and 2) examining the relationship between depression at the time of the myocardial infarction and longitudinal quality of life, with quality of life and anxiety before myocardial infarction controlled.


  METHOD

 
 TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 REFERENCES
 
Participants
We conducted this study at a large metropolitan teaching hospital from which we received institutional review board approval. Over an 18-month period, 696 patients were admitted to the hospital as a result of acute myocardial infarction, defined by the presence of at least two of the following: typical ischemic chest pain lasting ≥20 minutes, presence of ECG changes typical of ischemia/infarction, peak creatine phosphokinase [CPK] >1.5 times normal, or a CPK-myocardial band index >10 ng/ml with a simultaneous CPK exceeding the normal limits.

Of these 696 eligible patients admitted to the hospital because of acute myocardial infarction, 285 patients were interviewed. All patients were approached for consent except those excluded because of 1) comorbid noncardiac illness likely to lead to death within 6 months, 2) medical conditions precluding reliable verbal communication, 3) nonadmission to the cardiology service, 4) in-hospital death, 5) transfer to other facilities within the first 48 hours of hospitalization (patients requiring early angioplasty or cardiac surgery were immediately transferred to a different site because these services were not available at this hospital site) or 6) symptoms of dementia or delirium determined during clinical examination.

Analyses of available records of those excluded at baseline showed that they did not differ significantly from those who provided informed consent in terms of age, gender, diabetes status, prior myocardial infarction, living alone, cigarette use, Killip class, or peak CPK value. Reasons for loss to follow-up (N=89) included death (N=18), refusal to be reinterviewed (N=11), unreachable (N=43), and partial completion of interview (N=17). Participants at the follow-up evaluation tended to be more likely to have a left ventricular ejection fraction of 35 or above and less likely to be categorized in Killip classes II–IV than those lost to follow-up. Otherwise, participants at the follow-up evaluation did not differ on any demographic or health-related variable from those not reinterviewed 4 months after myocardial infarction.

Procedure and Materials
Participants provided informed consent and during the first 2–5 days following admission were assessed with the mood disorders module of the Structured Clinical Interview for DSM-III-R (SCID)24 to evaluate the presence of mood disorder before hospital admission, and both the Beck Depression Inventory25 and Beck Anxiety Inventory26 to measure postmyocardial infarction symptoms of depression and anxiety, respectively, present since admission. Quality of life was measured with the SF-36 Health Survey27 at baseline by asking participants to rate their quality of life before hospitalization. Quality of life was subsequently reassessed at the 4-month follow-up evaluation.

Demographic, medical, and treatment data were gathered by reviewing hospital charts after discharge. Myocardial infarction severity, comorbid conditions, and cardiac risk factor status were evaluated using standard criteria by one of two cardiologists (D.E.B., R.C.Z.) blind to the psychiatric and psychosocial status of the subjects at the time of the chart review. Cardiac risk factors examined included hypertension (defined as systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg, history of hypertension, or receiving antihypertensive medications), hyperlipidemia (total cholesterol ≥240 mg/dl, history of increased cholesterol, or receiving lipid-lowering medication at the time of admission), previous myocardial infarction (determined by a review of patient history or from electrocardiographic evidence), left ventricular ejection fraction (<35% versus ≥35%), and tobacco use (self-reported current status). Demographic variables were collected and then dichotomized as follows: age (≥65 versus <65 years), race (white versus non-white), living alone versus living with someone, and gender. Comorbid conditions examined included renal insufficiency or failure, chronic obstructive pulmonary disease (COPD), and diabetes mellitus. At the 4-month follow-up evaluation, 196 individuals were interviewed.

