Since several risk factors for the development of CAVS have been identified,
it seemed reasonable to explore the effects of their medical targeting on the rate of
progress of this disease.
Especially for lipid disorders and statins, hopes have been high. Statins have a proven
value for the treatment of lipid disorders in atheromatosis, which shares some risk
factors with CAVS. A proof of concept could also be derived from animal models.
Early non randomized and retrospective studies have seemed to confirm these hopes.
With appearance of the more recent trails (SEAS, SALTIRE and ASTRONOMER) it
has become clear that these hopes are unjustified. No difference in effect have been
found between statins and placebo on the rate of progression of CAVS.
Reasons for these findings are probably:
- The composition of the population: it is unethical to deny patients with lipid
disorders a treatment with statins. This limitation makes it difficult to compare
certain populations.
- The stage of CAVS: statins might work only very early in the course of the
disease, which is asymptomatic.
- The mechanisms of action: fibrosis of the aortic valve could be induced by statins.
A fibrotic cap in atheromatosis has a protective effect; in contrast, fibrosis in
CAVS could impair the mobility of the leaflets and worsens the disease.
Statins have probably also no role in the prevention of SVD of bioprostheses.
Other approaches such as ACE inhibitors, ATR blocking agents and endothelin receptor
antagonists need still investigations. The “window” of “opportunity” for their action
might be too short.
Keywords: Angiotensin converting enzyme, aortic valve area, calcium score, end
points, endothelin receptor antagonists, jet velocity, left ventricular ejection fraction
low density lipoproteins, randomized controlled trials, statins, transvalvular gradient.
