Aortic Valve Stenosis

The supplied grounding supports calcific aortic valve stenosis as a major disease form, but does not provide a complete aetiologic list for all aortic stenosis subtypes. It also identifies elevated lipoprotein(a) as a causal and continuous risk factor for aortic valve stenosis, and notes genetic loci and candidate causal genes associated with calcific aortic valve stenosis. Cardiac amyloidosis can also involve the valves and contribute to aortic stenosis in affected patients.

In calcific aortic valve stenosis, the valve undergoes progressive calcification, with high lipoprotein(a) associated with both microcalcification and macrocalcification of the aortic valve. Genomic analyses point to tissue-specific regulation, expression changes in valve tissue, and candidate genes involved in processes such as endothelial-mesenchymal transition. In cardiac amyloidosis, misfolded protein deposition in the valve can impair its structure and function and contribute to stenosis.

Elevated lipoprotein(a) is a supported risk factor for aortic valve stenosis, including at low levels of LDL cholesterol. Genetic susceptibility is also supported by genome-wide association findings and candidate causal genes for calcific aortic valve stenosis. Cardiac amyloidosis shares risk factors and disease mechanisms with aortic stenosis in the subset of patients who have both conditions.

The supplied grounding indicates that there is currently no medical therapy to prevent calcific aortic valve stenosis. Management is therefore centered on procedural treatment, including surgery and transcatheter aortic valve replacement in appropriate patients, with the literature also addressing complications, mortality, and therapy at the valve-disease level. The Lp(a) consensus statement discusses testing and treatment of elevated Lp(a) in the broader cardiovascular context, but does not establish a disease-specific medical therapy for aortic stenosis.