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Electronic Comments to:
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Electronic comments posted:
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Efstratios Apostolakis Cardiothoracic Surgery Department of University Hospital of Patras, 22500 Rion Patras, Greece, Ioanna Koniari
stratisapostolakis{at}yahoo.gr Efstratios Apostolakis, et al.
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Interactive CardioVascular and Thoracic Surgery 2008,
doi:10.1510/icvts.2008.178038A © 2008 European Association of Cardio-Thoracic Surgery There is no doubt that despite the controversial conclusions of your review [1], statins contribute to the deceleration of atherosclerosis of the stenotic aortic valve; fact that has been proved by various experimental studies [2]. Besides, early results of experimental trials in our department support the beneficial effect of statins, while we strongly believe that additional future randomized trials will confirm the above findings. However, future studies in order to be reliable should primarily examine the comparative deceleration of atherosclerosis in different subgroups, based on the patient lipid profile before the therapy initiation. Secondly, an 'objective' method should be applied concerning the 'quantitative measurement' of this deceleration. It is notable that the anti-inflammatory action of statins – as it is reported by the reduction of IL - 6 and CRP levels respectively - contributes to the deceleration of valve sclerosis, independently of their corresponding impact on serum lipids [3]. On the other side, it has been demonstrated that statins induce the angiogenesis, and as a consequence, statins contribute to the increase of the atherosclerotic plaque [4]. But if this beneficial action of statins will be supported by a great number of randomized trials in the future, what should we do? Could we administer a statin as an agent that slows the progression of a stenotic aortic valve in elderly people? Such an indication would be meaningful in selective cases, such as patients with type II hypercholesterolemia or with coronary artery disease; while in patients with normal cholesterol and LDL levels there is no significant difference concerning the velocity of valvular aortic sclerosis progression. However, the limitation of several studies is that their results are not being evaluated according to the hypercholesterolemic subgroups of the whole number of patients [1]. In conclusion, taking into consideration the low incidence of reported complications as well as the great cost concerning the prevention of CAD - that fluctuates from €6700 up to €11400 [5] - we should give the green light concerning the administration of statins only in selective cases of aortic valve stenosis. References [1] Tourmousoglou C, Lalos S, Psarros T. Do statins slow the progression of aortic valve stenosis? Interact CardioVasc Thorac Surg doi:10.1510/icvts.2008.178038. [2] Rajamannan N, Subramaniam M, Caira F, Stock S, Spelsberg T. Atorvastatin inhibits hypercholesterolemia-induced calcification in the aortic valves via the Lrp5 receptor pathway. Circulation 2005;112:I229–234. [3] Libby P, Ridker P, Maseri A. Inflammation and atherosclerosis. Circulation 2002;105:1135-1143. [4] Urbich C, Dembach E, Zeiher A, Dimmeler S. Double edged role of statins in angiogenesis signaling. Circ Res 2002;90:737-744. [5] Gaziano M, Manson J, Ridker P. Primary and secondary prevention of coronary heart disease. In: Zipes D, Libby P, Bonow R, Braunwald E, editors. Braunwald’s Heart Disease, 7th Ed, Elsevier Saunders, 2005:1068. |
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