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Psychosomatics 49:230-234, May-June
doi: 10.1176/appi.psy.49.3.230
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Cardiovascular Symptoms in Coronary-Artery Disease Patients Are Strongly Correlated With Emotional Distress

Mark W. Ketterer, Ph.D., W. Knysz, M.D., S.J. Keteyian, Ph.D., J. Schairer, D.O., S. Jafri, M.D., M. Alam, M.D., A.J. Farha, M.D., and S. Deveshwar, M.D.

Received January 14, 2007; revised June 4, 2007; accepted June 4, 2007. From the Department of Behavioral Health and the Heart and Vascular Institute, Henry Ford Hospital and Wayne State University. Send correspondence and reprint requests to Dr. Mark W. Ketterer, Henry Ford Hospital/CFP6, 2799 West Grand Blvd., Detroit MI 48202. e-mail: MarkWKetterer{at}cs.com
© 2008 The Academy of Psychosomatic Medicine


  ABSTRACT

 
TOP
 ABSTRACT
INTRODUCTION
 METHOD
 RESULTS
 CONCLUSIONS
 REFERENCES
 
BACKGROUND: The relationship of cardiovascular events and cardiovascular symptoms is unclear, and physical symptoms, including most cardiovascular symptoms, are known to be influenced by emotional distress. OBJECTIVE: Authors examined the relative strength of association of multiple measures of emotional distress and accepted cardiac risk factors with five common cardiac symptoms (chest pain, fatigue, palpitations, presyncope, and dyspnea). METHOD: The authors tested the association of multiple cardiovascular symptoms with various measures of emotional distress (i.e., the scales of the Symptom Checklist-90–Revised) and the putative risk factors for disease status in 109 patients with documented coronary artery disease. RESULTS: Measures of emotional distress were stronger correlates of patient-rated distress due to the symptoms than were traditional risk factors. CONCLUSION: Treatment of emotional distress may be a viable strategy for symptom-control in cardiovascular disease.

Key Words: Heart Disease • Emotional Distress

  INTRODUCTION

 
TOP
 ABSTRACT
 INTRODUCTION
METHOD
 RESULTS
 CONCLUSIONS
 REFERENCES
 
The relationship of cardiovascular events and cardiovascular symptoms is unclear. For example, at least 25% of myocardial infarctions are clinically "silent" (asymptomatic) or undiagnosed on occurrence.1 In coronary-artery disease (CAD) patients, most episodes of ischemia on Holter-monitor exams are also clinically silent, and most episodes of chest pain are ECG-negative for ischemia.2 The uncertainties of this relationship bedevil clinical care because treatment-seeking by patients and clinical decision-making by physicians are generally guided by patient reports about symptoms.

CAD patients with emotional distress show higher medical-system utilization than those without emotional distress.3–5 One plausible explanation for this relationship may be that emotional distress results in increased symptoms, thus leading to treatment-seeking by patients and more aggressive diagnostic work-ups and treatment by physicians.

Symptoms generally attributed to cardiovascular disease (e.g., chest pain, dyspnea, fatigue, presyncope, and palpitations) are also commonly found in patients with emotional distress.6 Because of the high prevalence of emotional distress in cardiovascular patients,7 it is reasonable to ask whether these symptoms are most likely due to the cardiovascular disease or the emotional distress. For example, anginal chest pain has been found to be reduced by treatment of emotional distress,8,9 and fatigue is a common manifestation of emotional distress in CAD10 and CHF.11

This article examines the relative strength of association of multiple measures of emotional distress and accepted cardiac risk factors with five common cardiac symptoms.


  METHOD

 
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 ABSTRACT
 INTRODUCTION
 METHOD
RESULTS
 CONCLUSIONS
 REFERENCES
 
This study was approved by our Institutional Review Board. Subjects were 109 patients with documented cardiovascular disease (positive catheterization or history of myocardial infarction) who were referred for "stress management." The sample is, thus, skewed toward distressed patients, as shown in Table 1.


