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Interact Cardiovasc Thorac Surg · Sep 2010
ReviewDo statins slow the process of calcification of aortic tissue valves?
- Daniyar Gilmanov, Stefano Bevilacqua, Annamaria Mazzone, and Mattia Glauber.
- Department of Adult Cardiac Surgery, G. Pasquinucci Heart Hospital, Massa, Italy. drgilmanov@hotmail.it
- Interact Cardiovasc Thorac Surg. 2010 Sep 1;11(3):297-301.
AbstractA best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was whether statins slow the process of calcification of aortic tissue valves. Altogether 207 papers were found using the reported search, of which eight represented the best evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results of these papers are tabulated. We acknowledge the limited evidence in this very specific field of cardiac surgery. Due to their pleiotropic effects, including anti-inflammatory properties, there has been speculation that statins could reduce and delay the degeneration and calcification of aortic bioprosthetic valves. Mainly, it was extrapolation of the recently discovered molecular similarities between atherosclerosis and native aortic valve stenosis (AS), with some evidence that statins may slow the progression of native aortic valve calcific degeneration, and the potential harmful impact of atherosclerotic risk factors on the development of native AS. Several studies have been conducted to evaluate the impact of hyperlipidemia and serum cholesterol levels on structural valve deterioration (SVD). Indeed, two studies suggested hyperlipidemia was a risk factor for SVD and correlated reoperation, from which one case-control study based on first-generation biological valves without specific anti-calcification treatment, while three - more convincing by number of patients observed and design of the study - reported contrary results. The other three studies focused on statin treatment in patients after aortic biological valve replacement. Two studies confirmed beneficial effects of statin therapy on valve hemodynamics or inflammatory damage in vivo, but another study, with significantly greater patients series, found lipid-lowering therapy futile in this clinical aspect. Currently, studies and their results are discordant, but statin therapy appears insufficient to result in better clinical outcomes. We conclude that even though the data is conflicting, statin therapy does not prevent SVD of bioprosthetic valves in the aortic position.
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