The following are key perspectives from the recent European Society of Cardiology (ESC) Position Paper on depression and coronary heart disease (CHD):

1. While some experts in the United States and American Heart Association have suggested that depression is an important factor in cardiovascular disease (CVD), particularly increasing CV events and poor outcome, little attention has been paid by clinicians and recent guidelines. This position paper from the ESC summarizes current knowledge linking depression and CHD within the intersecting fields of neuroscience, cardiovascular physiology, and behavioral medicine.
2. Major depression is prevalent, affecting about 10% of the population and growing. This a risk factor for CHD has been characterized from mild depressive symptoms to a clinical diagnosis of major depression. Major depression is defined by depressed mood or anhedonia (loss of interest or pleasure) for ≥2 weeks accompanied by significant functional impairment and additional somatic or cognitive symptoms. The prevalence of depression is 15–30% in patients with CHD and is approximately twice as high in women than men, and particularly affecting young women who have a high mortality post-myocardial infarction. Higher degrees of depression are associated with higher risk.
3. Most evidence is that the risk associated with depression for CHD, post-CV events, stable CHD, and post–coronary artery bypass grafting is related to noncompliance with prevention efforts including adverse lifestyle such as smoking, low level of physical activity, high fat diet, development of diabetes, hypertension, and decrease in compliance with evidence-based therapies and lower participation in cardiac rehabilitation. Studies suggest that specific subtypes of depression may be more strongly associated with CHD risk than others. Patients with new-onset depression after acute coronary syndrome (ACS), with treatment-resistant depression, or with somatic depressive symptoms as opposed to cognitive symptoms, are all at increased risk of developing adverse CHD outcomes and poorer quality of life (QoL). A reduction in depressive symptoms is the strongest predictor of improved 1-year health-related QoL after accounting for functional limitation and clinical variables including angina and heart failure.
4. Depression and sudden negative emotions have been associated with atrial fibrillation (AF) and recurrence after electrical cardioversion, and AF may worsen symptoms of depression. Depression is associated with increased inflammatory and adrenergic activity and reduced heart rate variability. These factors can shorten atrial refractory periods, trigger AF, and foster a substrate that perpetuates AF, suggesting a mechanism for the observed association of depression. Similarly, persons with depression, as well as those exposed to various forms of chronic and acute psychological distress, have increased risk of developing ventricular arrhythmias and sudden cardiac arrest, in both initially CHD-free populations and in patients with CHD. Whether treating depression would affect arrhythmias is not known.
5. The mechanisms linking depression to CHD are speculated based on neurochemical human and animal responses. Acute and chronic stress exposure can lead to disruptions in the synthesis or activity of norepinephrine, dopamine, serotonin, cortisol, aldosterone, and angiotensin II, each of which may influence mood and risk factors including hypertension, platelet reactivity, endothelial dysfunction, and diabetes and the metabolic syndrome, which can also cause depression. Several of these changes may affect the immune system leading to excessive secretion of cytokines such as interleukin (IL)-1, IL-6, and tumor necrosis factor-a. Inflammation is common in mood disorders and CVD and thus might play a role in plaque development and ACS, as well as AF. Twin studies have shown common genetic pathways involving neuroendocrine, immune, and inflammatory systems that may simultaneously increase the risk for both depression and CHD.
6. Brain areas that likely play a role in CV regulation for stress and memory are altered in major depression, and acute psychological stressors may reduce baroreflex sensitivity. Asymmetric sympathetic inputs from these brain areas to the heart may increase the risk of ventricular arrhythmias. Amygdala activity measured by ¹⁸fluorodeoxyglucose positron emission tomography independently predicted CV events, providing further evidence of brain mechanisms through which emotional or other causes of mental stress can lead to modulation of peripheral vascular and autonomic function, CVD, hypertension, and symptomatic and asymptomatic myocardial ischemia.
7. The guideline describes tools for assessment of depression that in my opinion are too complicated and time consuming for physicians and nonphysician providers to use in the clinical setting. Our system encourages primary care physicians and other providers to use the Patient Health Questionnaire (PHQ)-9 Questionnaire for Depression Scoring and Interpretation Guide that provides a point score with grading of severity and recommendations. Antidepressant medications are a useful tool for the treatment of depression in patients with CHD, especially those with moderate-to-severe depression. Amongst the most efficacious tools for treatment of depression is regular aerobic exercise, which can complement antidepressant medication. Cardiac rehabilitation enhanced with stress management is highly effective at improving mental health, including depression as well as future outcomes.
8. In summary: Clinicians should be aware of the “high” prevalence of depression in CHD. Screening for depression is recommended if patients have access to adequate care support systems. Patients with positive screening results should be referred to a qualified healthcare provider in the management of depression. Nonpharmacologic interventions such as exercise and psychotherapy should be considered as additional treatment options. Multidisciplinary cooperative efforts between healthcare providers is essential in patients with combined CHD and depression.

Keywords: Acute Coronary Syndrome, Anhedonia, Antidepressive Agents, Atrial Fibrillation, Cardiac Rehabilitation, Coronary Artery Bypass, Coronary Disease, Death, Sudden, Cardiac, Depression, Depressive Disorder, Major, Diabetes Mellitus, Diet, High-Fat, Exercise, Hypertension, Inflammation, Sedentary Behavior, Mental Health, Mood Disorders, Myocardial Infarction, Primary Prevention, Psychotherapy, Quality of Life, Risk Factors, Smoking, Stress, Psychological

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