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TABLE 1. Sample Means and Standard Deviations (SD) of the SCL-90–R Scores



We would point out that this causes a conservative bias in our analyses. By virtue of the range-restriction in one of our principal variables, emotional distress, the use of this particular sample weakens the likelihood of finding a relationship with the symptom measures. Patients were excluded if they were illiterate (N=0), refused inclusion of their data in a de-identified database (N=1), were on an SSRI antidepressant for longer than 1 week (N=1), or tested as cognitively impaired on the Mini-Mental State Exam (N=4).

The mean age of the sample was 59.4 years (standard deviation [SD]: 11.9 years). Mean years of education was 13.3 years (SD: 2.3 years); 49 patients (45%) were ethnic minority (one Hispanic patient and the remainder African American), and 39 (36%) of the patients were women.

Instruments
Demographic and traditional risk factors were assessed by semi-structured interview; these factors included age at initial diagnosis, pack-years of smoking (number of years smoking x maximum number of packs per day), history of diabetes, Body Mass Index (weight and height), hours of exercise per week, sex, family history of early CHD (onset or death before age 56 in at least one first- or second-degree relative), current smoker status, history of elevated cholesterol (baseline ≥240 mg/dL), history of hypertension (casual values >139/89 mmHg or on medication), history of myocardial infarction, or history of revascularization.

Emotional distress was assessed with the Symptom Checklist-90–Revised (SCL-90–R). The SCL-90–R is a well-known and widely-used omnibus measure of emotional distress.12

Cardiovascular symptoms were derived from the following items of the SCL-90–R: "During the last 7 days, including today, how much were you distressed by: (#4) faintness or dizziness; (#12) pains in the heart or chest; (#14) feeling low in energy or slowed down; (#39) heart pounding or racing; (#48) trouble getting your breath. The response-scale options were 0: "not at all;" 1: "a little bit;" 2: "moderately;" 3: "quite a bit;" and 4: "extremely."

Procedures
All patients underwent these evaluations at an initial meeting for "stress management." At this meeting, verbal assent to de-identified use of the patient’s data for research purposes was obtained according to IRB-approved protocol.

Statistical Analyses
Cardiovascular symptoms were tested for their association with cardiovascular risk factors and the SCL-90–R Scales by use of univariate statistics (t-tests and Pearson product-moment correlation [r] coefficients), exempting scales from which the items were drawn. Those risk factors and scales achieving statistical significance (p≤0.05) in the univariate tests were then entered in a series of multiple regression equations predicting each symptom.


  RESULTS

 
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 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
CONCLUSIONS
 REFERENCES
 
Emotional Distress
With only a few exceptions, all the SCL-90–R Scales were strongly associated with the cardiovascular symptoms (see Table 2).


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TABLE 2. Emotional Distress and Cardiovascular Symptoms (Pearson Product-Moment Correlation Coefficients [r])



Traditional Risk Factors
Female sex and history of hypertension were associated with higher levels of distress for each of the cardiovascular symptoms. Chest pain was positively associated with early-onset cardiovascular disease (p<0.05), and a history of diabetes was associated with more distress about fatigue (p<0.01). Dyspnea was associated with more pack-years of smoking (p<0.01), obesity (p<0.01), and a history of diabetes (p<0.01). Education was associated with less distress over palpitations (p<0.01; see Table 3).


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TABLE 3. Cardiovascular Risk Factors and Cardiovascular Symptoms (Pearson Product-Moment Correlation Coefficients [r])



For Stepwise Multiple Regressions
Anxiety was the strongest unique correlate of chest pain (p<0.001) and dyspnea (p<0.001), accounting for about 10% of the variance in each; somatization was the strongest unique correlate of palpitations (p<0.001) and fatigue (p<0.001), accounting for about one-third of the variance in each; and obsessive-compulsiveness was the strongest unique correlate of presyncope (p<0.001), accounting for about 10% of this symptom’s variance (see Table 4).


