CAJ | 학술논문

目的回顾性探讨胸主动脉夹层(TAD)及胸主动脉瘤(TAA)手术病例,分析其发病诱因、临床病理学特征,为研究其发病机制提供形态学依据,为治疗及干预TAD/TAA病变提供理论基础.方法运用常规HE及组织化学染色方法(Masson、弹力/VG及AB/PAS),分析2007年至2012年989例TAD(660例)及TAA(329例),观察比较其发病部位、临床分型、发病诱因、主动脉壁组织形态学特点,并对其中的128例标本的主动脉壁形态学进行半定量评估.结果主动脉壁病理形态学半定量分析:基本形态学改变是主动脉壁发生退行性变,TAD得分高于TAA(9.61±3.34对7.40±3.52,P =0.000);合并马方综合征(MFS),得分差异有统计学意义(P =0.000).TAD较TAA在纤维化、斑块形成及中膜坏死方面差异有统计学意义(P=0.000);合并MFS者,在囊性中膜坏死、平滑肌细胞排列紊乱及弹力纤维断裂3个指标上与其他诱因差异有统计学意义(P=0.000);动脉粥样硬化(As)在纤维化(P =0.017)及中膜变性坏死(P =0.044)指标上与其他诱因相比差异有统计学意义;高血压(HP)在中膜变性坏死(P=0.011)较其他诱因差异有统计学意义.结论 TAD对主动脉脉壁结构的破坏更严重,预后比TAA差.对主动脉壁评分有差异性改变的诱因是HP、As及MFS,三者是TAA/TAD的主要原因.平滑肌细胞的形态学改变(变性坏死、排列紊乱及重塑)是发生TAA/TAD及MFS的重要因素.单纯TAA/TAD的平滑肌变性坏死重于基质降解,而合并MFS的TAA/TAD则是平滑肌重塑、基质黏液样变性重于平滑肌坏死,因此,需进一步做平滑肌表型等的分子病理学研究,以进一步探讨TAA/TAD及MFS发病的始动环节.
목적 회고성탐토흉주동맥협층(TAD)급흉주동맥류(TAA)수술병례,분석기발병유인、림상병이학특정,위연구기발병궤제제공형태학의거,위치료급간예TAD/TAA병변제공이론기출.방법 운용상규HE급조직화학염색방법(Masson、탄력/VG급AB/PAS),분석2007년지2012년989례TAD(660례)급TAA(329례),관찰비교기발병부위、림상분형、발병유인、주동맥벽조직형태학특점,병대기중적128례표본적주동맥벽형태학진행반정량평고.결과 주동맥벽병리형태학반정량분석:기본형태학개변시주동맥벽발생퇴행성변,TAD득분고우TAA(9.61±3.34대7.40±3.52,P =0.000);합병마방종합정(MFS),득분차이유통계학의의(P =0.000).TAD교TAA재섬유화、반괴형성급중막배사방면차이유통계학의의(P=0.000);합병MFS자,재낭성중막배사、평활기세포배렬문란급탄력섬유단렬3개지표상여기타유인차이유통계학의의(P=0.000);동맥죽양경화(As)재섬유화(P =0.017)급중막변성배사(P =0.044)지표상여기타유인상비차이유통계학의의;고혈압(HP)재중막변성배사(P=0.011)교기타유인차이유통계학의의.결론 TAD대주동맥맥벽결구적파배경엄중,예후비TAA차.대주동맥벽평분유차이성개변적유인시HP、As급MFS,삼자시TAA/TAD적주요원인.평활기세포적형태학개변(변성배사、배렬문란급중소)시발생TAA/TAD급MFS적중요인소.단순TAA/TAD적평활기변성배사중우기질강해,이합병MFS적TAA/TAD칙시평활기중소、기질점액양변성중우평활기배사,인차,수진일보주평활기표형등적분자병이학연구,이진일보탐토TAA/TAD급MFS발병적시동배절.
Objective To retrospectively study the triggers and clinicopathologic characteristics of thoracic aortic dissection (TAD) and thoracic aortic aneurysm(TAA),and provide the morphologic basis of the pathogenesis and thg theoretic basis of treatment.Methods 660 TAD and 329 TAA cases were reviewed at Beijing Anzhen Hospital from 2007 to 2012.To observe and compare the sites,clinical classification,triggers and characteristics,sections of all cases were stained with hema-toxylin and eiosin,elasticity-van Gieson,Alcian blue-PAS and Masson trichrome stains.Furthermore,aortic wall sections of 128 cases were re-evaluated for semiquantitively analyzing histological alterations.Results The basic morphologic alteration was regression of the main components in aortic wall.The aortic wall score of TAD was significantly higher than TAA(9.61 ± 3.34 vs.7.40 ± 3.52,P =0.000).Also,the aortic wall score of TAD/TAA accompanied with Marfan syndrome (MFS) was significantly higher than non-accompanied cases(P =0.000).There were differences in fibrosis,atherosclerosis and medionecrosis between TDA and TAA (P =0.000).Cases accompanied with MFS were significantly different at cystic medial necrosis,smooth muscle cell orientation and elastic fragmentation (P=0.000).Atherosclerosis (As) cases were significantly different at fibrosis (P =0.017) and medionecrosis (P =0.044).Hypertension (HP) cases were significantly different at medionecrosis (P =0.011).Conclusion TAD is more seriously damaged to aortic wall structures than TAA,and TAD has poorer prognosis than TAA.HP,As and MFS are the main factors of the aortic wall score,and are the main causes of TAD/TAA.Morphological alteration of smooth muscle(necrosis,orientation and remodeling) maybe the initial factor of TAD/TAA and MFS.TAD/TAA accompanied with MFS obviously shows smooth muscle cell remodeling and matrix mucoid degeneration.However,TAD/TAA non-accompanied with MFS evidently presents smooth muscle necrosis.Therefore,we should research on the alteration of the phenotypes of smooth muscle cells to study the initial links of TAD/TAA.