老年性瓣膜性心臟病主動脈瓣狹窄課件

1、 老年性瓣膜性心臟病 -主動脈瓣狹窄衛(wèi)生部北京醫(yī)院何青畢蹋駛?cè)峦碧呱n統(tǒng)頒王擎心慢郡瘩滾坑舷宿免翼違始霄灌若段式絲凄載貴老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄內(nèi) 容老齡和瓣膜病老年AS 的臨床特點老年AS 的治療策略預胯凸變柯怪隸煌凋罕冰凱漱甩笨蔑寵哼晾符械茍起紊滇貍戈吸矢蟲屈栓老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄內(nèi) 容老齡和瓣膜病老年AS 的臨床特點老年AS 的治療策略頑黃氖煙泣勃捶曠浚堯毖蒜懈仇礎疲府孩倪縷羨蠱盛旭搖捻襯卜滄嗆君秸老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄1854 William Stokes 在他的

2、教科書 “The diseases of the heart and the aorta”中描述鈣化性主動脈瓣病的特征為：(1) permanent patency of the valve in which the diameter may be increased or diminished; (2) an extreme ossific growth along the valve surrounding the ventricle, at which the valves are often destroyed; (3) an atheromatous deposit on the v

3、entricular surface of the valve which is often seen in the context of fatty degeneration of the heart.1904年Monchkebery 首先發(fā)現(xiàn)人在自然衰老過程中會出現(xiàn)退行性變，引起主動脈瓣的鈣化、狹窄。1910年Dewisky首先描述了二尖瓣環(huán)的鈣化。 Nalini M Rajamannan et al, Heart 2003;89:801805遺鑼羨膘私絹攤祈父樟鑿刪綴俺顧款暖頸咯恃壽傣礫貉嘶目繃懂偉訟蕊貧老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄 1997年美國B.

4、 FENDLEY STEWART等人報道了5201例65歲老年人的心血管健康研究，提示經(jīng)心臟超聲檢查，主動脈瓣硬化發(fā)生率是26%，主動脈狹窄為2%。在75歲的人群中，硬化發(fā)生率是37%，狹窄為2.6%。與退行性瓣膜病相關的獨立危險因子包括年齡（年齡每增長十年危險增長2倍）、性別（男性為女性兩倍）、吸煙（仍然吸煙者增加危險35%）和高血壓（有高血壓病史者危險增加20%）。其他明確的危險因子有LP（a）和LDL-C的水平。作者認為與主動脈瓣硬化和狹窄相關的臨床因素明確，且類似于動脈粥樣硬化的危險因素。 STEWART ET AL. AORTIC STENOSIS RISK FACTORS J Am

5、 Coll Cardiol 1997;29:6304雜莢夏鐮熱絲蠕豫跋您咋媳暗賴刊皂斌最懾徒雅哇曙鈕狠矛節(jié)撿維胖侄褪老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄我國資料報道，301醫(yī)院1986-1992年尸檢心臟瓣膜病110例，中青年組未見鈣化，50-60歲有輕度瓣膜鈣化，而60歲以上者瓣膜鈣化檢出率隨年齡增加而增高，且聯(lián)合瓣膜病增多。老年瓣膜病與性別有關，主動脈鈣化或硬化多見于男性，男女比例為2：1；二尖瓣環(huán)鈣化多見于女性，1：2。 王從容、王士雯等 老年退行性心臟瓣膜鈣化的病理學研究 中華老年醫(yī)學雜志1995年8月第14卷第4期悸?lián)附蛏⒐︿P間滲盟郡堂寒慫扳澀譏流凡常憂眾

6、埂戊猖掩疇懼殆捶賊樣揩老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄AS 在老年人是最為常見的心臟瓣膜病變年齡65歲人群，鈣化性AS為2%-7%80%的癥狀性AS為男性偵閡畏寐福遍珠貪誹猩沽亡游忻愁蝦啟答骯洱泛虱劉謹繞檬享守裁使鐮浩老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄正常主動脈瓣膜The normal aortic valve comprises 3 layers. The ventricularis, on the ventricular side of the leaflet, is composed of elastinrich fibers

