[Depression, stress and coronary heart disease--epidemiology, prognosis and therapeutic sequelae].
Depression and coronary heart disease may be related in several ways: (1) There is epidemiological evidence that high levels of depressive symptoms in male and female patients are associated with an increased risk of myocardial infarction and a higher mortality following an acute cardiac event. Furthermore, patients developing depression after myocardial infarction have more complications, including cardiac arrhythmias. (2) In patients with a chronic coronary heart disease depression also results in a worse cardiac functional status with more frequent and severe chest pain, more physical limitation, less treatment satisfaction and a lower perceived quality of life. Non-compliance with drug therapy is also more prevalent in depressed cardiac patients. (3) The possible pathophysiological mechanisms leading to more frequent complications of coronary heart disease in patients with depression are not fully explained, but could partly be due to higher sympatho-adrenergic stimulation and increased platelet aggregation. Some anti-depressant medications, on the other hand, may also cause cardiac symptoms and increase the risk in patients with coronary heart disease. The use of tricyclic antidepressants has been shown to result in a higher relative risk of myocardial infarction even after adjustment for other cardiovascular risk factors. Tricyclic anti-depressants may have direct cardiac effects, such as QT-prolongation with ventricular arrhythmias, orthostatic hypotension and, less frequently, myocardial dysfunction. In contrast such associations were not found with the newer serotonin re-uptake inhibitors. What are the practical consequences of the observed association between coronary artery disease and depression? First of all depression should better and earlier be recognised also by non-psychiatrists and treatment indications be discussed with specialists. At present, however, there is no clear evidence that ant-depressant drugs or psychotherapy will reduce the risk of myocardial infarction and improve prognosis. Further data are urgently needed to clarify the role of therapeutic interventions. Therefore, a closer research co-operation between cardiologists and psychiatrists should be promoted in future.
Follath
F
F
Medizinische Klinik A, Departement für Innere Medizin, Universitätsspital Zürich.
D000928:Antidepressive Agents / Q000009:adverse effects / Q000627:therapeutic use; D001143:Arousal / Q000502:physiology; D015984:Causality; D003327:Coronary Disease / Q000401:mortality* / Q000503:physiopathology / Q000517:prevention & control / Q000523:psychology; D003430:Cross-Sectional Studies; D003866:Depressive Disorder / Q000188:drug therapy / Q000401:mortality* / Q000503:physiopathology / Q000523:psychology; D006801:Humans; D011379:Prognosis; D017367:Selective Serotonin Reuptake Inhibitors / Q000009:adverse effects / Q000627:therapeutic use; D013315:Stress, Psychological / Q000150:complications* / Q000453:epidemiology / Q000401:mortality / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology
D000928:Antidepressive Agents; D017367:Selective Serotonin Reuptake Inhibitors