Another option would be to treat the patient as if his symptoms represented depression. Exhibiting 4 of the necessary diagnostic criteria, the patient nearly qualifies for a diagnosis of current major depression. An antidepressant could be started, exercise could be prescribed, or a referral could be made for psychotherapy. However, again there is insufficient evidence that his subsyndromal depression will respond to standard treatments designed for major depressive disorder.
The patient returns as scheduled 2 weeks later. He has tolerated the change in blood pressure medications without difficulty, but he is experiencing persistent anhedonia, terminal insomnia, and low levels of concentration, energy, and libido. He has felt increasingly hopeless and worthless over the past 2 weeks, though he denies having thoughts of suicide. Results on CBC, serum chemistries, thyroid panel, and sleep study are all unremarkable.
The patient now clearly meets criteria for a major depressive episode. As a first step, he should be educated about depression. An excellent self-help book is Getting Your Life Back by Wright and Basco.6 The patient should be taught to monitor his symptoms with the BDI3 or the PHQ-94 to better assess the severity of the current episode, to monitor changes in his symptoms, and to rapidly identify relapses.
Most physicians would start an antidepressant, unless the patient had significant objections. Other treatment options, alone or in concert with antidepressant treatment, include exercise or psychotherapy. The patient is an excellent candidate for exercise, given that he has 3 risk factors for CAD: hypertension, a sedentary lifestyle, and obesity (4, if you include depression). Exercising for at least 30 minutes, 2 to 3 times per week, would likely benefit his physical and mental health. In addition to its cardiac benefits, exercise 3 times weekly was found in at least one trial to be as effective as sertraline in treating major depression in outpatients.7
Choosing an antidepressant. A number of factors should be considered in choosing antidepressants, including efficacy, side effect profile, and cost. Table 3 outlines some of the main considerations in the choice of antidepressants for this patient. Note that tricyclic antidepressants are not listed, being contraindicated in CAD because of their tendency to contribute to arrhythmias in the post-MI period. In this patient’s case, mirtazapine should be avoided because of the possibility of weight gain; venlafaxine should be avoided because of hypertension. Sertraline would be an appropriate choice, given that it has been relatively well-studied in persons with CAD.
The patient begins treatment with fluoxetine (10 mg/d, which is then increased to 20 mg/d after several days). His depressive symptoms gradually diminish; he achieves a “50%” reduction of symptoms at follow-up visit 3 weeks later. Two months after fluoxetine was initiated, the patient is nearly euthymic, reporting only 2 depressive symptoms, and is again engaging in usual recreational activities.
TABLE 3
A comparison of antidepressants in the treatment of depressed patients in cardiac populations
| Medication | Class/mechanism | Risks/side effects | Benefits |
| Citalopram | SSRI | Low cost, minimal drug-drug interactions | |
| Escitalopram | SSRI | Newest/least studied agent | Low cost, minimal drug-drug interactions, possibly faster onset and fewer side effects |
| Fluoxetine | SSRI | Long half-life, more drug-drug interactions | |
| Paroxetine | SSRI | Sedation, mild anticholinergic effects | |
| Sertraline | SSRI | Sedation, mild | Best studied in CAD; few drug interactions |
| Mirtazapine | Atypical antidepressant (5HT2, 5HT3, and alpha2 refceptor blockade) | Sedation, weight gain, possible elevation of lipids | No sexual dysfunction |
| Venlafaxine | Selective serotonin and norepinephrine receptor blockade | Elevated blood pressure in 13% at doses of 300 mg or greater | |
| Bupropion | Increases noradrenergic and dopaminergic activity | Initial anxiety | No sexual dysfunction |
| SSRI, selective serotonin reuptake inhibitor; CAD, coronary artery disease | |||
Conclusions
Q: Is depression, like hypertension, a risk factor for the development of coronary artery disease (CAD)? A:____________________________________________________ _____________________________________________________ _____________________________________________________
Whether depression is a risk factor for CAD depends on how one defines a risk factor and whether one is discussing “major” or “minor” risk factors. At least 15 narrative reviews have been written on the relationship between depression and heart disease, but none has examined the epidemiologic evidence for depression as a major risk factor for CAD (Table 4).8
In looking at the 7 main epidemiologic criteria for a risk factor, depression does very well on 4: strength of association, consistency, dose-response effect, and predictability. Numerous studies have shown that depression is clearly and consistently associated with the development of CAD, and that clinical depression appears to predict CAD more robustly than does depressed mood alone.9-12
On 2 of the criteria, specificity and biological plausibility, there is fair evidence for depression as a CAD risk factor. We do not yet know the relative importance of recurrent major depression, dysthymia, BDI scores of 10 or greater, or some other marker of depression as predictors of CAD.
Because mild depressive symptoms may predict CAD, it is unclear what levels of depression increase the risk of CAD and require intervention. Excellent work exists regarding the development of plausible mechanisms by which depression may lead to CAD; however, these mechanisms have yet to be proven. Therefore, the evidence in this domain can only be rated as fair.