Lack of response to antidepressant treatment in depressed patients with a recent heart attack may signify a high risk of more cardiac events. De Jonge et al. (CME, p. 1371) assessed 70 patients treated for depression after suffering a myocardial infarction. Over 18 months, major heart problems occurred in 26% of the patients whose depression did not respond but only 7% of the responders. Otte et al. (p. 1379) report a possible genetic connection between heart disease and depression. The 5-HTTLPR polymorphism is part of a gene that influences intercellular serotonin transport. Among 557 cardiac patients, those with one or two copies of the 5-HTTLPR short allele had more depression, perceived stress, and urinary norepinephrine excretion than patients with two long alleles. Norepinephrine excretion is believed to reflect activity of the sympathetic nervous system, a possible link between heart disease and depression. Drs. Robert Carney and Kenneth Freedland discuss depression in cardiac patients in an editorial on p. 1307.
Hyperprolactinemia caused by antipsychotic drugs may respond to the addition of aripiprazole, an antipsychotic with a distinct pharmacological profile. Shim et al. (p. 1304) added aripiprazole to the haloperidol treatment of 26 patients with schizophrenia. Hyperprolactinemia was alleviated in 85%, compared to 4% for placebo. This normalization may be due to aripiprazole’s high affinity for dopamine D2 receptors. Using positron emission tomography, Mamo et al. (p. 1411) measured aripiprazole’s binding to D2 receptors. Therapeutic doses bound to more than 80% of available D2 receptors in the striatum of patients with schizophrenia or schizoaffective disorder. For most other antipsychotics, occupancy is 60%–65%. The threshold for producing extrapyramidal side effects was 90% for aripiprazole, compared to 80% for other antipsychotics. The clinical pharmacology of aripiprazole is discussed by Dr. Robert Kessler in an editorial on p. 1310.