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Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow

Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow Letter to the Editor Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow Masafumi Kuzuya, Takeshi Sasaki In Response: thrombotic occlusion of the artery at the site of the presumed The criticism of Falk et al is based on the lack of evidence rupture. These events observed in the Sasaki model appear to be of consecutive events in the Sasaki model : plaque break- analogous to the events in some parts of human plaque rupture. down first, then thrombosis formation. As cited by Falk et al, Obviously, this model does not completely reproduce human we have previously demonstrated that the simultaneous treat- plaque rupture, the final event in a long and complex pathophys- ment of ligation and cuff placement in the mouse carotid iological process. However, we should take advantage of bene- artery induced occlusive thrombosis which was accompanied ficial parts in this incomplete model, and should also avoid with endothelial cell damage in wild-type mice. Falk et al rejecting animal models simply because they do not generate may speculate that thrombus formation in our new rupture human-like lesions, as described in the editorial by Jackson. model was also mediated through the combined application- Finally, we believe that the plaque vulnerability and induced endothelial damage but not through plaque break- rupture in the Sasaki model partially overlap with human down, or that plaque disruption and thrombus formation may disease, and improve several disadvantages in previous mod- occur independently. We cannot neglect the possibility that els of plaque rupture. This model can be used as a useful plaque disruption (rupture) may not always be necessary for model of some aspects of human plaque rupture until an occlusive thrombus formation in the Sasaki model, although animal model with ideal features of human plaque rupture we clearly demonstrated the association of neointima cracks without the need for artificial manipulations is developed. with the thrombus formation. To demonstrate the direct relationship between plaque breakdown and thrombus forma- tion, a careful time course study is needed. However, it is Disclosures very difficult to clarify the time course of plaque disruption None. and thrombosis formation, because these two events seem to generate at almost the same time. Fibrous cap, which was References stained with smooth muscle cell-marker, was detected in the 1. Sasaki T, Kuzuya M, Nakamura K, Cheng XW, Shibata T, Sato K, Iguchi most of the neointima lesions, and cracks were observed at A. A simple method of plaque rupture induction in apolipoprotein the fibrous cap region, although there was no necrotic core in E-deficient mice. Arterioscler Thromb Vasc Biol. 2006;26:1304–1309. the lesions of Sasaki model. Nevertheless, we believe that 2. Sasaki T, Kuzuya M, Cheng XW, Nakamura K, Tamaya-Mori N, Maeda K, Kanda S, Koike T, Sato K, Iguchi A. A novel model of occlusive our model is still useful for investigating the pathophysiolog- thrombus formation in mice. Lab Invest. 2004;84:1526–1532. ical mechanisms underlying the development of the vulnera- 3. Jackson CL. Ruptures of delight? A new mouse model of plaque rupture. ble lesion and plaque rupture of humans, because this model Arterioscler Thromb Vasc Biol. 2006;26:1191–1192. represents similar features observed during the process of 4. Cullen P, Baetta R, Bellosta S, Bernini F, Chinetti G, Cignarella A, von Eckardstein A, Exley A, Goddard M, Hofker M, Hurt-Camejo E, Kanters human plaque rupture: a reduction of collagen content, the E, Kovanen P, Lorkowski S, McPheat W, Pentikainen M, Rauterberg J, presence of matrix metalloproteinases, an increase in apoptot- Ritchie A, Staels B, Weitkamp B, de Winther M; MAFAPS Consortium. ic cells and inflammatory cells in the plaque lesions before Rupture of the atherosclerotic plaque: does a good animal model exist? the thrombosis formation, followed by neointima cracks and Arterioscler Thromb Vasc Biol. 2003;23:535–542. From the Department of Geriatrics (M.K.), Nagoya University Graduate School of Medicine, and the Department of Anatomy and Neuroscience (T.S.), Hamamatsu University School of Medicine, Hamamatsu, Japan. Correspondence to Masafumi Kuzuya, Department of Geriatrics, Nagoya University Graduate School of Medicine, 65 Tsurama-Cho, Showa-Ku, Nagoya, Japan. (Arterioscler Thromb Vasc Biol. 2007;27:252.) © 2006 American Heart Association, Inc. Arterioscler Thromb Vasc Biol. is available at http://www.atvbaha.org DOI: 10.1161/01.ATV.0000249619.75202.1e http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis, Thrombosis, and Vascular Biology Wolters Kluwer Health

Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow

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ISSN
1079-5642
eISSN
1524-4636
DOI
10.1161/01.ATV.0000249619.75202.1e

