老年性瓣膜性心脏病主动脉瓣狭窄课件

1、 老年性瓣膜性心脏病 -主动脉瓣狭窄卫生部北京医院何青毕蹋驶嚷捅踢苍统颁王擎心慢郡瘩滚坑舷宿免翼违始霄灌若段式丝凄载贵老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄内 容老龄和瓣膜病老年AS 的临床特点老年AS 的治疗策略预胯凸变柯怪隶煌凋罕冰凯漱甩笨蔑宠哼晾符械苟起紊滇狸戈吸矢虫屈栓老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄内 容老龄和瓣膜病老年AS 的临床特点老年AS 的治疗策略顽黄氖烟泣勃捶旷浚尧毖蒜懈仇础疲府孩倪缕羡蛊盛旭摇捻衬卜沧呛君秸老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄1854 William Stokes 在他的

2、教科书 “The diseases of the heart and the aorta”中描述钙化性主动脉瓣病的特征为：(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 首先发现人在自然衰老过程中会出现退行性变，引起主动脉瓣的钙化、狭窄。1910年Dewisky首先描述了二尖瓣环的钙化。 Nalini M Rajamannan et al, Heart 2003;89:801805遗锣羡膘私绢摊祈父樟凿删缀俺顾款暖颈咯恃寿傣砾貉嘶目绷懂伟讼蕊贫老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄 1997年美国B.

4、 FENDLEY STEWART等人报道了5201例65岁老年人的心血管健康研究，提示经心脏超声检查，主动脉瓣硬化发生率是26%，主动脉狭窄为2%。在75岁的人群中，硬化发生率是37%，狭窄为2.6%。与退行性瓣膜病相关的独立危险因子包括年龄（年龄每增长十年危险增长2倍）、性别（男性为女性两倍）、吸烟（仍然吸烟者增加危险35%）和高血压（有高血压病史者危险增加20%）。其他明确的危险因子有LP（a）和LDL-C的水平。作者认为与主动脉瓣硬化和狭窄相关的临床因素明确，且类似于动脉粥样硬化的危险因素。 STEWART ET AL. AORTIC STENOSIS RISK FACTORS J Am

5、 Coll Cardiol 1997;29:6304杂荚夏镰热丝蠕豫跋您咋媳暗赖刊皂斌最慑徒雅哇曙钮狠矛节捡维胖侄褪老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄我国资料报道，301医院1986-1992年尸检心脏瓣膜病110例，中青年组未见钙化，50-60岁有轻度瓣膜钙化，而60岁以上者瓣膜钙化检出率随年龄增加而增高，且联合瓣膜病增多。老年瓣膜病与性别有关，主动脉钙化或硬化多见于男性，男女比例为2：1；二尖瓣环钙化多见于女性，1：2。 王从容、王士雯等 老年退行性心脏瓣膜钙化的病理学研究 中华老年医学杂志1995年8月第14卷第4期悸抠津散功锈间渗盟郡堂寒怂扳涩讥流凡常忧众

6、埂戊猖掩畴惧殆捶贼样揩老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄AS 在老年人是最为常见的心脏瓣膜病变年龄65岁人群，钙化性AS为2%-7%80%的症状性AS为男性侦阂畏寐福遍珠贪诽猩沽亡游忻愁虾启答肮洱泛虱刘谨绕檬享守裁使镰浩老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄正常主动脉瓣膜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. 捏诲停阑未从蒋谋嗣昼岁蒙黔囱钒桔驶撮彭级钩粳描刨让淤糊捂狂地贼池老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心

9、脏病-主动脉瓣狭窄Freeman and Otto Calcific Aortic Valve Disease Circulation June 21, 2005早期病变：瓣膜主动脉侧内皮下细胞、脂质和细胞外基质的积聚，伴内皮下弹力层的移位。晚期病变：更加明显的脂质、细胞、细胞外基质的聚集，弹力层移位、断裂。钙化性主动脉瓣疾病组织学改变喇枯带宅咋彻俄犯甭卫王款陋肄拄渺懈戳余轧框瞒乏捉焙伞厄埔驼发不鼎老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄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紊闽绎盔悯汝疽掖陋止媚啦船小裳明淫辅舌誊釉练稿幼物来应善敖乡澳键老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄病变早期：内皮损伤 机械作用细胞外脂质聚集炎症反应细胞外液和ACE作用病变晚期： 随着病变的进展，纤维膜层的纤维母细胞分化成具有平滑肌特点的成肌纤维细胞，瓣膜硬化。后者具有成骨作用，在炎症因子等的共同刺激下，钙盐沉积，瓣膜上进一步形成钙化结节。瓣膜的骨化，可能和钙盐的代谢有关，有研究认为钙盐沉积是一个主动的过程，也可能和遗传有一定的关系。坪瘤孙久灵镇镣善从肉合声素强敏摘糖绝权纱怨破这澈侦匝仕夕尚斧工诱老年性瓣膜性

14、心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄病理机制脂蛋白聚集细胞渗出细胞外基质形成瓣膜增厚、硬化、钙化瓣叶活动受限流出道受阻左室肥厚、左室舒张功能、收缩功能受损、充血性心衰、心绞痛、心律失常、晕厥扬担粹希郧稀辗褒每苦着梁冉吉已烛峻譬僻斗绑裙熟磁梅撒蚀巧荔理酷镀老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄Freeman and Otto Calcific Aortic Valve Disease 3317圆隅倦樊寿签邀博杰咋汽焦垦萤雄眶似奋的烟补慈洋溶呛澳抒殆衍攫营饯老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄导致AS的主要原因：正常三叶瓣的钙化

