Depression and heart disease: What do we know, and where are we headed?
ABSTRACTDepression and heart disease have an intricate association and perhaps a causal relationship. We review the current status of depression and heart disease and provide an algorithm for diagnosing and treating depression in cardiac patients that internists and cardiologists can use in their daily patient encounters.
KEY POINTS
- Depression is a risk factor for new cardiac disease and has a detrimental impact in established cardiac disease.
- Numerous mechanistic pathways have been implicated.
- In clinical trials, drug therapy and psychotherapy have not clearly decreased the rate of cardiac death in depressed cardiac patients, but they did improve depression, adherence to drug therapy, and quality of life.
- Clinicians should routinely screen for depression in cardiac patients and should not hesitate to treat it.
- Eligible patients should routinely be referred to cardiac rehabilitation programs.
IN TRIALS, LESS DEPRESSION BUT NO EFFECT ON DEATHS, RECURRENT MI
Major behavioral and drug trials conducted in the last 15 years have focused on how to best treat depression in cardiac patients.80–85
The Montreal Heart Attack Readjustment Trial (MHART)81 used telephone calls and home nursing visits to explore and monitor psychological distress for up to 1 year after an MI. The overall trial did not show these interventions to have any impact on survival compared with usual care. In fact, in women receiving the telephone intervention, there was a trend toward higher rates of cardiac and all-cause death, which was quite unexpected. Uncovering stresses and problems without resolving them, rather than encouraging patients to place these on the “back burner,” may partially explain these results.
SADHART82 studied the safety of sertraline in depressed post-MI patients. No major differences in cardiac function were noted between the sertraline and placebo groups, showing that sertraline was safe for these patients. The sertraline group had fewer cardiovascular events, but the difference was not statistically significant.
The Enhancing Recovery in Coronary Heart Disease (ENRICHD) study83 was primarily designed to see whether a psychosocial intervention would decrease deaths in depressed cardiac patients. Much to the chagrin of behavioral medicine, the group undergoing cognitive behavioral therapy did not have a higher rate of event-free survival, although the intervention had a favorable impact on depression and social support.
The Myocardial Infarction Depression Intervention Trial (MIND-IT)84 looked at whether the antidepressant mirtazapine (Remeron) would improve long-term depression and cardiovascular outcomes in depressed post-MI patients. In 18 months of follow-up, neither objective was obtained.
The Cardiac Randomized Evaluation of Antidepressant and Psychotherapy Efficacy (CREATE) trial85 tested the efficacy of the SSRI citalopram (Celexa) and interpersonal therapy in a short-term intervention. Here, the antidepressant was superior to placebo in the primary outcome of treating depression, but interpersonal therapy had no advantage over “clinical management,” ie, a shorter, 20-minute supportive intervention.
Common threads in these studies.
- In ENRICHD and MIND-IT, patients whose depression did not respond to treatment were at higher risk of cardiac events during follow-up.86–88
- In SADHART and CREATE, which used drug treatment, the antidepressant response was more robust in patients with a history of depression before their heart attacks, suggesting that a patient with recurrent depression at the time of a cardiac event should receive medication for it.85,89
CLINICAL RECOMMENDATIONS
Use a depression screening tool
Ziegelstein et al90 recently studied the ability of clinical personnel to detect depression in hospitalized MI patients. If a screening tool was not used, the results were abysmal, indicating the need to use formal screening for symptoms of depression in acute MI patients.
Many self-rating scales are available, among which are the Beck Depression Inventory (BDI) and the Hospital Anxiety and Depression Scale (HADS). Others are:
The PHQ-2 consists of the two first questions of the PHQ-9, which deal with mood and lack of pleasure. A cut-off score of 3 or higher has a sensitivity of 83% and a specificity of 92%,96 fulfilling the need for a quick and reliable depression screening tool. The clinician can also ask for a yes-or-no answer to the two questions of the PHQ-2 (Table 1). A yes to either of the two questions is up to 90% sensitive and 75% specific.92,97
When to suspect depression in cardiac patients
Which type of psychotherapy is best?
The negative results of psychosocial interventions (phone calls and home visits from a nurse) in MHART and of cognitive behavioral therapy in ENRICHD raise questions about which type of psychotherapy is best for depression in heart disease. CREATE found that 50-minute weekly sessions of interpersonal psychotherapy were no more beneficial than clinical management, ie, 20-minute weekly sessions that focused on compliance with treatment and education about depression and overall management. Perhaps a type of therapy akin to “clinical management” in this study or the brief behavior-based and targeted therapy used in the Improving Mood Promoting Access to Collaborative Care Treatment (IMPACT) trials of depression in primary care99 could be designed specifically to treat depression in cardiac disease. However, it is also quite possible that treatments that focus on uncovering stresses or problems may not be timely for these patients.
Which therapy is best for women is another area of consideration. In MHART, even after 5 years of follow-up,100 women who received the psychosocial support intervention did marginally worse. In the ENRICHD study, women did not experience a benefit from cognitive behavioral therapy. Further studies must address sex differences in response to different therapies.
