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1、急性冠脈綜合征痰瘀證與炎癥關(guān)系的臨床研究【摘要】目的:本研究試圖針對ACS痰瘀證研究的空白,從免疫炎癥的角度出發(fā),探討急性冠脈綜合征痰瘀證的實質(zhì),并分析了炎癥因子與血脂分組間的相關(guān)性。方法:將90例急性冠脈綜合征患者按照中醫(yī)辨證標(biāo)準(zhǔn)分為痰瘀證組(55例)及非痰瘀證組(35例),另設(shè)健康對照組70例。分別檢測CRP、FIB、IL-6、TNF-α及D-二聚體在痰瘀證及非痰瘀證組中的數(shù)值,分析急性冠脈綜合征痰瘀證與炎癥相關(guān)因子的關(guān)系。檢測痰瘀證組、非痰瘀證組間TC、TG及LDL-C的數(shù)值變化。結(jié)果:急性冠脈綜合征痰瘀證組CRP、TNF-α及D-二聚體顯著高于非痰瘀證組(P<0.05、P&
2、lt;0.05、P<0.01),痰瘀證組FIB、IL-6雖高于非痰瘀證組,但差異未見顯著性(P>0.05)。ACS痰瘀證組TC數(shù)值顯著高于非痰瘀證組(P=0.025),其余TG及LDL-C在兩組間的比較未見顯著差異(P均>0.05)。結(jié)論:本研究顯示CRP、TNF-α及D-二聚體等炎癥因子介導(dǎo)的免疫炎癥活動與ACS痰瘀證的形成密切相關(guān),可能是ACS痰瘀證形成的始動因素;而高血脂是急性冠脈綜合征痰瘀證形成的物質(zhì)基礎(chǔ);CRP、TNF-α、D-二聚體等免疫、炎癥因子有可能成為ACS痰瘀證劃分的客觀指標(biāo)?!娟P(guān)鍵詞】急性冠脈綜合征;痰瘀證;炎癥介質(zhì)〔Abstract〕Object
3、ivePointingtothevacancyinthe14researchofphlegm-bloodstasissyndromeofACS,wetrytoexploreintotherelationshipamongphlegm-bloodstasissyndrome,weanalyzesomekindofinflammationmediumsandbloodlipid.Methods90ACSpatientsweredividedintophlegm-bloodstasisgroup(55)andnon-phlegm-bloodstasisgroup(35)inaccordance
4、withthestandardofthesyndromedifferentiationofTCM.70healthypeoplewereinthecontrolgrou.DetectedthelevelofC-reactiveprotein(CRP),fibrinogen(FIB),interleukin-6(IL-6),tumornecrosisfactor-alpha(TNF-α)D-Dimer(D-D)ofthephlemgm-bloodStasisgroupandthenon-phlegm-bloodstasisgroup,inthemeantime,analyzedtherel
5、ationshipbetweenthephlegm-bloodstasisofACSandheinflammationmediums.Thevarietyofthethreekindsoflipid(TC,TG,LDL-C)betweenthephlegm-bloodstasisgroupandthenon-phlegm-bloodstasisgroupwerealsostudied.ResultsThelevelsofCRP,TNF-αandD-Dinthephlegm-bloodstasisgroupofACSwereallsignificantlyhigherthanthosein
6、thenon-phlegm-bloodstasisgroup(P<0.05、P<0.05、P<0.01).FIBandIL-6inthephlegm-bloodstasisgroupwereallhigherthanthoseinthenon-phlegm-bloodstasisgroup,butallthedifferenceswerenotsignificant(P>0.05).ThenumericalvalueofTCwassignificantlyhigherinphlegm-blood14stasisgroupofACSthanthatinnon-phl
7、egm-bloodstasisgroup(P=0.025),butthedifferenceofTGbetweenthetwogroupswasnotsignificant(P>0.05),neitherwasthatofLDL-C.ConclusionThisstudysuggeststhattheimmunityandinflammationactivitiesleadedbyCRP,TNF-α,D-D,etalarehi