Letter by Williams and Tabas Regarding Article “Atherosclerosis 2005: Recent Discoveries and Novel Hypotheses”
2006; Lippincott Williams & Wilkins; Volume: 113; Issue: 21 Linguagem: Inglês
10.1161/circulationaha.105.606962
ISSN1524-4539
AutoresKevin Jon Williams, Ira Tabas,
Tópico(s)Diabetes, Cardiovascular Risks, and Lipoproteins
ResumoHomeCirculationVol. 113, No. 21Letter by Williams and Tabas Regarding Article “Atherosclerosis 2005: Recent Discoveries and Novel Hypotheses” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Williams and Tabas Regarding Article “Atherosclerosis 2005: Recent Discoveries and Novel Hypotheses” Kevin Jon Williams, MD Ira Tabas, MD, PhD Kevin Jon WilliamsKevin Jon Williams Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pa Search for more papers by this author Ira TabasIra Tabas Columbia University, College of Physicians and Surgeons, New York, NY Search for more papers by this author Originally published30 May 2006https://doi.org/10.1161/CIRCULATIONAHA.105.606962Circulation. 2006;113:e782To the Editor:Although the ideas put forth by Goldschmidt-Clermont et al1 are intriguing, we believe that their article underplays a large body of work, much of it from the past 2 decades, that has clarified how normal arteries become atherosclerotic.2–5 Low-density lipoprotein (LDL) is not mysteriously injurious. Instead, as experimentally demonstrated by Skålén et al,4 LDL causes harm only if it becomes retained, or trapped, within the arterial wall. Moreover, without LDL retention, atherosclerosis does not develop, even if other known risk factors are present. There are no known circumstances in humans or in animal models in which atherosclerosis is caused by stem cell defects, inflammation, senescence, or endothelial injury per se in the absence of unhealthy levels of LDL or related particles in plasma (meaning above a therapeutically attainable goal of ∼70 mg/dL).2 Retained LDL provokes a series of responses in the arterial wall that accounts for all known features of this disease, including the development of the lipid-rich vulnerable plaque. The therapeutic implications of these hard-won insights are clear: We should lower unhealthy plasma levels of LDL and modify other conventional risk factors, and we should enhance “reverse” lipid transport out of plaques. Benefits from these approaches have been demonstrated in animal models and in humans.5 In contrast, clinical trials of antioxidants, antiinflammatory agents, and antibacterials have shown no benefits in this disease to date,5 and the potential utility of stem cells remains highly speculative. We agree with Goldschmidt-Clermont et al1 that there is a need for further study and therapeutic improvements,5 but it is important to emphasize that our field already has robust, proven remedies that are based on a well-tested understanding of the pathogenesis of this major killer.Sources of FundingDr Williams was supported by research grants NIH HL56984 and NIH HL73898. Dr Tabas was supported by research grant NIH HL56984.DisclosuresDr Williams is the inventor of a number of patents on the use of phospholipid liposomes to promote reverse lipid transport in vivo (now held by Pfizer). Dr Williams received honoraria as a member of the ARA Research Awards Committee, Pfizer. Dr Tabas received honoraria from Merck and Schering-Plough and is a consultant for Merck.1 Goldschmidt-Clermont PJ, Creager MA, Losordo DW, Lam GKW, Wassef M, Dzau VJ. Atherosclerosis 2005: recent discoveries and novel hypotheses. Circulation. 2005; 112: 3348–3353.LinkGoogle Scholar2 Williams KJ, Tabas I. The response-to-retention hypothesis of early atherogenesis. Arterioscler Thromb Vasc Biol. 1995; 15: 551–561.CrossrefMedlineGoogle Scholar3 Hurt-Camejo E, Olsson U, Wiklund O, Bondjers G, Camejo G. Cellular consequences of the association of apoB lipoproteins with proteoglycans: potential contribution to atherogenesis. Arterioscler Thromb Vasc Biol. 1997; 17: 1011–1017.CrossrefMedlineGoogle Scholar4 Skålén K, Gustafsson M, Rydberg EK, Hultén LM, Wiklund O, Innerarity TL, Borén J. Subendothelial retention of atherogenic lipoproteins in early atherosclerosis. Nature. 2002; 417: 750–754.CrossrefMedlineGoogle Scholar5 Williams KJ, Tabas I. Lipoprotein retention and clues for atheroma regression. Arterioscler Thromb Vasc Biol. 2005; 25: 1536–1540.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Ishida K, Morimoto S, Horiuchi S, Kimura M, Ishikawa T, Kimura S, Yamashita K, Takano N, Seki Y, Bokuda K, Sasaki N, Watanabe D and Ichihara A (2021) Comparison of the usefulness of the cardio-ankle vascular index and augmentation index as an index of arteriosclerosis in patients with essential hypertension, Hypertension Research, 10.1038/s41440-021-00823-x, 45:3, (455-463), Online publication date: 1-Mar-2022. Terentes-Printzios D and Vlachopoulos C (2022) Arterial stiffness for cardiovascular risk stratification in clinical practice Textbook of Arterial Stiffness and Pulsatile Hemodynamics in Health and Disease, 10.1016/B978-0-323-91391-1.00033-9, (503-525), . 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