Statistical Analyses
The depressed group comprised individuals with SCID-diagnosed mood disorder or Beck Depression Inventory scores ≥10 at baseline on the basis of previous work in this area.2,3 Analyses comparing the depressed and nondepressed groups with regard to anxiety, demographics, coronary disease risk factors, and indices of myocardial infarction severity and cardiac function are presented in Table 1. Significance of differences between the groups on these variables was evaluated with chi-square tests for dichotomized variables (Fisher’s exact test where appropriate) and t tests for continuous variables. The relationship between depression status and quality of life was evaluated with t tests of group differences. Analysis of covariance (ANCOVA) was applied to assess for an association between depression at baseline and quality of life at 4 months after we controlled for quality of life before myocardial infarction.


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TABLE 1. Demographic and Clinical Characteristics of 196 Patients With or Without Depression Following Hospitalization Due to Acute Myocardial Infarction




  RESULTS

 
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 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 REFERENCES
 
Patient Characteristics
The characteristics of participants in the depressed and nondepressed groups who were followed at both baseline and 4 months are described in Table 1. Of the depressed group (N=44), 26 had a DSM-III-R mood disorder at the time of the myocardial infarction, and 33 had a Beck Depression Inventory score of 10 or greater within 5 days of hospitalization. Individuals scoring below 10 on the Beck Depression Inventory and not meeting criteria for a current mood disorder comprised the nondepressed group (N=152). Participants in the depressed group, relative to the nondepressed group, were more likely to be white and female. The depressed group also scored significantly higher than the nondepressed group on measures of baseline anxiety (mean= 36.5 [SD=11.5] versus 30.2 [SD=10.1], respectively; t = –4.45, df=194, p<0.01). There were no significant differences on any other demographic variables, coronary disease risk factors, or indices of myocardial infarction severity or cardiac function. Gender, race, and anxiety at baseline were used as control variables in the subsequent evaluation of the relationship between depression at baseline and quality of life at 4 months.

Relationship Between Depression and Quality of Life at the Time of Hospitalization and After 4 Months
The aggregate SF-36 mental and physical domain scores for the depressed and nondepressed groups differed significantly at both baseline and 4 months. At baseline, the mean SF-36 mental domain score for the depressed group was 42.7 (SD=11.0), which was significantly lower than that of the nondepressed group (mean=51.8, SD=6.2) (t=7.0, df=194, p<0.01). The baseline score for the SF-36 physical domain was also lower for the depressed group (mean=37.4, SD=10.4) relative to the nondepressed group (mean=40.9, SD=9.6) (t=2.1, df=194, p=0.04). At the 4-month follow-up evaluation, the depressed group again had lower scores than the nondepressed group in both mental domain functioning and physical domain functioning (Table 2). There was no significant change in physical domain scores across time for depressed patients (baseline: mean=37.4 [SD=10.4]; 4 months: mean=36.9 [SD=12.8]) and nondepressed patients (baseline: mean=40.9 [SD=9.6]; 4 months: mean=42.1 [SD=12.0]), although physical functioning tended to decline slightly for the depressed group and improve slightly for the nondepressed group. Mental domain scores improved significantly for both the depressed patients (baseline: mean=42.7, SD=11.0; 4 months: mean=49.8, SD=13.5 [t=3.1, df=43, p<0.01]) and nondepressed patients (baseline: mean=51.8, SD=6.2; 4 months: mean=58.7, SD=7.4 [t=10.4, df=151, p< 0.01]).


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TABLE 2. Quality of Life After 4 Months in 196 Patients With and Without Depression Following Hospitalization for Acute Myocardial Infarction



