ABSTRACT
Cardiovascular disease and depression are intimately related illnesses. Cardiovascular mortality is more common in persons with depression, and depression following a myocardial infarction is associated with significantly poorer cardiac outcome. Safe and effective simultaneous treatment of depression and cardiovascular illness can be difficult because of the interplay between these conditions. We examine the evidence for cardiovascular effects of depression, as well as the proposed mechanism for these effects. We also review the cardiovascular effects of antidepressant treatments and the mood-altering effects of common cardiovascular medications. Articles reviewed were derived from a Medline search of English-language articles published between 1970 and 1998 (search terms: cardiovascular disease, antidepressants, psychiatry, myocardial infarction, antihypertensive agents, depression).
Subject(s)
Cardiovascular Diseases/etiology , Depressive Disorder/drug therapy , Depressive Disorder/psychology , Adrenergic beta-Antagonists/therapeutic use , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Antidepressive Agents, Tricyclic/therapeutic use , Calcium Channel Blockers/therapeutic use , Central Nervous System Stimulants/therapeutic use , Electroconvulsive Therapy/methods , Humans , Monoamine Oxidase Inhibitors/therapeutic use , Selective Serotonin Reuptake Inhibitors/therapeutic useABSTRACT
The potential role of macrophages and T lymphocytes in the destruction of the corpus luteum at the end of the luteal phase was investigated by treating pseudopregnant rabbits with the immunosuppressant glucocorticoid methylprednisolone. Eleven specific pathogen-free New Zealand White rabbits were injected with pregnant mares' serum gonadotrophin (40 iu, i.m.), followed 2 days later by human chorionic gonadotrophin (40 iu, i.v.) to stimulate ovulation. The following day (day 1 of pseudo-pregnancy) all animals had an oestradiol-filled Silastic capsule implanted s.c., to ensure that oestradiol, the luteotrophic hormone in this species, would not be limiting. From day 10 of pseudopregnancy, three animals were injected with a low dose of methylprednisolone (2 mg kg-1 per day) until day 20. Three other animals were injected with a higher dose of methylprednisolone (20 mg kg-1 per day) from day 13 of pseudopregnancy until day 19. Five animals served as control, vehicle-injected animals. Blood samples were taken at intervals and assayed for progesterone. Immunofluorescence was used to stain luteal tissue for macrophages, T lymphocytes and class II antigens, and positive cells were counted under high-power magnification. Methylprednisolone treatment reduced (by about 70%), but did not eliminate, the macrophages in the regressing corpora lutea. In contrast, the high dose of methylprednisolone essentially eliminated T lymphocytes, and reduced (by about 90%) the number of cells expressing class II antigen in the luteal tissue. Despite the effects of methylprednisolone on these cells, serum progesterone profiles were not altered by treatment with methylprednisolone, and pseudopregnancy was of normal duration.(ABSTRACT TRUNCATED AT 250 WORDS)
