Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions

Zenshiro Onouchi; Akiko Hamaoka-Okamoto; Chinatsu Suzuki; Kenji Hamaoka

doi:doi:10.11648/j.ccr.20210501.12

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Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions

Zenshiro Onouchi, Akiko Hamaoka-Okamoto, Chinatsu Suzuki, Kenji Hamaoka

Published in Cardiology and Cardiovascular Research (Volume 5, Issue 1)

Received: 21 November 2020 Accepted: 25 December 2020 Published: 15 January 2021

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Abstract

Backgrounds. The mechanism causing coronary artery lesions in Kawasaki disease (KD) has not yet been fully clarified. Objective. We hypothesized that the main coronary artery (MCA) segment perfused by the vasa vasorum (VV) arose from the atrial and ventricular branches of peripheral coronary arteries in the myocardium (Type 1 VV externa) is more prone to aneurysm formation than that perfused by Type 2 VV originated from the ostium. Methods and Results. We reviewed the coronary angiography and two-dimensional echocardiogram (2DE) data of KD patients in our hospital and measured the distances from the left coronary ostium to the proximal point of the aneurysm in the left MCA (D1) and to the MCA bifurcation (D2). We found that the ratio of the distances (D1/D2) was negatively correlated with the patients’ age of KD onset, indicating that longitudinal extension of the left MCA aneurysms coincided with the development of Type 1 VV externa. We performed a literature review of KD cases with extracardiac aneurysms and found that 15 patients also had giant aneurysms in the MCA. Also, 8 of 9 extracardiac aneurysm cases whose clear 2DE images were available in the reports, the giant MCA aneurysms seemed to have developed at positions immediately adjacent to the ostium. We assume that the giant coronary aneurysms might be a consequence of the coincidence of aneurysms in the MCA segments perfused by Type 1 and 2 VV externas and reflect a severe inflammation where Type 2 VV externa which is less susceptible to blood flow reduction than Type 1 VV externa is affected. Conclusions. Vasculitis in VV externa with the unique structure originating from and distributing most richly across coronary arteries might induce a vicious circle of hypoperfusion of VV externa and reduced coronary blood flow.

Published in	Cardiology and Cardiovascular Research (Volume 5, Issue 1)
DOI	10.11648/j.ccr.20210501.12
Page(s)	7-15
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2021. Published by Science Publishing Group

Keywords

Coronary Artery Aneurysm, Coronary Artery Ischemia, Coronary Blood Flow, Coronary Vasa Vasorum, Endothelial Dysfunction