Quality of Life 4 Months After Discharge in the Depressed and Nondepressed Groups, With Premyocardial Infarction Quality of Life Controlled
ANCOVA was used to test the hypothesis that 4-month postmyocardial infarction aggregate SF-36 mental and physical domain scores and the eight component subscales would differ between depressed and nondepressed groups at the 4-month follow-up evaluation after the influence of baseline (premyocardial infarction) SF-36 subscale scores, anxiety, gender and race (i.e., the univariate correlates of baseline depression status) was controlled. Table 2 presents both unadjusted and adjusted SF-36 subscale means and 95% confidence intervals for the depressed and nondepressed groups at the follow-up evaluation. After removing the effect of the covariates, there remained a significant multivariate effect of depression on postmyocardial infarction quality of life in the aggregate mental domain (F=8.06, df=5, 195, p<0.01). There was not a significant adjusted effect of depression on aggregate physical domain score (F=0.11, df=5, 195, p=0.57). Comparisons of adjusted means of the eight SF-36 subscales at 4 months indicated that patients who were depressed at the time of baseline assessment scored significantly lower than those in the nondepressed group at 4 months on measures of global health (F=7.45, df=5, 195, p<0.01), mental health (F=6.53, df=5, 195, p=0.01), role interference by emotional problems (F=7.27, df=5, 195, p<0.01), vitality (F=9.83, df=5, 195, p<0.01), and social functioning (F=7.99, df=5, 195, p<0.01). Significant differences between groups on adjusted means were evaluated using Hochberg’s Sequential Method28 for multiple mean comparisons to maintain the family-wise error rate at p≤0.05. Partial eta squared values are also provided in Table 2. Following Cohen’s guidelines,29 the estimates of effect sizes for the mental domain and significant subscale domain effects were in the small to medium range.


  DISCUSSION

 
 TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 REFERENCES
 
Patients depressed at the time of hospitalization following acute myocardial infarction reported significantly poorer aggregated physical and psychological health at baseline and at a 4-month follow-up evaluation. Even after we controlled for baseline quality of life, anxiety, and demographic variables, depression at baseline was significantly associated with reduced global health, psychological health, vitality, social function, and psychological problems interfering with function 4 months later. Aggregated mental domain scores of both groups improved significantly over the follow-up period. While significant changes in the aggregated physical domain scores were not evident, physical function tended to decline slightly for the depressed group and improve slightly for the nondepressed group.

These results replicate and extend previous work in several areas. For example, whereas previous studies have focused on global measures, using the SF-36 Health Survey in the current study permitted the identification of specific areas of function affected by postmyocardial infarction depression. Also, previous work has shown that patients with depression who underwent elective cardiac catheterization experienced poorer 12-month physical functioning outcomes relative to those who were not depressed, and that both anxiety and baseline health status predicted 6-month physical and social quality of life.22,23 The current investigation detected the same pattern of poorer perceived global health and psychological and social outcomes at an earlier time point, with potentially confounding baseline anxiety and preinfarction quality of life controlled. This suggests that the biopsychosocial link between depression and poor outcome from myocardial infarction is influential within a few months after myocardial infarction, and that specific aspects of depression determine this relation, as opposed to a causal role being attributed to general negative affectivity per se.30

Several limitations of the present study should be addressed. This prospective cohort study can only establish correlations and not definitive causal relationships. However, the major known physical (e.g., left ventricular ejection fraction, age, diabetes mellitus, prior history of myocardial infarction) and psychosocial (e.g., living alone) determinants of postmyocardial infarction outcome were examined directly or statistically controlled where indicated, and therefore were unlikely to confound the observed relationships between depression and various postmyocardial outcome measures. It is also possible that results were affected by differential recruitment, since the consenting subjects had a higher rate of prior myocardial infarction than the total population of myocardial infarction admissions in the hospital, and it is possible that similar findings would not have been seen in patients following their first myocardial infarction. Study attrition might have influenced findings, since participants at the follow-up evaluation tended to be more likely to have a left ventricular ejection fraction of 35 or above and less likely to be categorized in Killip classes II–IV.

In conclusion, the present results underscore the important relationship between depression and perceived poor quality of life, and the negative impact of both of these factors in long-term health following myocardial infarction. These results, when considered with previous findings, underscore the importance of early identification and treatment of depression among patients following acute myocardial infarction to minimize long-term morbidity and disability.


  REFERENCES

 
 TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 REFERENCES
 

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