Two Views on Plaque Rupture

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HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 27, No. 4Two Views on Plaque Rupture Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBTwo Views on Plaque Rupture Göran K. Hansson and Donald D. Heistad Göran K. HanssonGöran K. Hansson From the Center for Molecular Medicine (G.K.H.), Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; and the University of Iowa Carver College of Medicine and VA Medical Center (D.D.H.), Iowa City, Ia. Search for more papers by this author and Donald D. HeistadDonald D. Heistad From the Center for Molecular Medicine (G.K.H.), Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; and the University of Iowa Carver College of Medicine and VA Medical Center (D.D.H.), Iowa City, Ia. Search for more papers by this author Originally published1 Apr 2007https://doi.org/10.1161/01.ATV.0000261344.03489.0cArteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:697Plaque rupture probably is the most important cause of myocardial infarction. Plaque rupture is thought to be precipitated by proteases that attack a weakened fibrous cap overlying an inflamed atherosclerotic plaque. Obviously, plaque rupture is of major interest for atherosclerosis researchers and a major target for development of therapy in the pharmaceutical and biotechnology industries.See pages 705 and 714There is an urgent need for good models to study plaque rupture in our laboratories. Studies of gene-targeted mice that model atherosclerosis in humans have led to in-depth understanding regarding the initiation and progression of atherosclerosis. In contrast, studies of plaque activation, rupture, and thrombosis have been hampered by a paucity of animal models. Histopathologic analyses of human lesions, largely from autopsy material, have provided important data on cellular properties and histochemical composition of ruptured plaques. These data are of great importance, but they cannot substitute for experimental models that permit investigators to intervene in the pathological process in a controlled fashion.In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Christopher Jackson and his colleagues review their development of a mouse model for plaque instability and rupture.1 They have found that the brachiocephalic artery (also known as the innominate artery) of hypercholesterolemic mice contains atherosclerotic plaques with histopathologic features that are suggestive of plaque instability and, in some cases, overt rupture. They have presented their evidence for plaque instability and rupture at this site in a series of original articles published in ATVB and elsewhere, and now summarize their findings in a Brief Review. They argue that plaques in mice by necessity differ from those in humans and propose a new set of criteria to define plaque rupture in mice.Back-to-back with the article by Jackson et al, we publish another Brief Review, which presents a different point of view on the topic.2 The authors, Stephen Schwartz and his colleagues, use their experience from analysis of human lesions to assess the evidence for plaque rupture in mouse models. In their Brief Review, they question the histopathologic criteria used for identifying plaque rupture in mice and criticize the interpretation of “buried caps” as indirect evidence for previous plaque ruptures. They point out that different strains of mice seem to develop different lesion phenotypes in the brachiocephalic artery and emphasize the need for further studies of genes associated with atherosclerosis.These two Brief Reviews reflect the current need for models of plaque rupture and the interest in the cardiovascular community to develop and evaluate such models. They differ in their approach and arrive at contrasting conclusions. The Editors of ATVB do not wish to censor the ongoing debate by providing space for only one view on plaque rupture. By publishing the Brief Reviews back-to-back, and by providing the authors with an opportunity to respond to the other Brief Review in a Letter to the Editor,3,4 we give the readers of ATVB the opportunity to judge for themselves the state of the art. We hope that the exchange of views will stimulate additional studies in this important area of research.See pages 969 and 973DisclosuresNone.FootnotesCorrespondence to Göran K. Hansson, Center for Molecular Medicine L8:03, Karolinska Hospital, SE-171 76, Stockholm, Sweden. E-mail [email protected] References 1 Jackson CL, Bennett MR, Biessen EAB, Johnson JL, Krams R. Assessment of unstable atherosclerosis in mice. Arterioscler Thromb Vasc Biol. 2007; 27: 714–720.LinkGoogle Scholar2 Schwartz SM, Galis ZS, Rosenfeld ME, Falk E. Plaque rupture in humans and mice. Arterioscler Thromb Vasc Biol. 2007; 27: 705–713.LinkGoogle Scholar3 Falk E, Schwartz SM, Galis ZS, Rosenfeld ME. Putative murine models of plaque rupture. Arterioscler Thromb Vasc Biol. 2007; 27: 969–972.LinkGoogle Scholar4 Jackson CL. Defining and defending murine models of plaque rupture. Arterioscler Thromb Vasc Biol. 2007; 27: 973.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited ByChen Y, Huang A, Kyaw T, Bobik A and Peter K (2016) Atherosclerotic Plaque Rupture, Arteriosclerosis, Thrombosis, and Vascular Biology, 36:8, (e63-e72), Online publication date: 1-Aug-2016. Heiden K, Hoogendoorn A, Daemen M and Gijsen F (2018) Animal models for plaque rupture: a biomechanical assessment, Thrombosis and Haemostasis, 10.1160/th15-07-0614, 115:03, (501-508), . Riou L, Broisat A, Ghezzi C, Finet G, Rioufol G, Gharib A, Pettigrew R and Ohayon J (2014) Effects of mechanical properties and atherosclerotic artery size on biomechanical plaque disruption – Mouse vs. human, Journal of Biomechanics, 10.1016/j.jbiomech.2014.01.020, 47:4, (765-772), Online publication date: 1-Mar-2014. Campbell I, Weiss D, Suever J, Virmani R, Veneziani A, Vito R, Oshinski J and Taylor W (2013) Biomechanical modeling and morphology analysis indicates plaque rupture due to mechanical failure unlikely in atherosclerosis-prone mice, American Journal of Physiology-Heart and Circulatory Physiology, 10.1152/ajpheart.00620.2012, 304:3, (H473-H486), Online publication date: 1-Feb-2013. McNeill E, Channon K and Greaves D (2010) Inflammatory cell recruitment in cardiovascular disease: murine models and potential clinical applications, Clinical Science, 10.1042/CS20090488, 118:11, (641-655), Online publication date: 1-Jun-2010. April 2007Vol 27, Issue 4 Advertisement Article InformationMetrics https://doi.org/10.1161/01.ATV.0000261344.03489.0cPMID: 17377145 Originally publishedApril 1, 2007 PDF download Advertisement