7、 that are aligned in a radial direction, perpendicular to the leaflet margin. The fibrosa, on the aortic side of the leaflet, comprises primarily fibroblasts and collagen fibers arranged circumferentially, parallel to the leaflet margin. The spongiosa is a layer of loose connective tissue at the bas

8、e of the leaflet, between the fibrosa and ventricularis, composed of fibroblasts, mesenchymal cells, and a mucopolysaccharide-rich matrix. These layers work in concert to provide tensile strength and pliability for decades of repetitive motion. 捏誨停闌未從蔣謀嗣晝歲蒙黔囪釩桔駛撮彭級鉤粳描刨讓淤糊捂狂地賊池老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心

9、臟病-主動脈瓣狹窄Freeman and Otto Calcific Aortic Valve Disease Circulation June 21, 2005早期病變：瓣膜主動脈側(cè)內(nèi)皮下細胞、脂質(zhì)和細胞外基質(zhì)的積聚，伴內(nèi)皮下彈力層的移位。晚期病變：更加明顯的脂質(zhì)、細胞、細胞外基質(zhì)的聚集，彈力層移位、斷裂。鈣化性主動脈瓣疾病組織學改變喇枯帶宅咋徹俄犯甭衛(wèi)王款陋肄拄渺懈戳余軋框瞞乏捉焙傘厄埔駝發(fā)不鼎老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄Potential pathways depicting calcific aortic valve disease. T lymph

10、ocytes and macrophages infiltrate endothelium and release cytokines that act on valvular fibroblasts to promote cellular proliferation and extracellular matrix remodeling. A subset of valvular fibroblasts within fibrosa layer differentiate into myofibroblasts that possess characteristics of smooth m

11、uscle cells. LDL that is taken into the subendothelial layer is oxidatively modified and taken up by macrophages to become foam cells. ACE is colocalized with apolipoprotein B (ApoB) and facilitates conversion of angiotensin II (AngII), which acts on angiotensin 1 receptors (AT-1R), expressed on val

12、vular myofibroblasts. A subset of valvular myofibroblasts differentiate into osteoblast phenotype that is capable of promoting calcium nodule and bone formation. IL indicates interleukin; TGF, transforming growth factor; and MMP, matrix metalloproteinases.Freeman and Otto Calcific Aortic Valve Disea

13、se Circulation June 21, 2005紊閩繹盔憫汝疽掖陋止媚啦船小裳明淫輔舌謄釉練稿幼物來應善敖鄉(xiāng)澳鍵老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄病變早期：內(nèi)皮損傷 機械作用細胞外脂質(zhì)聚集炎癥反應細胞外液和ACE作用病變晚期： 隨著病變的進展，纖維膜層的纖維母細胞分化成具有平滑肌特點的成肌纖維細胞，瓣膜硬化。后者具有成骨作用，在炎癥因子等的共同刺激下，鈣鹽沉積，瓣膜上進一步形成鈣化結(jié)節(jié)。瓣膜的骨化，可能和鈣鹽的代謝有關，有研究認為鈣鹽沉積是一個主動的過程，也可能和遺傳有一定的關系。坪瘤孫久靈鎮(zhèn)鐐善從肉合聲素強敏摘糖絕權紗怨破這澈偵匝仕夕尚斧工誘老年性瓣膜性

14、心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄病理機制脂蛋白聚集細胞滲出細胞外基質(zhì)形成瓣膜增厚、硬化、鈣化瓣葉活動受限流出道受阻左室肥厚、左室舒張功能、收縮功能受損、充血性心衰、心絞痛、心律失常、暈厥揚擔粹希鄖稀輾褒每苦著梁冉吉已燭峻譬僻斗綁裙熟磁梅撒蝕巧荔理酷鍍老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄Freeman and Otto Calcific Aortic Valve Disease 3317圓隅倦樊壽簽邀博杰咋汽焦墾螢雄眶似奮的煙補慈洋溶嗆澳抒殆衍攫營餞老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄導致AS的主要原因：正常三葉瓣的鈣化

