To assess whether therapy with two widely used antidepressants influences platelet counts.

In 90 patients hospitalized for treatment of a major depressive episode according to DSM-IV, platelet counts were performed after a 6 d antidepressant-free run-in period and again after 35 d of active standardized treatment with amitriptyline (n = 40) or paroxetine (n = 50).

There was a trend for platelet counts to increase during treatment with amitriptyline (from 245.5 ± 68.6 to 256.8 ± 69 cells × 109 L-1, P < 0.06); no change was observed during treatment with paroxetine (from 232.6 ± 58.3 to 234.6 ± 68.9 cells × 109 L-1, n.s).

Treatment with amitriptyline tends to be associated with elevated platelet counts. The cause for this increase is not known, but may be relevant in terms of patients’ long-term thromboembolic risk.

Repeatedly, it has been demonstrated that depression increases the risk of developing cardiovascular disorders; vice versa, in subjects with pre-existing heart disease, comorbid depression was found to predict an unfavourable cardiovascular prognosis. However, several studies failed to observe that treatment of depression positively influences cardiac risk. Therefore, focus of research has shifted to identification of subjects, who would benefit from antidepressant therapy that is tailored to their individual needs.

Search of literature databases, focusing latest goals and advances in diagnosis and therapy of depression in subjects with cardiovascular disease.

Screening cardiac patients for depression seems to result in a different population of depressed patients, as compared with most trials testing antidepressant agents. This different inclusion process obviously favoured oversampling of subjects with minor or reversible depressive syndromes such as adjustment disorders. It is known that in these conditions placebo treatment is powerful, sometimes equalling verum condition in effectiveness.

This hypothesis is supported by re-analysis of former studies revealing selective serotonin reuptake inhibitors (SSRI) to be more effective in subjects with severe or recurrent depression or in patients, in whom depression had begun prior to the onset of cardiovascular disease (e.g., myocardial infarction). Surprisingly, some data support the notion that treatment with SSRIs ameliorates cardiac prognosis irrespective of their antidepressant action. Ongoing studies deal with treatment of depression in patients with heart failure or stroke, and with psychotherapy aimed at reducing cardiac risk factors.