綜述綜述南華大學碩士學位論文南華大學碩士學位論文抑郁與冠心病的研究進展綜述論文目錄TOC\o"1-2"\h\u10885抑郁與CHD患者的預后： 15864CHD患者合并抑郁的可能發病機制 24276 210597 217477 27996-- 315433 32360 327732 3694CHD患者合并抑郁的早期篩查 426655CHD患者合并抑郁的治療 418219 48544 532036展望： 531070參考文獻 6摘要：后的影響、發病機制、早期篩查、治療方案等幾個方面進行綜述。關鍵詞：冠心病、抑郁、機制、治療（Coronaryheartdisease，CHD）5名CHD1人患有抑郁癥，其3倍[1-2]“生物-心理-醫學”抑郁共病的現象越來越受到臨床醫師的關注。抑郁與CHD患者的預后：新診斷的CHD12內會增加一倍[3]量-[4]名因AMI12個月的隨訪研究顯示，260名抑郁癥患者的直接醫療再入院時間延長[5]654名疑似CHD33%21%。而總社會成本也可能在抑郁的CHD患者中增加，這可能是延遲返回工作導致的生產力損失而造成的[6]CHD定程度上造成了醫療資源的浪費，成為嚴重的社會公共衛生問題。CHD患者合并抑郁的可能發病機制研究表明，A型性格的人更容易患CHD。其性格特征主要體現在三個方面：AMI并與MACE的發生率增加相關。D型人格性格特征主要包括：負性情感和社會抑制性[8]。除了性格因素的影響外，CHD合并抑郁患者的不良行為改變也在疾病的進過度疲勞也被證明是心源性猝死的前兆。ratevariability，HRV）的降低與該調節功能受損有關[10]。而心率增快與的降低均可誘發心源性猝死[11]。--抑郁與白細胞介素-1、白細胞介素-6、腫瘤壞死因子-α等參與非特異性免疫反應的促炎性細胞因子的過度分泌有關omega-3和脂肪酸的血清濃度卻平行下降[13]激活，進一步加重炎癥反應和氧化應激[9]。在軸的作用下，血清皮質醇濃度增加，不僅誘導胰島素抵抗和脂質代謝紊亂，還可破壞海馬神經元，以致于對軸的負反饋作用減弱，形成惡性循環[14]。抑郁可通過介導內皮功能障礙以及增強血小板反應性來影響CHD患者的預后。研究表明，血小板反應性增強是抑郁癥患者AS血栓形成易感性增加的潛在機制[15]5-5-5-羥色胺密度也可能增加血小板的反應性[16]減弱[17]。切相關[18-19]。腸道微生物群代謝產物可產生神經活性物質來影響大腦發育和功交互作用可能導致抑郁的發生[20-21]可通過炎癥反應影響中樞神經系統的功能、神經遞質的信號傳導，導致抑郁癥[22-23]神經系統的生理皮質醇水平、炎癥因子和神經遞質調節來改善抑郁癥狀[24-25]。內分泌因子通過旁分泌和自分泌途徑調節器官的生長、代謝和功能。IGF-1生長激素的調控。IGF-1是預防冠心病的有效保護因素[26]。血清IGF-1水平過高CHD的風險[26]IGF-1[27]。認知能力較低的個體如果IGF-1水平較低，則更容易患抑郁癥[28-29]。FGF21善動脈粥樣硬化和減輕心肌缺血再灌注損傷。Liu等證明FGF21水平與男性受試者貝克抑郁量表得分之間存在顯著的負相關，表明FGF21具有預防抑郁的功能[30]IGF-1FGF21可能參與了CHDCHD患者合并抑郁的早期篩查的CHD患者，因為非精神?？漆t師對于抑郁的識別及診治往往是不甚了解的。所有CHD成年患者，包括急性起病或慢性進展患者，都應進行抑郁篩查及風險評估[31]。美國心臟病協會建議首先使用PHQ-2量表進行基線評估，若PHQ-2篩PHQ-9量表對于病情嚴重程度進行評估[32]慮每年度或者更頻繁的進行抑郁的篩查、評估。CHD患者合并抑郁的治療CHD患者合并抑郁的藥物治療可以有效緩解其抑郁情緒[33]，但無法減輕抑郁帶來的心臟損害以及死亡率的增加[34]。目前抗抑郁藥物主要包括三環類藥物、5-5-羥色胺和去甲腎上腺素再5-羥色胺再攝取抑制劑是治療CHD5-羥色胺和去甲腎上腺素再攝取抑制劑是一種新型抗[36]規律的生活作息以及適當的運動訓練，提升生活質量，加強CHD二級預防從而一定程度的改善，但并沒有較強的證據可以表明心里干預治療可以降低CHD患者的全因死亡率及相關并發癥風險[38]。展望：近期研究發現，腸道微生物群及一些內分泌因子可能參與了CHD合并抑郁的發生、發展，但其相關機制仍需進一步的基礎實驗和臨床研究去探討及證實。目前中藥聯合抗抑郁藥物治療并未在臨床上較大范圍應用，相關副作用尚未可參考文獻LaneD,CarrollD,RingC,etal.Theprevalenceandpersistenceofdepressionandanxietyfollowingmyocardialinfarction[J].Britishjournalofhealthpsychology,2002,7(Pt1):11-21.RuoB,RumsfeldJS,HlatkyMA,etal.Depressivesymptomsandhealth-relatedqualityoflife:theHeartandSoulStudy[J].Jama,2003,290(2):215-221.CarneyRM,RichFreedlandKE,etal.Majordepressivedisorderpredictscardiaceventsinpatientswithcoronaryarterydisease[J].Psychosomaticmedicine,1988,50(6):627-633.Frasure-SmithN,LespéranceReflectionsondepressionasacardiacriskfactor[J].Psychosomaticmedicine,2005,67(Suppl1):S19-25.Frasure-SmithN,LespéranceGravelG,etal.Depressionandhealth-carecostsduringthefirstyearfollowingmyocardialinfarction[J].Journalofpsychosomaticresearch,2000,48(4-5):471-478.RutledgeJohnsonBD,etal.Depressionandcardiovascularhealthcarecostsamongwomenwithsuspectedmyocardialischemia:prospectiveresultsfromtheWISEIschemiaSyndromeEvaluation)Study[J].JournaloftheAmericanCollegeofCardiology,2009,53(2):176-183.ConsoliSM,CordierS,DucimetierePJPM.ApsychologicalmodelaccountingfortheriskfordepressionintheFrenchGAZELcohort[J].PsychosomaticMedicine,1997,59.LinLiL,etal.Dpersonality,butnotAbehaviorpattern,isassociatedwithcoronaryplaquevulnerability[J].Psychology,health&medicine,2018,23(2):216-223.ZornSchürRR,Boksetal.Cortisolstressreactivityacrosspsychiatricdisorders:Asystematicreviewandmeta-analysis[J].Psychoneuroendocrinology,2017,77:25-36.李愛民. 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