Department of Cardiology, MUMC+ and CARIM, P. Debyelaan 25, HX Maastricht, the Netherlands.
Department of Clinical Chemistry, MUMC+, P. Debyelaan 25, HX Maastricht, the Netherlands.
Eur Heart J. 2018 Jul 21;39(28):2618-2624. doi: 10.1093/eurheartj/ehx653.
Calcific aortic valve stenosis (CAVS) is common in the ageing population and set to become an increasing economic and health burden. Once present, it inevitably progresses and has a poor prognosis in symptomatic patients. No medical therapies are proven to be effective in holding or reducing disease progression. Therefore, aortic valve replacement remains the only available treatment option. Improved knowledge of the mechanisms underlying disease progression has provided us with insights that CAVS is not a passive disease. Rather, CAVS is regulated by numerous mechanisms with a key role for calcification. Aortic valve calcification (AVC) is actively regulated involving cellular and humoral factors that may offer targets for diagnosis and intervention. The discovery that the vitamin K-dependent proteins are involved in the inhibition of AVC has boosted our mechanistic understanding of this process and has opened up novel avenues in disease exploration. This review discusses processes involved in CAVS progression, with an emphasis on recent insights into calcification, methods for imaging calcification activity, and potential therapeutic options.
钙化性主动脉瓣狭窄（CAVS）在老年人群中很常见，且将成为日益严重的经济和健康负担。一旦出现，在有症状的患者中，它不可避免地会进展，并预后不良。没有医学疗法被证明能有效阻止或减缓疾病进展。因此，主动脉瓣置换仍然是唯一可行的治疗选择。对疾病进展机制的深入了解使我们认识到，CAVS 不是一种被动的疾病。相反，CAVS 受多种机制调节，钙化起关键作用。主动脉瓣钙化（AVC）是受多种细胞和体液因素主动调节的，这些因素可能为诊断和干预提供靶点。发现维生素 K 依赖性蛋白参与抑制 AVC，这提高了我们对这一过程的机制理解，并为疾病探索开辟了新途径。本文讨论了 CAVS 进展涉及的过程，重点介绍了钙化的最新见解、钙化活性成像方法以及潜在的治疗选择。
