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HomeCirculationVol. 137, No. 6Letter by Koh Regarding Article, “Effect of Rosuvastatin on Carotid Intima-Media Thickness in Children With Heterozygous Familial Hypercholesterolemia: The CHARON Study (Hypercholesterolemia in Children and Adolescents Taking Rosuvastatin Open Label)” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Koh Regarding Article, “Effect of Rosuvastatin on Carotid Intima-Media Thickness in Children With Heterozygous Familial Hypercholesterolemia: The CHARON Study (Hypercholesterolemia in Children and Adolescents Taking Rosuvastatin Open Label)” Kwang Kon Koh, MD, PhD Kwang Kon KohKwang Kon Koh Department of Cardiovascular Medicine, Heart Center, Gachon University, Gil Medical Center, and Gachon Cardiovascular Research Institute, Incheon, Korea. Search for more papers by this author Originally published6 Feb 2018https://doi.org/10.1161/CIRCULATIONAHA.117.030934Circulation. 2018;137:639–640To the Editor:Dr Braamskamp and colleagues1 assessed the effect of 2-year treatment with rosuvastatin on carotid intima-media thickness (IMT) in children with heterozygous familial hypercholesterolemia. In children with heterozygous familial hypercholesterolemia who were ≥6 years of age, carotid IMT was significantly greater at baseline in comparison with unaffected siblings. Rosuvastatin treatment for 2 years resulted in significantly less progression of increased carotid IMT in children with heterozygous familial hypercholesterolemia than in untreated unaffected siblings. As a result, no difference in carotid IMT could be detected between the 2 groups after 2 years of rosuvastatin.The combined thickness of carotid IMT is associated with the prevalence of cardiovascular disease. Increases in the thickness of carotid IMT are directly associated with an increased risk of myocardial infarction and stroke in older adults without a history of cardiovascular disease.2 Measuring carotid IMT is noninvasive and can be repeated, and thus it is widely used as a surrogate marker of atherosclerosis and cardiovascular events. Therefore, the present study clearly demonstrated that early initiation of statin treatment will prevent the rapid development of atherosclerosis and cardiovascular events. They assumed it was because of low-density lipoprotein (LDL)–cholesterol reduction.Most believe that statins reduce cardiovascular risk by lowering LDL-cholesterol levels, but some believe that statins reduce risk through multiple actions called pleiotropic effects.3,4 Statins may exert cardiovascular protective effects that are independent of LDL-cholesterol lowering. The relative contributions of statin pleiotropy to clinical outcomes, however, remain a matter of debate and are hard to quantify despite the many randomized controlled trials denying pleiotropic effects, because the degree of isoprenoid inhibition by statins correlates to some extent with the amount of LDL-cholesterol reduction. Indeed, this hypothesis is difficult to prove despite its clinical importance. This issue has been disputed recently. Namely, the primary mechanism of its effect is to reduce LDL-cholesterol and atherogenic lipoproteins. Recent metaregression analysis showed that lower achieved LDL-cholesterol levels were associated with lower rates of major coronary events. Statins are like other LDL-lowering agents and are not unique except in LDL-lowering potency.5However, statins alone are sometimes not sufficient to lower LDL-cholesterol levels in children with heterozygous familial hypercholesterolemia. Combination therapy with statins and other classes of drugs such as ezetimibe, PCSK9 (proprotein convertase subtilisin kexin 9) inhibitors, inclisiran, or angiopoietin-like 3 antisense oligonucleotides is a promising approach to maximize therapeutic benefit while reducing the inherent metabolic risks of potent statins.Kwang Kon Koh, MD, PhDDisclosuresDr Koh holds certificate of patent no. 10-1579656 (pravastatin + valsartan).FootnotesCirculation is available at http://circ.ahajournals.org.
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