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：心脏的硬疾


摘要 钙化性主动脉瓣狭窄（CAVS）在老龄化人口中很常见，并将成为日益严重的经济和健康负担。一旦出现，就不可避免地会进展，并且有症状的患者预后较差。没有任何药物疗法被证明可以有效控制或减少疾病进展。因此，主动脉瓣置换术仍然是唯一可用的治疗选择。对疾病进展机制的进一步了解使我们认识到 CAVS 不是一种被动疾病。相反，CAVS 受到多种机制的调节，对钙化起着关键作用。主动脉瓣钙化（AVC）受到细胞和体液因素的积极调节，可能为诊断和干预提供目标。维生素 K 依赖性蛋白参与 AVC 抑制的发现增强了我们对该过程的机制理解，并为疾病探索开辟了新途径。这篇综述讨论了 CAVS 进展的过程，重点是对钙化的最新见解、钙化活动成像方法以及潜在的治疗选择。