References

[1]	Fujiwara H, Hamashima Y. Pathology of the heart in Kawasaki disease. Pediatrics 1978; 61: 100-107.
[2]	Burns JC, Glodé MP. Kawasaki disease. Lancet 2004; 364: 533-544.
[3]	Kato H, Sugimura T, Akagi T, Sano N, Hashino K, Maeno Y, et al. Long-term consequences of Kawasaki disease. A 10- to 21-year follow-up study of 594 patients. Circulation 1996; 94: 1379-1385.
[4]	Amano S, Hazama F, Hamashima Y. Pathology of Kawasaki disease. I. Pathology and morphogenesis of the vascular changes. Jpn Circulation J 1979; 43: 633-643.
[5]	Terai M, Kohno Y, Niwa K, Umemiya T, Mikata A, Nakajima H. Imbalance among circulating T cell subsets and staining from HLA-DR antigen in coronary endothelial cells in Kawasaki disease. [Arerugi], Jpn J Allergol 1987; 36: 394-403.
[6]	Sato N, Sagawa K, Sasaguri Y, Inoue O, Kato H. Immunopathology and cytokine detection in the skin lesions of patients with Kawasaki disease. J Pediatr 1993; 122: 198-203.
[7]	Nagata, S, Yamashiro Y, Maeda M, Ohtsuka Y, Yabuta K. Immuno- histochemical studies on small intestinal mucosa in Kawasaki disease. Pediatr Res 1993; 33: 557-563.
[8]	Terai M, Honda T, Yasukawa K, Higashi K, Kohno Y. Prognostic impact of vascular leakage in acute Kawasaki disease. Circulation 2003; 108: 325-330.
[9]	Yasukawa K, Terai M, Shulman ST, Toyozaki T, Yajima S, Kohno Y, et al. Systematic production of vascular endothelial growth factor and fms-like tyrosin-kinase1 receptor in acute Kawasaki disease. Circulation 2002; 105: 766-769.
[10]	Senzaki H, Kobayashi T, Nagasaka H, Nakano H, Kyo S, Yokote Y, et al. Plasminogen activator inhibitor-1 in patients with Kawasaki disease: diagnostic value for the prediction of coronary artery lesion and implication for a new mode of therapy. Pediatr Res 2003; 53: 983-988.
[11]	Furui J, Ishii M, Ikeda H, Muta H, Egami K, Sugahara Y, et al. Soluble forms of the selectin family in children with Kawasaki disease: predilection for coronary lesions. Acta Pediatr 2002; 91: 1183-1188.
[12]	Kariyazono H, Ohno T, Khajoee V, Ihara K, Kusuhara K, Kinukawa N, et al. Association of vascular endothelial growth factor (VEGF) and VEGF receptor polymorphisms with coronary artery lesions of Kawasaki disease. Pediatr Res 2004; 56: 953-959.
[13]	Furuno K, Takada H, Yamamoto K, Ikeda K, Ohno T, Khajoee V, et al. Tissue inhibitor of metalloproteinase 2 and coronary artery lesions in Kawasaki disease. J Pediatr 2007; 151: 155-160.
[14]	Hamamichi Y, Ichida F, Yu X, Hirono K, Uese KI, Hashimoto I, et al. Neutrophil and mononuclear cells express vascular endothelial growth factor in acute Kawasaki disease: its possible role in progression of coronary artery lesions. Pediatr Res 2001; 49: 74-80.
[15]	Suzuki H, Noda E, Miyawaki M, Takeuchi T, Uemura S, Koike M. Serum levels of neutrophil activation cytokines in Kawasaki disease. Pediatr Int 2001; 43: 115-119.
[16]	Onouchi Y, Gunji T, Burns JC, Shimizu C, Newburger JW, Yashiro M, et al. ITPKC functional Polymorphism associated with Kawasaki disease susceptibility and formation of coronary artery aneurysms Nature Genetics 2008; 40: 35-42.
[17]	Onouchi Y, Ozaki K, Burns JC, Shimizu C, Hamada H, Honda T, et al. Common variants in CASP3 confer susceptibility to Kawasaki disease. Hum Mol Genet 2010; 19: 2898-2906.
[18]	Onouchi Y, Ozaki K, Burns JC, Shimizu C, Terai M, Hamada H, et al. A genome-wide association study identified three new risk loci for Kawasaki disease Nature Genetics 2012; 44: 517-521.
[19]	Tanaka K, Onouchi Z, Tomizawa M, Goto M, Kinpara S, Kusunoki T, et al. A study of Kawasaki disease. Part 2. A presentation of an autopsy case and relationship with infantile periarteritis nodosa [Nippon Shonika Gakkai Zasshi], J Jpn Pediatr Soc 1973; 77: 397-411.
[20]	Onouchi Z, Tomizawa N, Goto M, Nakata K, Fukuda M. Cardiac involvement and prognosis in acute mucocutaneous lymph node syndrome Chest 1975; 68: 297-301.
