Original articles
Severe depression is associated with markedly reduced heart rate variability in patients with stable coronary heart disease

https://doi.org/10.1016/S0022-3999(99)00085-9Get rights and content

Abstract

Objective: The purpose of this study was to investigate the relationship between depression and heart rate variability in cardiac patients. Methods: Heart rate variability was measured during 24-hour ambulatory electrocardiographic (ECG) monitoring in 40 medically stable out-patients with documented coronary heart disease meeting current diagnostic criteria for major depression, and 32 nondepressed, but otherwise comparable, patients. Patients discontinued β-blockers and antidepressant medications at the time of study. Depressed patients were classified as mildly (n = 21) or moderately-to-severely depressed (n = 19) on the basis of Beck Depression Inventory scores. Results: There were no significant differences among the groups in age, gender, blood pressure, history of myocardial infarction, diabetes, or smoking. Heart rates were higher and nearly all indices of heart rate variability were significantly reduced in the moderately-to-severely versus the nondepressed group. Heart rates were also higher and mean values for heart rate variability lower in the mildly depressed group compared with the nondepressed group, but these differences did not attain statistical significance. Conclusion: The association of moderate to severe depression with reduced heart rate variability in patients with stable coronary heart disease may reflect altered cardiac autonomic modulation and may explain their increased risk for mortality.

Introduction

There is considerable evidence that clinical depression is a risk factor for cardiac morbidity and mortality in patients with coronary heart disease; that is, heart disease resulting from coronary atherosclerosis 1, 2, 3, 4, 5, 6, 7, 8. Moreover, relatively severe forms of depression are associated with a greater risk for cardiac events; for example, myocardial infarction, need for balloon angioplasty, coronary artery bypass surgery, or other cardiac-related hospitalizations. Lésperance et al. [9], for instance, found that 40% of acute myocardial infarction patients with both a history of major depression and major depression at the time of their myocardial infarction (MI) died in the year following the myocardial infarction, compared with 10% of patients who were depressed for the first time with relatively mild depression. Similarly, Barefoot et al. [2] found that patients with documented coronary heart disease who had moderate to severe depression had an 84% greater risk for mortality, and those with mild depression had a 57% greater risk, than did nondepressed patients with coronary disease.

These adverse effects of depression in coronary heart disease patients are believed to be due, at least in part, to dysregulation of the autonomic nervous system. Autonomic dysregulation, that is, a predominance of adrenergic activation and/or lack of parasympathetic modulation, has been found in medically well patients with major depressive disorder, as evidenced by elevated plasma and urinary catecholamines and their metabolites 10, 11, 12, 13, 14, 15, altered cardiac autonomic balance as measured by elevated resting heart rate 4, 16, 17, and decreased heart rate variability 18, 19, 20, 21, 22.

Attenuated heart rate variability is a well-known independent risk factor for mortality after myocardial infarction 23, 24. Decreased heart rate variability has been shown to predict subsequent mortality even when it is measured in stable patients 1 year after myocardial infarction [25] and in unselected consecutive patients without any recent cardiac events involving cardiac catheterization [26]. We have previously shown that heart rate variability is significantly lower in depressed patients with newly diagnosed coronary disease than in otherwise comparable nondepressed patients [18]. Although there were no significant differences between the depressed and nondepressed groups with respect to prescribed medications, the fact that some patients were taking cardiac medications, such as β-blockers, may have affected the heart rate variability results in the sample as a whole. Furthermore, the sample was too small to determine whether heart rate variability was lower in more severely depressed patients than in mildly depressed ones. Thus, the purpose of the present study was to determine whether moderately-to-severely depressed, unmedicated patients with stable coronary heart disease have lower heart rate variability than comparable mildly depressed or nondepressed patients.

Section snippets

Subjects

Medically stable patients with angiographically documented coronary disease were eligible to participate if they were ⩽75 years old and had no history or current evidence of congestive heart failure (the inability of the heart to pump sufficient blood to meet the needs of the body), a recent (within 6 months) myocardial infarction (heart attack), severe systemic illness, a noncardiac medical illness that could influence autonomic function, recent coronary artery bypass surgery or angioplasty,

Results

Of the 54 depressed and 40 nondepressed patients recruited for the study, 40 depressed and 30 nondepressed patients had recordings that were adequate for 24-hour heart rate variability analysis. As can be seen in Table 1, the groups were similar with respect to demographic and medical characteristics, except for a significantly greater pack-year smoking history among the severely depressed. The mean Beck Depression Inventory score for the moderately-to-severely depressed subjects was 28.2 ±

Discussion

In a previous study, we found that heart rate variability was lower in depressed than in nondepressed patients with newly diagnosed coronary disease, some of whom were taking cardiac medications such as β-blockers 9, 18. The present study extends this finding by documenting reduced heart rate variability in clinically depressed patients with stable coronary heart disease who had temporarily discontinued all cardiac medications. Although it is possible that there was a rebound effect on heart

Acknowledgements

This study was supported in part by Grant No. 2 R01 HL42427-04 from the National Heart, Blood and Lung Institute, National Institutes of Health, Bethesda, Maryland (Robert M. Carney, PhD, Principal Investigator).

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