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TABLE 4. Stepwise Regression Models Predicting Cardiovascular Symptoms




  CONCLUSIONS

 
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 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 CONCLUSIONS
REFERENCES
 
Measures of emotional distress are stronger unique correlates of cardiovascular symptoms than the traditional risk factors, and, therefore, they must be considered possible causes of these symptoms. Although the existence of this relationship is well established, particularly for chest discomfort,9 the nature of this relationship remains ambiguous. Basically, four possible types of relationship might account for these findings: First, cardiovascular symptoms in CAD patients may sometimes represent "somatized" emotional distress. Because of the stigma (and thus, denial) associated with emotional distress,13–15 patients may present only the physical symptoms of depression (i.e., fatigue) or anxiety (i.e., chest pain, dyspnea, presyncope, or palpitations) to their physicians. In the absence of a careful biopsychosocial examination, apparently common in cardiac care,16,17 the possibility of emotional distress as a causal/aggravating factor will be missed. A second possibility is that the acute, recurring arousal seen in anxious/angry patients, or the associated noncompliance with treatment, may sometimes precipitate cardiovascular events such as ischemia, thrombogenesis, or myocardial stunning,9,18–20 which, in turn, account for the increased symptoms. A third possibility is that patients experiencing emotional distress are, by virtue of reduced beta-endorphin production,21,22 hypersensitive to cardiovascular events. A final possibility is that increased symptoms may cause increased emotional distress. The nature of this relationship can be clarified by one, and only one, kind of study: a random-assignment, controlled clinical trial targeting emotional distress and measuring both emotional distress and symptom intensity as outcomes.23 By randomly assigning patients, manipulating (i.e., treating) one group, and observing consequent outcomes, the rigor of a true experiment can be met. The causal argument can be further enhanced by using change-in-emotional distress as a covariate, after first achieving improvement in the symptom. If the effect ceases to be significant after introducing change-in-emotional distress as a covariate, it clearly implies that the improvement in symptom-intensity is accounted for by improvement in the emotional-distress measure. Our results suggest several likely emotional-distress measures that might succeed as such mechanistic covariates.

The notion that emotional distress worsens symptom intensity is not new,24 but, surprisingly, it has been neglected in routine clinical care, perhaps leading clinicians to "bark up the wrong tree" in many cases of symptomatic CHD. We believe that routine clinical care must now include brief, psychometric screening of CHD patients in cardiac settings to identify those most likely to benefit from evaluation/treatment of emotional distress.

Such screening may be accomplished by several brief bedside/clinic measures of emotional distress,25–28 but we believe the best is the Patient’s Health Questionnaire, or PHQ–9.29 The PHQ–9 appears to be the most sensitive and efficient first step in screening for emotional distress.30 The next step requires circumvention of patient denial so as to capture patients who minimize their distress self-ratings.13–15

We believe that the present results take on greater meaning in light of the results from the COURAGE trial,31 which compared routine medical care with such care plus PTCA/stenting in 2,287 patients with stable angina. The findings from COURAGE confirm the absence of a mortality/MI benefit, and only modest effects on the percentage of patients who were pain-free at 1 year (66% versus 58%; p<0.001), 3 years (72% versus 67%; p=0.02), and total absence of difference at 5 years (74% versus 72%; NS.)

Thus, a procedure costing $40,000 per patient helps only 1 patient in 12 achieve freedom from pain at 1 year, and 1 person in 20 at 3 years. The possibility that treating emotional distress, which costs perhaps one-tenth of PTCA/stenting over the patient’s lifetime and is entirely noninvasive, may achieve the same goal for many patients seems like a major potential boon to patient care. Treatment of emotional distress should be tested as a strategy for diminishing cardiovascular symptoms. Several studies already indicate that there is a decrease in chest pain with treatment of emotional distress.9

Present results must be interpreted in light of study limitations. The present results are taken from a group of patients referred for "stress management," and, thus, they represent a sample skewed by clinical referral processes. Patients who died before diagnosis of their CAD, who refused referral, who were entirely asymptomatic and therefore undiagnosed for CAD, or whose behavior in the clinic may not have suggested the presence of distress to the cardiologists are not included here. We suspect that clinical selection processes may have caused a conservative bias in our results because of the restricted range of one of our emotional-distress measures, but only the study of an unselected sample can confirm this possibility.


  ACKNOWLEDGMENTS

 
This work was presented at the Annual Meeting of the American Psychosomatic Society, Vancouver, BC, March 2005.


  REFERENCES

 
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 CONCLUSIONS
 REFERENCES
 

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