[21]	Booth RF, Martin JF, Honey AC, Hassall DC, Beesley JE, Moncada S. Rapid development of atherosclerotic lesions in the rabbit carotid artery induced by perivascular manipulation. Atherosclerosis 1989; 76: 257-268.
[22]	Barker SG, Tilling LC, Miller GC, Beesley JE, Fleetwood G, Stavri GT, Baskerville PA, Martin JF. The adventitia and atherogenesis: removal initiates intimal proliferation in the rabbit which regresses on generation of a ‘neoadventitia’. Atherosclerosis 1994; 105: 131-144.
[23]	Nakata T, Shionoya S. Vascular lesions due to obstruction of the vasa vasorum. Nature 1966; 212: 1258-1259.
[24]	Martin JF, Booth RFG, Moncada S. Arterial wall hypoxia following hyperfusion through the vasa vasorum is an initial lesion in atherosclerosis. Eur J Clin Invest 1990; 20: 588-592.
[25]	Barker SGE, Talbert A, Cottam S, Baskerville PA, Martin JF. Arterial intimal hyperplasia after occlusion of the adventitial vasa vasorum in the pig. Arterioscler Thromb 1993; 13: 70-77.
[26]	Wilcox JN, Scott NA. Potential role of the adventitia in arteritis and atherosclerosis Int J Cardiol 1996; 54: S21-35.
[27]	Clarke JA. An X-ray microscopic study of the vasa vasorum of normal human coronary arteries. J Anat 1964; 98: 539-543.
[28]	Clarke JA. An X-ray microscopic study of the postnatal development of the vasa vasorum of normal human coronary arteries. Acta Anat (Basel) 1966; 64: 506-516.
[29]	Kwon HM, Sangiorgi G, Ritman EL, McKenna C, Holmes DR Jr, Schwartz RS, et al. Enhanced coronary vasa vasorum neovascularization in experimental hypercholesterolemia. J Clin Invest 1998; 101: 1551-1556.
[30]	Tanaka N, Naoe S, Masuda H, Ueno T. Pathological study of sequelae of Kawasaki disease (MCLS). With special reference to the heart and coronary arterial lesions. Acta Pathol Jpn 1986; 36: 1513-1527.
[31]	Jennette JC. Implications for pathogenesis of patterns of injury in small- and medium-sized-vessel vasculitis. Cleve Clin J Med 2002; 69: S11 33-38.
[32]	Landing BH, Larson EJ. Are infantile periarteritis nodosa with coronary artery involvement and fatal mucocutaneous lymph node syndrome the same? Comparison of 20 patients from North America with patients from Hawaii and Japan. Pediatrics 1977; 59: 651-662.
[33]	Igarashi H, Hatake K, Tomizuka H, Yamada M, Gunji Y, Momoi MY. High serum levels of M-CSF and G-CSF in Kawasaki disease. Br J Haematol 1999; 105: 613-615.
[34]	Xu H, Manivannan A, Jiang HR, Liversidge J, Sharp PF, Forrester JV, et al. Recruitment of IFN-gamma-producing (Th1-like) cells into the inflamed retina in vivo is preferentially regulated by P-selectin glycoprotein ligand 1: P/E-selectin interactions. J Immunol 2004; 172: 3215-3224.
[35]	Rodrigues SF, Granger DN. Role of blood cells in ischemia-reperfusion induced endothelial barrier failure. Cardiovasc Res 2010; 87: 291-299.
[36]	Niwa Y, Sohmiya K. Enhanced neutrophilic functions in mucocutaneous lymph node syndrome, with special reference to the possible role of increased oxygen intermediate generation in the pathogenesis of coronary thromboarteritis. J Pediatr 1984; 104: 56-60.
[37]	Viemann D, Strey A, Janning A, Jurk K, Klimmek K, Vogl T, et al. Myeloid-related proteins 8 and 14 induce a specific inflammatory response in human microvascular endothelial cells. Blood 2005; 105: 2955-2962.
[38]	Furukawa S, Matsubara T, Jujoh K, Yone K, Sugawara T, Sasai K, et al. Peripheral blood monocyte/macrophages and serum tumor necrosis factor in Kawasaki disease. Clin Immunol Immunopathol 1988; 48: 247-251.
[39]	Ritman EL, Lehman A. The dynamic vasa vasorum. Cardiovasc Res 2007; 75: 649-658.
[40]	Scotland RS, Vallance PJ, Ahluwalia A. On the regulation of tone in vasa vasorum. Cardiovasc Res 1999; 41: 237-245.
[41]	Masuda H, Naoe S, Tanaka N. A pathologic study of coronary artery in Kawasaki disease (MCLS): with special reference to morphogenesis of aneurysm [Myakkangaku, J Jpn Coll Angiol] 1981; 21: 899-912.
[42]	Breier G, Albrecht U, Sterrer S, Risau W. Expression of vascular endothelial growth factor during embryonic angiogenesis and endothelial cell differentiation. Development 1992; 114: 521-532.