Abstract

Letter to the Editor Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow Masafumi Kuzuya, Takeshi Sasaki In Response: thrombotic occlusion of the artery at the site of the presumed The criticism of Falk et al is based on the lack of evidence rupture. These events observed in the Sasaki model appear to be of consecutive events in the Sasaki model : plaque break- analogous to the events in some parts of human plaque rupture. down first, then thrombosis formation. As cited by Falk et al, Obviously, this model does not completely reproduce human we have previously demonstrated that the simultaneous treat- plaque rupture, the final event in a long and complex pathophys- ment of ligation and cuff placement in the mouse carotid iological process. However, we should take advantage of bene- artery induced occlusive thrombosis which was accompanied ficial parts in this incomplete model, and should also avoid with endothelial cell damage in wild-type mice. Falk et al rejecting animal models simply because they do not generate may speculate that thrombus formation in our new rupture human-like lesions, as described in the editorial by Jackson. model was also mediated through the combined application- Finally, we believe that the plaque vulnerability and induced endothelial damage but not through plaque break- rupture in the Sasaki model partially overlap with human down, or that plaque disruption and thrombus formation may disease, and improve several disadvantages in previous mod- occur independently. We cannot neglect the possibility that els of plaque rupture. This model can be used as a useful plaque disruption (rupture) may not always be necessary for model of some aspects of human plaque rupture until an occlusive thrombus formation in the Sasaki model, although animal model with ideal features of human plaque rupture we clearly demonstrated the association of neointima cracks without the need for artificial manipulations is developed. with the thrombus formation. To demonstrate the direct relationship between plaque breakdown and thrombus forma- tion, a careful time course study is needed. However, it is Disclosures very difficult to clarify the time course of plaque disruption None. and thrombosis formation, because these two events seem to generate at almost the same time. Fibrous cap, which was References stained with smooth muscle cell-marker, was detected in the 1. Sasaki T, Kuzuya M, Nakamura K, Cheng XW, Shibata T, Sato K, Iguchi most of the neointima lesions, and cracks were observed at A. A simple method of plaque rupture induction in apolipoprotein the fibrous cap region, although there was no necrotic core in E-deficient mice. Arterioscler Thromb Vasc Biol. 2006;26:1304–1309. the lesions of Sasaki model. Nevertheless, we believe that 2. Sasaki T, Kuzuya M, Cheng XW, Nakamura K, Tamaya-Mori N, Maeda K, Kanda S, Koike T, Sato K, Iguchi A. A novel model of occlusive our model is still useful for investigating the pathophysiolog- thrombus formation in mice. Lab Invest. 2004;84:1526–1532. ical mechanisms underlying the development of the vulnera- 3. Jackson CL. Ruptures of delight? A new mouse model of plaque rupture. ble lesion and plaque rupture of humans, because this model Arterioscler Thromb Vasc Biol. 2006;26:1191–1192. represents similar features observed during the process of 4. Cullen P, Baetta R, Bellosta S, Bernini F, Chinetti G, Cignarella A, von Eckardstein A, Exley A, Goddard M, Hofker M, Hurt-Camejo E, Kanters human plaque rupture: a reduction of collagen content, the E, Kovanen P, Lorkowski S, McPheat W, Pentikainen M, Rauterberg J, presence of matrix metalloproteinases, an increase in apoptot- Ritchie A, Staels B, Weitkamp B, de Winther M; MAFAPS Consortium. ic cells and inflammatory cells in the plaque lesions before Rupture of the atherosclerotic plaque: does a good animal model exist? the thrombosis formation, followed by neointima cracks and Arterioscler Thromb Vasc Biol. 2003;23:535–542. From the Department of Geriatrics (M.K.), Nagoya University Graduate School of Medicine, and the Department of Anatomy and Neuroscience (T.S.), Hamamatsu University School of Medicine, Hamamatsu, Japan. Correspondence to Masafumi Kuzuya, Department of Geriatrics, Nagoya University Graduate School of Medicine, 65 Tsurama-Cho, Showa-Ku, Nagoya, Japan. (Arterioscler Thromb Vasc Biol. 2007;27:252.) © 2006 American Heart Association, Inc. Arterioscler Thromb Vasc Biol. is available at http://www.atvbaha.org DOI: 10.1161/01.ATV.0000249619.75202.1e

Journal

Arteriosclerosis, Thrombosis, and Vascular BiologyWolters Kluwer Health

Published: Jan 1, 2007

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