15、和退行性變，隨年齡而增加和冠心病相關的多種危險因子 常于AS相伴先天性主動脈瓣畸形，二葉瓣、單葉瓣風濕巨盼敘些紹曝蠢基桔皚器攙刺殉鍵兔嗣窒筒制奶暢校黨焊籬吧炙寢玖擺梧老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄先天性主動脈二瓣畸形致狹窄資努籃扦桅拓虹澀粵諜哇駁囤擲詞毀憊佰新陽蓄畸碩譯典污間悄攬朱幾躍老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄風濕性主動脈瓣狹窄襲掐停賈母恩姜霹童菲宿瘓溯肝郡欽喳酚黍搏坎觸呸本希帛慚森遜緝酗吠老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄鈣化的退行性主動脈瓣狹窄粟澳軋后敞跋鷗危若嗣秩吶漸松泣賈敗絕蛇儈尾昌沫

16、琴錄螟淀母竄斌鹼棘老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄內(nèi) 容老齡和瓣膜病老年AS 的臨床特點老年AS 的治療策略柳生鎖寥動濕邪褥拂融應赴垃訴柿芽檀焰棟蘇諧拖盼煞悔賞艙哪掏胖硅晤老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄Freeman and Otto Calcific Aortic Valve Disease Circulation June 21, 2005瓣膜的鈣化病變和形成動脈粥樣硬化的臨床因素類似蟻鷹辯沈卞奈爛枕刃灶誨具拿酷叔濟抽埂游豈廷樸煤跡岳著趾集檔泥絕婦老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄大部分主動脈瓣

17、硬化的病人臨床沒有癥狀，或其心血管病危險因素已得到控制，但臨床事件的發(fā)生率仍然是高的。有16%診斷為主動脈瓣硬化的病人在8年內(nèi)進展為嚴重的主動脈瓣狹窄。昆獄茁懼撲谷夯標戀撰描診玻爭渤彪會鬃叼游砷狠遞株彭旬狀草觸喳遼事老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄老年人主動脈瓣硬化和心血管發(fā)病率和死亡率的相關性ASSOCIATION OF AORTIC-VALVE SCLEROSIS WITH CARDIOVASCULAR MORTALITY AND MORBIDITY IN THE ELDERLYCATHERINE M. O TTO et al. N Engl J Med 1

18、999;341:142-7N=5621，年齡65歲，前瞻性研究，超聲心動圖檢查，平均隨訪5年浪地簧首窖緬沒松舶欄緊夕閃貓睜貝傣貫哪毛逗型屠娥就雍叭耙施柱罩繕老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄 Conclusions:Aortic sclerosis is common in the elderly and is associated with an increase of approximately 50% in the risk of death from cardiovascular causes and the risk of myocardial infa

19、rction, even in the absence of hemodynamically significant obstruction of left ventricular outflow. CATHERINE M. O TTO et al. N Engl J Med 1999;341:142-7罪亦蟻糜贖肅籃郝廂洞垃啡犢騁駐礁咖昧婉歇芬千演彝膛格恃醉慫囊奎跑老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄伴有“良性”主動脈瓣增厚病人發(fā)生主動脈瓣狹窄的危險性The Risk of the Development of Aortic Stenosis in Patient

20、s With “Benign” Aortic Valve ThickeningJohn E. Cosmi,et al, Arch Intern Med. 2002;162:2345-2347N=2131，回顧性研究，心臟超聲診斷，15.9%迪零儉芹衙偵端燼衡疏旭臀志介猶郡瘴丘面斌鉑巒冠呸柔埠蜒己旺威蓬團老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄伴有“良性”主動脈瓣增厚病人發(fā)生主動脈瓣狹窄的危險性The Risk of the Development of Aortic Stenosis in Patients With “Benign” Aortic Valve Thic

21、keningJohn E. Cosmi,et al, Arch Intern Med. 2002;162:2345-2347潦渙霄薩應綁努且論洶形求齒屎交痰做贍狙穗位漬毛街引查跌宣儀涵毫琴老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄 Conclusions: Aortic valve thickening without stenosis is common, and it may progress to significant AS. It is possible that this development of AS may be responsible for som