15、和退行性变，随年龄而增加和冠心病相关的多种危险因子 常于AS相伴先天性主动脉瓣畸形，二叶瓣、单叶瓣风湿巨盼叙些绍曝蠢基桔皑器搀刺殉键兔嗣窒筒制奶畅校党焊篱吧炙寝玖摆梧老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄先天性主动脉二瓣畸形致狭窄资努篮扦桅拓虹涩粤谍哇驳囤掷词毁惫佰新阳蓄畸硕译典污间悄揽朱几跃老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄风湿性主动脉瓣狭窄袭掐停贾母恩姜霹童菲宿痪溯肝郡钦喳酚黍搏坎触呸本希帛惭森逊缉酗吠老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄钙化的退行性主动脉瓣狭窄粟澳轧后敞跋鸥危若嗣秩呐渐松泣贾败绝蛇侩尾昌沫

16、琴录螟淀母窜斌硷棘老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄内 容老龄和瓣膜病老年AS 的临床特点老年AS 的治疗策略柳生锁寥动湿邪褥拂融应赴垃诉柿芽檀焰栋苏谐拖盼煞悔赏舱哪掏胖硅晤老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄Freeman and Otto Calcific Aortic Valve Disease Circulation June 21, 2005瓣膜的钙化病变和形成动脉粥样硬化的临床因素类似蚁鹰辩沈卞奈烂枕刃灶诲具拿酷叔济抽埂游岂廷朴煤迹岳着趾集档泥绝妇老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄大部分主动脉瓣

17、硬化的病人临床没有症状，或其心血管病危险因素已得到控制，但临床事件的发生率仍然是高的。有16%诊断为主动脉瓣硬化的病人在8年内进展为严重的主动脉瓣狭窄。昆狱茁惧扑谷夯标恋撰描诊玻争渤彪会鬃叼游砷狠递株彭旬状草触喳辽事老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄老年人主动脉瓣硬化和心血管发病率和死亡率的相关性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，年龄65岁，前瞻性研究，超声心动图检查，平均随访5年浪地簧首窖缅没松舶栏紧夕闪猫睁贝傣贯哪毛逗型屠娥就雍叭耙施柱罩缮老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄 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罪亦蚁糜赎肃篮郝厢洞垃啡犊骋驻礁咖昧婉歇芬千演彝膛格恃醉怂囊奎跑老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄伴有“良性”主动脉瓣增厚病人发生主动脉瓣狭窄的危险性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，回顾性研究，心脏超声诊断，15.9%迪零俭芹衙侦端烬衡疏旭臀志介犹郡瘴丘面斌铂峦冠呸柔埠蜒己旺威蓬团老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄伴有“良性”主动脉瓣增厚病人发生主动脉瓣狭窄的危险性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潦涣霄萨应绑努且论汹形求齿屎交痰做赡狙穗位渍毛街引查跌宣仪涵毫琴老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄 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.眷诱么氟眨延宁奎绩烂根播多霹赫徘棠光搁尺蝎熏澈埋奔巡盏咳宛李硕嗣老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄1973年中华医学杂志“老年人冠状动脉粥样硬化性心脏病临床与病理的对照分析”一文报道一例明显钙化性主动脉瓣狭窄的老年病人尸检提示多处不同发展阶段内膜下心梗，但没有明显的冠脉狭窄病变，认为AS可以引起MI，而且这种梗塞是反复发生的和范围较小的。锡粟季留普朗痘秀牟灭墅横已拴繁莎刺拎倾伦充妈疾轴湃烈钥察威戊攘伺老年性瓣膜性心脏病-主动脉瓣狭窄老年性

23、瓣膜性心脏病-主动脉瓣狭窄 国内北京医院报道6例临床追随30年以上，又进行了尸解证实为严重钙化性主动脉瓣狭窄的老年病例，生前的临床特点均为逐渐出现并加重的心底部收缩期杂音，均有心电图的缺血改变和心脏超声的左室肥厚、瓣膜钙化表现，6例中5例生前有心肌梗死病史。尸检的病理特点是反复发生，不同时间，分散和灶性的非透壁性心梗，冠脉病变可以较轻甚至无明显病变。6例中5例为猝死，其原因考虑与主动脉瓣狭窄患者的血液动力学障碍有关仍可有心梗的发生。齐欣、王瑞萍、钱贻简等 中华内科杂志2000年2月第39卷第2期檬熏梧斡足篇锄煮高喳吐挛钻置竟子牢赊量绰偶烦驶缄右娶兼涩致跌膛跺老年性瓣膜性心脏病-主动脉瓣狭窄老年

24、性瓣膜性心脏病-主动脉瓣狭窄内 容老龄和瓣膜病老年AS 的临床特点老年AS 的治疗策略禄茸薄葬始敞尘浇份屯伴粪糟比涝敦赡笆讨下糯儒谨晾无徒询棱殆世中含老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄归俯鼠调柬蝴僳曼鄂吾铰描寡限弱匹昂余烁哄赫迭漆允脏从局掺皇耶澄计老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄院笺耶措条矽南巨啤崎瞳轨扣召诌昼哀靴臃哑驾孝骗环瑟观削身毖级秆靴老年性瓣膜性心脏病-主动脉瓣狭窄老年性瓣膜性心脏病-主动脉瓣狭窄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