[43]	Kai H, Kuwahara F, Tokuda K, Shibata R, Kusaba K, Niiyama H, et al. Coexistence of hypercholesterolemia and hypertension impairs adventitial vascularization. Hypertension 2002; 39: 455-459.
[44]	Dvorak HF, Brown LF, Detmar M, Dvorak AM. Vascular permeability factor/vascular endothelial growth factor, microvascular hyperpermeability, and angiogenesis. Am J Pathol 1995; 146: 1029-39.
[45]	Heistad DD, Marcus ML, Martins JB. Effects of neural stimuli on blood flow through vasa vasorum in dogs Circ Res 1979; 45: 615-620.
[46]	Hashimoto Y, Yoshinoya S, Aikawa T, Mitamura T, Miyoshi Y, Muranaka M, et al. Enhanced endothelial cell proliferation in acute Kawasaki disease (muco-cutaneous lymph node syndrome). Pediatr Res 1986; 20: 943-946.
[47]	Sakata K, Kita M, Imanishi J, Onouchi Z, Liu Y, Mitsui Y. Effect of Kawasaki disease on migration of human umbilical vein endothelial cells. Pediatr Res 1995; 38; 501-505.
[48]	Sakata K, Hamaoka K, Ozawa S, Niboshi A, Yahata T, Fujii M, et al. Matrix Metalloproteinase-9 in vascular lesions and endothelial regulation in Kawasaki disease. Circ J 2010; 74: 1670-1675.
[49]	Hotchi M. Pathologic concept of vasculitis. [in Japanese]. Jpn J Clin Med 1985; 43: 2017-2025.
[50]	Onouchi Z. Echocardiographic diagnosis of coronary artery lesions in Kawasaki disease. In: Kawasaki T, Shigematsu I, Hamashima Y, Yanagawa H, Kato H, editors. Kawasaki Disease. Japan: Nankodo Publications, 1988: 178-185.
[51]	Galili O, Herrmann J, Woodrum J, Sattler KJ, Lerman LO, Lerman A. Adventitial vasa vasorum heterogeneity among different vascular beds. J Vasc Surg 2004; 40: 529-535.
[52]	Munro-Faure H. Necrotizing arteritis of the coronary vessels in infancy; case report and review of the literature. Pediatrics 1959; 23: 914-926.
[53]	Amano S, Hazama F, Hamashima Y. Pathology of Kawasaki disease. II. Distribution and incidence of the vascular lesions. Jpn Circulation J 1979; 43: 741-748.
[54]	Naoe S, Asaji A, Takahashi K, Masuda H, Tanaka N. Coronary artery lesions in children. Particular focus to the coronary artery aneurysm. [Byouri to Rinsho], Pathol Clin Med 1988; 6: 184-192.
[55]	Ichinose E. Prognosis of coronary aneurysms due to Kawasaki disease: Search of risk factors using multivariate analyses. [Nippon Shonika Gakkai-Zasshi], J Jpn Pediatr Soc 1985; 89: 1595-1603.
[56]	Ohmochi Y, Onouchi Z, Oda Y, Hamaoka K. Assessment of effects of intravenous dipyridamole on regional myocardial perfusion in children with Kawasaki disease without angiographic evidence of coronary stenosis using positron emission tomography and H2(15)O. Coronary Artery Dis 1995; 6: 555-559.
[57]	Lavi S, Yang EH, Prasad A, Mathew V, Barsness GW, Rihal CS, et al. The interaction between coronary endothelial dysfunction, local oxidative stress, and endogenous nitric oxide in humans. Hypertension 2008; 51: 127-133.
[58]	Onouchi Z, Hamaoka K, Ozawa S, Sakata K, Kiyosawa N, Ito H. Neutropenia in the acute phase of Kawasaki disease and prevention of coronary artery aneurysm. Pediatr Int 2009; 51: 448-452.
[59]	Kalogeris T, Baines CP, Krenz M, Korthuis RJ. Cell biology of ischemia /reperfusion injury. Int Rev Cell Mol Biol 2012; 298: 229-317.
[60]	Huelmann WC, Dubelaar MI. Carnitine requirement of vascular endothelial and smooth muscle cells in imminent ischemia. Mol Cell Biochem 1992; 116: 125-129.
[61]	Pachori AS, Melo LG, Hart MI, Noiseux N Zhang L, Morello F, et al. Hypoxia-regulated therapeutic gene as a preemptive strategy against ischemia/reperfusion tissue injury. Proc Natl Acad Sci U S A 2004; 101: 12282-12287.
[62]	US patent 6630507. (https:/worldwide.espacenet.com/textdoc?
[63]	DB-EPODOC&IDX=US6630507), Hampson Aidan J, Axelrod Julius, Grimaldi Maurizio, “cannabinoids as antioxidants and neuroprotectants”, issued 200310-07.
[64]	Ahmed LA, Salem HA, Attia AS, Agha AM. Pharmacological preconditioning with nicorandil and pioglitazone attenuates myocardial ischemia/reperfusion injury in rats. Eur J Pharmacol 2011; 663: 51-58.

