Akat K, Borggrefe M, Kaden J J
First Department of Medicine (Cardiology), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany.
Heart. 2009 Apr;95(8):616-23. doi: 10.1136/hrt.2007.134783. Epub 2008 Jul 16.
Calcific aortic valve stenosis is the result of regulated cell processes. The histological hallmarks are inflammation and a remodelling of the extracellular matrix leading to bone formation. In the last 15 years the view has changed from it being an unmodifiable degenerative disease to an active biological process regulated by highly conserved ubiquitous cellular pathways. Many mechanisms and risk factors are the same as in atherosclerosis. Thus, statins and angiotensin II antagonists seemed promising treatment options. However, clinical trials failed to support this. This review describes the current understanding of major molecular mechanisms and discusses their role in clinical practice and possible therapy.
钙化性主动脉瓣狭窄是细胞调节过程的结果。组织学特征是炎症和细胞外基质重塑导致骨形成。在过去15年里,人们的观点已从它是一种不可改变的退行性疾病转变为一种由高度保守的普遍细胞途径调节的活跃生物学过程。许多机制和危险因素与动脉粥样硬化相同。因此,他汀类药物和血管紧张素II拮抗剂似乎是有前景的治疗选择。然而,临床试验未能证实这一点。本综述描述了对主要分子机制的当前理解,并讨论了它们在临床实践中的作用及可能的治疗方法。