Depressive illness and the heart: Identifying the relation between affective disorders and coronary heart disease

严重抑郁症在全球疾病负担的十大主要原因中排名第四，如果流行病学预测是正确的，到2020年，它将排在第二位。抑郁症患者患冠心病的风险增加。这种增加的风险是独立于传统的危险因素，如吸烟，肥胖，高脂血症，糖尿病和高血压。同样确凿地证明了心肌梗死（MI）后患者抑郁的不良影响，这大大增加了死亡率。抑郁症导致心脏风险增加的机制目前尚不清楚，但交感神经系统的激活、血小板反应性的增强和/或气压反射功能的改变可能是最重要的。我们实验室的初步数据表明，全身和心脏交感神经活动和心脏压力反射敏感性在抗抑郁治疗后发生改变。确定导致情感行为改变的潜在神经化学机制，直接和间接量化心脏和全身交感神经活动，并测试治疗和行为干预是否能影响脑神经递质转换，并以可能降低心脏风险的方式改变心脏交感神经张力、血小板反应性和压力反射功能。将是减轻社区抑郁症负担的重要一步。

Major depression is ranked fourth among the 10 leading causes of the global burden of disease and, if epidemiological projections are correct, by 2020 it will reach second place. Patients with depression are at increased risk of developing coronary heart disease. This elevated risk is independent of conventional risk factors such as smoking, obesity, hyperlipidaemia, diabetes and hypertension. Also conclusively demonstrated is the adverse effect of depression in patients following myocardial infarction (MI), which materially increases mortality. The mechanism of increased cardiac risk attributable to depressive illness is at present uncertain but activation of the sympathetic nervous system, exaggerated platelet reactivity and-or altered baroreflex function are likely to be of prime importance. Preliminary data from our laboratory indicates that whole body and cardiac sympathetic nervous activity and cardiac baroreflex sensitivity are modified following antidepressant therapy. Identifying the underlying neurochemical mechanisms responsible for alterations in affective behaviour, and quantifying cardiac and whole body sympathetic activity directly and indirectly, and testing whether therapeutic and behavioural interventions can influence brain neurotransmitter turnover and modify cardiac sympathetic tone, platelet reactivity, and baroreflex function in a fashion likely to reduce cardiac risk, will be an important step forward in alleviating the burden of depressive illness on the community.