Introduction to the Aortic Valve Disease Review Series.
Introduction to the Aortic Valve Disease Review Series.
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DOI：
10.1161/circresaha.121.319286
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发表时间：
2021-04-30
影响因子：
20.1
通讯作者：
St Hilaire C
中科院分区：
文献类型：
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作者：
Cuevas RA;St Hilaire C
熟悉的“滴滴”、“滴滴”的心跳声来自心脏瓣膜关闭时产生的湍流。主动脉瓣与肺动脉瓣一起产生瓣膜，平均每分钟打开和关闭 75 次，每天 108 000 次，到您 50 岁的时候，这种运动已经发生了近 20 亿次。主动脉瓣叶的正确密封可确保血液从左心室单向流入主动脉。由于二尖瓣主动脉瓣 (BAV) 等先天性形态异常或硬化、增厚和钙化的慢性进展，瓣叶稳态的改变会导致流出道紊乱和阻塞，从而可能诱发血栓事件，导致中风或心力衰竭。人们曾经认为，纤维钙化重塑，通常在本文中称为钙化性主动脉瓣疾病（CAVD），是这种重复运动的退行性结果，然而，现在人们充分认识到CAVD发病机制是一个生物活性和复杂的过程。在本综述系列中，重点关注主动脉瓣，我们选择了该领域的领导者来介绍和讨论有关促进病理性瓣膜重塑的遗传、发育和外部压力的作用的当前进展，目前用于进一步阐明这些过程的下一代技术，以及严重 CAVD 患者可用的治疗方案的状况。该系列首先介绍了形态正常和畸形瓣膜中主动脉瓣狭窄的遗传和发育因素。虽然人们普遍认为出生时出现瓣膜畸形可能是发育缺陷的结果
The familiar lub-dub, lub-dub of your beating heart, comes from the turbulence created by the closure of the heart valves. The aortic valve, which along with the pulmonary valve creates the dub, opens and closes on average 75 times a minute, 108 000 times a day, and by the time you are 50, this movement has occurred nearly 2 billion times. Proper sealing of the aortic valve leaflets ensures the unidirectional flow of blood from the left ventricle into the aorta. Alterations in valve leaflet homeostasis, due to congenital morphological anomalies such as bicuspid aortic valve (BAV), or the chronic progression of stiffening, thickening, and calcification, cause disturbed and obstructed outflow, which may induce thrombotic events leading to stroke or heart failure. It was once thought that the fibrocalcific remodeling, commonly and herein referred to as calcific aortic valve disease (CAVD), was a degenerative consequence of this repetitive movement, however, it is now fully appreciated that CAVD pathogenesis is a biologically active and complex process.For this review series focused on the aortic valve, we have selected leaders in the field to introduce and discuss the current advances regarding the role of genetics, development, and external stresses that promote pathological valve remodeling, the next-generation technologies that are currently being used to further elucidate these processes, as well as the state of therapeutic options available to patients with severe CAVD. The series begins with a primer on the genetic and developmental contributors to aortic stenosis in morphologically normal and malformed valves. While it is accepted that the presence of valve malformations at birth is likely the result of a faulty developmental