Volume 3 Issue 1 January, 2013
Consultation Liaison Psychiatry Focus Cardiology
Depressive symptoms are common among post myocardial infarction (MI) patients and may cause negative impacts on cardiac prognosis. Depression is observed in 35-45% of MI patients. While depression is an independent risk factor for MI, post-MI depression has been shown to be a risk factor for mortality, morbidity, and decreased quality of life in patients.
The link between depression and MI is bidirectional in which behavioral and biological mechanisms have been proposed to be involved. Individuals with a history of recurrent depression, who are otherwise healthy, show increased inflammation, platelet activation, endothelial dysfunction, and reduced heart rate variability and baroreceptor sensitivity. The combination of these mechanisms is likely to involve in increasing the risk of mortality. However, the MIND-IT trial, which studied depression in MI patients, revealed that the rate of depression and the severity of depressive symptoms are significantly related to the severity of LV dysfunction. Hence, it may be relevant to acknowledge the association between depression and LV dysfunction when evaluating the prognostic effects of depression in cardiac patients.
Epidemiological studies, on the other hand, have shown the link between depression and increased risk for development of cardiovascular disease, MI, and cardiac mortality. The adverse impact of depression on prognosis of heart disease is preventable with the right treatment. A number of therapeutic approaches including cardiac rehabilitation, social support, cognitive behavioral therapy, and antidepressants have been suggested for post-MI depression. However, due to their adverse effects, tricyclic antidepressants are not recommended for treating post-MI depression. On the other hand, administering selective serotonin reuptake inhibitors (SSRIs) shortly after MI would lessen their major side effects. The SADHART and CREATE trials provide convincing evidence of the cardiac safety and antidepressant efficacy of two SSRIs (sertraline and citalopram) in depressed cardiac patients. However, with the exception of platelet function, which improves with selective serotonin reuptake inhibitors, the other abnormalities are not corrected by antidepressant treatment. Furthermore, endothelial function and baroreceptor sensitivity, which can lead respectively to progression of the atherosclerotic process and to sudden cardiac death, do not improve when depressive symptoms are in remission.
In many studies, drug therapy and psychotherapy did improve depression, adherence to drug therapy, and quality of life. Given current observations and recent data from interventional trials coupled with the safe drug-interaction profile of sertraline and citalopram, these two SSRIs are recommended for treating depression in cardiac patients. If the patient is also receiving an anticoagulant, one should monitor for bleeding, as all SSRIs are associated with risk of prolonged bleeding time. Monitoring for rare cases of hyponatremia and bradycardia should also be part of early follow-up.
Liaison with psychiatrist may be beneficial whenever physicians come across patients with depression.
Manipal Hospital, Bangalore
