Abstract 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.

中文翻译：

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钙化性主动脉瓣狭窄：心脏的硬病

摘要钙化性主动脉瓣狭窄（CAVS）在老年人群中很常见，并且将成为日益严重的经济和健康负担。一旦出现，它不可避免地会进展并且在有症状的患者中预后不良。没有医学疗法被证明可有效抑制或减少疾病进展。因此，主动脉瓣置换术仍然是唯一可用的治疗选择。对疾病进展机制的深入了解为我们提供了 CAVS 不是被动疾病的见解。相反，CAVS 受多种机制调节，对钙化起关键作用。主动脉瓣钙化 (AVC) 受到积极调节，涉及可能为诊断和干预提供目标的细胞和体液因素。维生素 K 依赖性蛋白参与 AVC 抑制的发现增强了我们对这一过程的机制理解，并开辟了疾病探索的新途径。这篇综述讨论了涉及 CAVS 进展的过程，重点是最近对钙化的认识、钙化活动的成像方法和潜在的治疗选择。