Dr. David B. Adams – Psychological Blog

Psychology of Injury, Pain, Anxiety and Depression

Depression and Heart Disease

The relationship between depression and heart disease (and stroke) is a reciprocal one. Those who are depressed are more likely to have a stroke or myocardial infarction, and in turn, depression is a common outcome to both of these physical events. Anti-depressant medication and psychotherapy can serve as a form of prevention, but choice in the incorrect medication may actually potentiate both heart disease and stroke.

Although routine screening for depression is controversial, the incidence and effects of depression among heart patients and stroke survivors are persuasive arguments for screening among these subgroups.

However, depression appears to be the more enduring predictor of mortality. Only recently has the magnitude of the interaction between heart disease and depression been appreciated. The relationship between depression and heart disease is reciprocal, with each condition contributing excess, potentially avoidable, morbidity and mortality to the other.

The majority of studies in patient populations with cardiovascular disease. showed a significant relationship between depression and mortality, but inferences were confounded by treatment and the effects of associated behaviors. More recent epidemiologic studies demonstrate that even when the effects of smoking are controlled, depression remains a significant independent predictor of mortality among heart patients and stroke survivors.

The acute disability following myocardial infarction is associated with a substantial incidence of major depression. And the loss of social roles and independence due to cardiomyopathy and arrhythmia may also cause depression.

Similarly, apathy, lack of physical activity, inability to stop smoking, alcohol abuse, and hypercortisolemia associated with depression also predispose the individual to heart disease. Depression following heart attack or stroke interferes with physical rehabilitation, return to sexual function, and adherence to the therapeutic regimen (eg, antiarrhythmia medications and anticoagulants).

It is recommended that antidepressants that do not promote arrhythmias, lower blood pressure, or interfere with anticoagulant therapy be used for treatment.

The effects of new antidepressants (“SSRI’s” such as Prozac, Paxil, etc) on cortisol, catecholamines, heart rate variability, platelet aggregation, and arteriosclerosing lipids are only now being appreciated. The choice of antidepressants was formerly determined by avoidance of cardiovascular side effects. In contrast, newer generations of antidepressants may also offer protective effects for both the heart and brain.

For optimum effects, antidepressant medication should be combined with lifestyle counseling and psychotherapy for both the depressed patient and his or her spouse or partner. Both behavioral and mental health interventions will be required to fully reduce the excess morbidity and mortality of heart disease and stroke complicated by depression.

Research indicates that cardiovascular mortality has been linked to a variety of mental disorders and behavioral and psychological attributes, including sedentary lifestyle, hostility, cynicism, personality type (time urgency), smoking, alcohol abuse, and bereavement.

If you would like to know how this occurs:

Several articles describe diverse mechanisms by which depression’s physiologic effects promote stroke and heart attack. Depression increases the cardiotoxic neurohumoral effects of emotional stress. Elevated cortisol described in major depression amplifies the cardiotoxic effects of catecholamines and accelerates arteriosclerosis. Depression and cardiac arrhythmias are linked through the autonomic nervous system seen in the measurement of heart rate variability. Some depressed persons exhibit decreased heart rate variability that has been related to arrhythmia vulnerability.

(In a comparison of indices of platelet activation (platelet factor 4 and beta-thromboglobulin) between depressed and nondepressed elderly subjects, the serotonin transporter protein and the serotonin transporter-linked promoter region are shared by platelets and brain neurons so that both central and peripheral effects would be expected. Platelet activation was significantly elevated among the depressed group both in the presence and absence of ischemic heart disease. These results suggest a common pathway to ischemic events both in the brain and the heart though which depression, via physiologic rather than behavioral effects, increases mortality.)

Several speakers described diverse mechanisms by which depression’s physiologic effects promote stroke and heart attack. Depression increases the cardiotoxic neurohumoral effects of emotional stress.

Elevated cortisol described in major depression amplifies the cardiotoxic effects of catecholamines and accelerates arteriosclerosis. Depression and cardiac arrhythmias are linked through the autonomic nervous system seen in the measurement of heart rate variability. Some depressed persons exhibit decreased heart rate variability that has been related to arrhythmia vulnerability.

A comparison of indices of platelet activation (platelet factor 4 and beta-thromboglobulin) between depressed and nondepressed elderly subjects. The serotonin transporter protein and the serotonin transporter-linked promoter region are shared by platelets and brain neurons so that both central and peripheral effects would be expected. Platelet activation was significantly elevated among the depressed group both in the presence and absence of ischemic heart disease.

These results suggest a common pathway to ischemic events both in the brain and the heart though which depression, via physiologic rather than behavioral effects, increases mortality.

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