
Depression and the Risk for Cardiovascular Events
Depression is a risk factor for the development of coronary heart disease in healthy patients, as well as a predictor of adverse cardiovascular outcomes in patients with diagnosed heart disease. One-fifth of patients with coronary heart disease and one-third of patients with congestive heart failure show signs of depression. Many of these cases of depression are undiagnosed or untreated, but identifying and treating depression in patients at risk for cardiovascular disease can improve quality of life and improve cardiovascular outcomes.
A new study published in JAMA reports that treating depression through behavior modification — particularly physical activity — may reduce the incidence of cardiovascular events. The prospective Heart and Soul Study was conducted in San Francisco from 2000 to 2008, and followed more than 1000 outpatients with diagnosed coronary heart disease. Depressive symptoms were assessed using the Patient Health Questionnaire, and 199 patients were determined to show depressive symptoms at baseline.
During the nearly 5 years of follow-up, 341 cardiovascular events occurred across both depressed and non-depressed patients, including heart attack, stroke, transient ischemic attack, hospitalization for heart failure, and death. Depression was associated with a 50% higher risk of cardiovascular events. The annual rate of these events was 10% in the group with depressive symptoms, versus 6.7% in the non-depressed group. After adjusting for severity of cardiovascular disease as well as comorbid conditions, depressive symptoms were associated with a 31% higher rate of cardiovascular events. Physical inactivity was associated with a 44% increased risk of cardiovascular events in people with depressive symptoms, though this association was not significant. The researchers postulate that patients with depressed symptoms are less likely to be compliant with medication regimens, or adhere to diet and exercise guidelines, explaining some of the increased risk.
While the association between physical activity and decreased cardiovascular risk was not statistically significant in this study, researchers theorize that cardiovascular risk could be attenuated by behavioral modification, including exercise. A combination of antidepressant medication and regular exercise may reduce the risk of cardiovascular events in patients with depression. Currently, a follow-up clinical trial is underway to evaluate the effects of antidepressants versus exercise on depression and cardiovascular risk factors.
While this latest study did not reveal significant findings in the relationship between exercise, depression, and cardiovascular disease, many studies show that cardiovascular risk is higher in depressed patients, as well as those with other mental health disorders. However, the appropriate identification and treatment of depression is challenging for health care providers due to the range of presentations and causes of stress. Mental health needs to be treated the same as traditional cardiovascular risk factors like smoking, obesity, and high blood pressure. Treatment through medication, psychotherapy, or behavior modification may have significant benefit in reducing the morbidity and mortality of cardiovascular disease.
References
Arslan A, Uzun M. Does the lower nitric oxide level cause cardiovascular changes in major depressed women? Eur Rev Med Pharmacol Sci. Sep-Oct 2008;12(5):309-313.
J DENOLLET, K MAAS, A KNOTTNERUS, J KEYZER, V POP (2008). Anxiety predicted premature all-cause and cardiovascular death in a 10-year follow-up of middle-aged women Journal of Clinical Epidemiology DOI: 10.1016/j.jclinepi.2008.08.006
H Lester, A Howe (2008). Depression in primary care: three key challenges Postgraduate Medical Journal, 84 (996), 545-548 DOI: 10.1136/pgmj.2008.068387
Sowden GL, Huffman JC. The impact of mental illness on cardiac outcomes: A review for the cardiologist. Int J Cardiol. Nov 10 2008.
M. A. Whooley (2006). Depression and Cardiovascular Disease: Healing the Broken-Hearted JAMA: The Journal of the American Medical Association, 295 (24), 2874-2881 DOI: 10.1001/jama.295.24.2874
M. A. Whooley, P. de Jonge, E. Vittinghoff, C. Otte, R. Moos, R. M. Carney, S. Ali, S. Dowray, B. Na, M. D. Feldman, N. B. Schiller, W. S. Browner (2008). Depressive Symptoms, Health Behaviors, and Risk of Cardiovascular Events in Patients With Coronary Heart Disease JAMA: The Journal of the American Medical Association, 300 (20), 2379-2388 DOI: 10.1001/jama.2008.711
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One of the major challenges when exploring the effects of any cardiac risk factor is the actual relationship between the risk factor and the illness which is the case for depression and CAD.
It is well known now that CAD and depression often co-occur; however, it is not clear whether depression precedes CAD, CAD precedes depression, or if both occur simultaneously.
There have been a number of studies evaluating the physiological effects depression has and thereby affects cardiovascular health. One speculation is that depression adversely affects autonomic nervous system functioning and heart rate variability which in turn affects cardiac health (Carney et al., 2005; Carney & Freeland, 2009; Krittayaphong et al., 1997). Medically healthy but depressed patients often have significantly elevated resting catecholamine concentrations and altered hypothalamic-pituitary adrenal axis and autonomic nervous system functioning (Carney & Freeland, 2009; Wyatt et al., 1971).
Low heart rate variability (HRV) is a sign of increased sympathetic nervous system modulation, meaning increased heart rate and stress response. According to a study by Krittayaphong et al. (1997), patients with high depression scores exhibited much lower heart rate variability.
Depression impacts heart rate variability and results in a decrease in the parasympathetic but increased sympathetic nervous system activity. This has an effect on vascular walls and presents a cardiac risk factor. Also, ventricular premature contractions (VPCs) are found to be a predictor of CAD events. Those physiological changes may result in myocardial ischemia, ventricular fibrillation, ventricular tachycardia and sudden cardiac death (Carney & Freeland, 2009).