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Aortic stenosis is a growing worldwide health burden with no approved therapies beyond surgical or transcatheter valve replacement procedures. Calcification of aortic valve leaflets is a major contributor to aortic stenosis, subsequent heart failure and ultimately death. A small number of genetic contributors to valvular calcification have been identified, with elevated lipoprotein(a) (Lp(a)) being one of the strongest risk factors for calcific aortic valve disease (CAVD).1 Despite >1 billion people globally having elevated Lp(a) (>30 to 50 mg/dL or >75 to 125 nmol/L),2 the normal physiological function of Lp(a) and how Lp(a) mechanistically promotes CAVD progression have not been established. As such, identifying the roles that Lp(a) plays in human disease is a major unmet medical need with far-reaching therapeutic potential. In their Heart paper, Capoulade et al 3 assessed Lp(a) complexes with apolipoproteins and oxidised phospholipids (OxPLs) in patients from the Aortic Stenosis Progression Observation: Measuring Effects of Rousvastatin trial. This new clinical report demonstrates the novel finding that complexes of Lp(a) with apolipoprotein CIII (apoCIII) are associated with accelerated CAVD progression, in addition to validating4 the association of apolipoprotein(a) (apo(a))-OxPL complexes with accelerated CAVD progression.
Lp(a) is a low-density lipoprotein-like particle with apo(a) covalently …
MAR and EA are joint senior authors.
Contributors MAR wrote the manuscript and EA edited and critically revised the manuscript.
Funding This work is supported by National Institutes of Health grants R01HL136431, R01HL14917 and R01HL147095.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.