2016
DOI: 10.1016/j.atherosclerosis.2016.01.023
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The effect of statins on valve function and calcification in aortic stenosis: A meta-analysis

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Cited by 60 publications
(36 citation statements)
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“…Finally, plaque stabilization in coronary atherosclerotic lesions is the major mechanism responsible for the beneficial effects of statins, but plaque rupture is not the cause of symptoms in CAVD and not a mechanism for CAVD progression. 29,30 The inhibition of PCSK9 and the maximally increasing LDLR as a result probably have synergistic advantages. The LDLR contributes to the clearance of atherogenic lipoproteins other than LDL-C, such as intermediate-density lipoproteins and remnant particles, the latter via APoE affinity.…”
Section: Contribution Of Pcsk9 To Cavd By Modulating Lipid Levelsmentioning
confidence: 99%
“…Finally, plaque stabilization in coronary atherosclerotic lesions is the major mechanism responsible for the beneficial effects of statins, but plaque rupture is not the cause of symptoms in CAVD and not a mechanism for CAVD progression. 29,30 The inhibition of PCSK9 and the maximally increasing LDLR as a result probably have synergistic advantages. The LDLR contributes to the clearance of atherogenic lipoproteins other than LDL-C, such as intermediate-density lipoproteins and remnant particles, the latter via APoE affinity.…”
Section: Contribution Of Pcsk9 To Cavd By Modulating Lipid Levelsmentioning
confidence: 99%
“…46 Al gengustu einkenni ósaeðarlokuþrengsla eru maeði, hjartaöng og yfirlið en auk þess geta hjartsláttartruflanir komið fyrir og jafn vel valdið skyndidauða. 6,7 Lyfjameðferð hefur lítil áhrif á gang sjúkdómsins 8 og þegar einkenna hjartabilunar verður vart versna lífslíkur einstaklinga hratt. 4 Hefðbundin meðferð er opin hjarta aðgerð þar sem lokunni er skipt út; ýmist fyrir ólífraena loku úr hertu kolefni eða lífraena loku úr svíni eða gollurshúsi kálfs.…”
Section: Inngangurunclassified
“…This lack of association to diet and the complexing of molecules with Lp(a) presents therapeutic challenges as well as opportunities. Firm evidence supports the finding that statins increase receptor-mediated uptake of low-density lipoprotein, but there is no clear evidence that statins reduce Lp(a) or work as an effective therapy for cardiovascular calcification and aortic stenosis 5. This suggests mechanistic differences between low-density lipoprotein and Lp(a) metabolism, along with the conundrum of how circulating Lp(a) interacts with and mediates its effects in cardiovascular cells.…”
mentioning
confidence: 99%