CAJ | 학술논문

心肌梗死后抑郁障碍的发生使人们认识到心脑在病理上存在一定联系。患有急性心肌梗死患者具有三倍的风险发展为抑郁。反之，抑郁症状可以增加心血管病的风险。这两种情况的并存与患者预后不良有密切关系。尽管导致这一交互作用的潜在机制尚不明确，但是有人认为炎性反应可能在其中发挥巨大作用。急性心肌梗死诱发的外周组织细胞因子的释放可以引发脑内皮渗漏和血脑屏障完整性的破坏，因此可以诱发神经炎性反应的发生。本文试图从心肌梗死后抑郁发生机制中揭示心脑之间的关系，并为临床心肌梗死后抑郁的治疗提供生物学依据。
심기경사후억욱장애적발생사인문인식도심뇌재병리상존재일정련계。환유급성심기경사환자구유삼배적풍험발전위억욱。반지，억욱증상가이증가심혈관병적풍험。저량충정황적병존여환자예후불량유밀절관계。진관도치저일교호작용적잠재궤제상불명학，단시유인인위염성반응가능재기중발휘거대작용。급성심기경사유발적외주조직세포인자적석방가이인발뇌내피삼루화혈뇌병장완정성적파배，인차가이유발신경염성반응적발생。본문시도종심기경사후억욱발생궤제중게시심뇌지간적관계，병위림상심기경사후억욱적치료제공생물학의거。
The incidence of depression after myocardial infarction brings people to realize that there is a cardio-cerebral pathologi-cal connection.Patients experiencing an acute myocardial infarction ( AMI) have a three times higher chance to develop depres-sion.Vice versa,depressive symptoms increase the risk of cardiovascular incidents.The co-existence of both conditions is associated with substantially worse prognosis.Although the underlying mechanism of the interaction is largely unknown, inflammation is thought to be of pivotal importance.AMI-induced peripheral cytokines release may cause cerebral endothelial leakage and the integ-rity of the blood-brain barrier damage and hence induces a neuroinflammatory reaction.The neuroinflammation may persist even longer after the initial peripheral inflammation has been subsided.This paper attempts to reveal the relationship between the heart and brain from the mechanism of depression after myocardial infarction and provide a biological basis for the treatment of depression after myocardial infarction for clinical application.