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The readership of Heart will require no introduction to the epidemiology, assessment and treatment of calcific aortic stenosis in 2020. Although transcatheter aortic valve implantation has revolutionised the interventional paradigm and is an unequivocal success, we recognise that a prosthesis is not a cure for aortic valve disease, and that complications—both short- and long-term—cannot be completely abolished. Consequently, although recent clinical research has largely focused on iterative improvements in devices, procedural techniques and risk assessment with a view to optimising the delivery and timing of valve replacement, the search for an effective medical therapy to retard the inexorable progression of aortic stenosis continues.
The only drugs to be tested prospectively in randomised controlled trials as disease modifiers are statins, with conclusively negative results.1 Observational data have hinted at possible roles for other therapies such as renin–angiotensin–aldosterone system blockade and antiosteoporosis medications (figure 1), but it is not possible to confirm causal relationships and draw actionable conclusions from these non-randomised data. Meanwhile, a deeper understanding of the complex processes governing aortic stenosis has shifted the field away from a purely degenerative disease model, with more emphasis on valve mineralisation, lipoprotein infiltration, active inflammation and tissue remodelling. This has led to the identification of multiple possible therapeutic targets, beyond simple correlations between clinical parameters and disease progression.2 Dipeptidyl peptidase-4 (DPP-4) has recently been proposed as one such target. DPP-4 inhibitors are most commonly used as oral hypoglycaemics for the treatment of diabetes mellitus. However, DPP-4 cleaves a variety of substrates beyond incretin hormones. The authors of the current study previously demonstrated that valve endothelial cell …
Contributors All authors have contributed to the creation of this editorial and its content. RB is the corresponding author.
Funding This work was supported by the British Heart Foundation (PG/19/40/34422) and the Sir Jules Thorn Charitable Trust (15/JTA).
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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