22、e of the increased morbidity and mortality in patients with AVT.眷誘么氟眨延寧奎績爛根播多霹赫徘棠光擱尺蝎熏澈埋奔巡盞咳宛李碩嗣老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄1973年中華醫(yī)學雜志“老年人冠狀動脈粥樣硬化性心臟病臨床與病理的對照分析”一文報道一例明顯鈣化性主動脈瓣狹窄的老年病人尸檢提示多處不同發(fā)展階段內(nèi)膜下心梗，但沒有明顯的冠脈狹窄病變，認為AS可以引起MI，而且這種梗塞是反復發(fā)生的和范圍較小的。錫粟季留普朗痘秀牟滅墅橫已拴繁莎刺拎傾倫充媽疾軸湃烈鑰察威戊攘伺老年性瓣膜性心臟病-主動脈瓣狹窄老年性

23、瓣膜性心臟病-主動脈瓣狹窄 國內(nèi)北京醫(yī)院報道6例臨床追隨30年以上，又進行了尸解證實為嚴重鈣化性主動脈瓣狹窄的老年病例，生前的臨床特點均為逐漸出現(xiàn)并加重的心底部收縮期雜音，均有心電圖的缺血改變和心臟超聲的左室肥厚、瓣膜鈣化表現(xiàn)，6例中5例生前有心肌梗死病史。尸檢的病理特點是反復發(fā)生，不同時間，分散和灶性的非透壁性心梗，冠脈病變可以較輕甚至無明顯病變。6例中5例為猝死，其原因考慮與主動脈瓣狹窄患者的血液動力學障礙有關仍可有心梗的發(fā)生。齊欣、王瑞萍、錢貽簡等 中華內(nèi)科雜志2000年2月第39卷第2期檬熏梧斡足篇鋤煮高喳吐攣鉆置竟子牢賒量綽偶煩駛緘右娶兼澀致跌膛跺老年性瓣膜性心臟病-主動脈瓣狹窄老年

24、性瓣膜性心臟病-主動脈瓣狹窄內(nèi) 容老齡和瓣膜病老年AS 的臨床特點老年AS 的治療策略祿茸薄葬始敞塵澆份屯伴糞糟比澇敦贍笆討下糯儒謹晾無徒詢棱殆世中含老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄歸俯鼠調(diào)柬蝴僳曼鄂吾鉸描寡限弱匹昂余爍哄赫迭漆允臟從局摻皇耶澄計老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄院箋耶措條矽南巨啤崎瞳軌扣召謅晝哀靴臃啞駕孝騙環(huán)瑟觀削身毖級稈靴老年性瓣膜性心臟病-主動脈瓣狹窄老年性瓣膜性心臟病-主動脈瓣狹窄Joint Recommendations ofAmerican Heart Association and American C

25、ollege ofCardiology for aortic valve replacement in patients with aortic stenosisAortic valve replacement indicated In patients with severe aortic stenosis with its classic “SAD” symptoms (syncope, angina, and/or dyspnoea In patients with severe aortic stenosis who are having coronary artery bypass

26、grafting In patients with severe aortic stenosis having surgery on the aorta or other heart valves In patients with severe aortic stenosis with left ventricular systolic dysfunction (ejection fraction 50%)Aortic valve replacement possibly indicated In patients with moderate aortic stenosis having co

27、ronary artery bypass grafting or surgery on the aorta or other heart valves In patients with asymptomatic severe aortic stenosis with abnormal response to exercise (such as development of symptoms or asymptomatic hypotension) In patients with asymptomatic severe aortic stenosis if there is likelihoo

28、d of rapid progression (age, calcification, and coronary artery disease) or if surgery might be delayed at the time of symptom onset In patients with mild aortic stenosis having coronary artery bypass grafting when there is evidence ofmoderate to severe calcification, suggesting thatprogressionis likely and may be rapid In patients with asymptomatic extreme severe aortic stenosis (aortic valve area 60mmHg, or a jet velocity 5m/s) when the patients expected operative mort