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APA Style

Zenshiro Onouchi, Akiko Hamaoka-Okamoto, Chinatsu Suzuki, Kenji Hamaoka. (2021). Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions. Cardiology and Cardiovascular Research, 5(1), 7-15. https://doi.org/10.11648/j.ccr.20210501.12

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ACS Style

Zenshiro Onouchi; Akiko Hamaoka-Okamoto; Chinatsu Suzuki; Kenji Hamaoka. Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions. Cardiol. Cardiovasc. Res. 2021, 5(1), 7-15. doi: 10.11648/j.ccr.20210501.12

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AMA Style

Zenshiro Onouchi, Akiko Hamaoka-Okamoto, Chinatsu Suzuki, Kenji Hamaoka. Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions. Cardiol Cardiovasc Res. 2021;5(1):7-15. doi: 10.11648/j.ccr.20210501.12

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@article{10.11648/j.ccr.20210501.12,
  author = {Zenshiro Onouchi and Akiko Hamaoka-Okamoto and Chinatsu Suzuki and Kenji Hamaoka},
  title = {Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions},
  journal = {Cardiology and Cardiovascular Research},
  volume = {5},
  number = {1},
  pages = {7-15},
  doi = {10.11648/j.ccr.20210501.12},
  url = {https://doi.org/10.11648/j.ccr.20210501.12},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ccr.20210501.12},
  abstract = {Backgrounds. The mechanism causing coronary artery lesions in Kawasaki disease (KD) has not yet been fully clarified. Objective. We hypothesized that the main coronary artery (MCA) segment perfused by the vasa vasorum (VV) arose from the atrial and ventricular branches of peripheral coronary arteries in the myocardium (Type 1 VV externa) is more prone to aneurysm formation than that perfused by Type 2 VV originated from the ostium. Methods and Results. We reviewed the coronary angiography and two-dimensional echocardiogram (2DE) data of KD patients in our hospital and measured the distances from the left coronary ostium to the proximal point of the aneurysm in the left MCA (D1) and to the MCA bifurcation (D2). We found that the ratio of the distances (D1/D2) was negatively correlated with the patients’ age of KD onset, indicating that longitudinal extension of the left MCA aneurysms coincided with the development of Type 1 VV externa. We performed a literature review of KD cases with extracardiac aneurysms and found that 15 patients also had giant aneurysms in the MCA. Also, 8 of 9 extracardiac aneurysm cases whose clear 2DE images were available in the reports, the giant MCA aneurysms seemed to have developed at positions immediately adjacent to the ostium. We assume that the giant coronary aneurysms might be a consequence of the coincidence of aneurysms in the MCA segments perfused by Type 1 and 2 VV externas and reflect a severe inflammation where Type 2 VV externa which is less susceptible to blood flow reduction than Type 1 VV externa is affected. Conclusions. Vasculitis in VV externa with the unique structure originating from and distributing most richly across coronary arteries might induce a vicious circle of hypoperfusion of VV externa and reduced coronary blood flow.},
 year = {2021}
}

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TY  - JOUR
T1  - Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions
AU  - Zenshiro Onouchi
AU  - Akiko Hamaoka-Okamoto
AU  - Chinatsu Suzuki
AU  - Kenji Hamaoka
Y1  - 2021/01/15
PY  - 2021
N1  - https://doi.org/10.11648/j.ccr.20210501.12
DO  - 10.11648/j.ccr.20210501.12
T2  - Cardiology and Cardiovascular Research
JF  - Cardiology and Cardiovascular Research
JO  - Cardiology and Cardiovascular Research
SP  - 7
EP  - 15
PB  - Science Publishing Group
SN  - 2578-8914
UR  - https://doi.org/10.11648/j.ccr.20210501.12
AB  - Backgrounds. The mechanism causing coronary artery lesions in Kawasaki disease (KD) has not yet been fully clarified. Objective. We hypothesized that the main coronary artery (MCA) segment perfused by the vasa vasorum (VV) arose from the atrial and ventricular branches of peripheral coronary arteries in the myocardium (Type 1 VV externa) is more prone to aneurysm formation than that perfused by Type 2 VV originated from the ostium. Methods and Results. We reviewed the coronary angiography and two-dimensional echocardiogram (2DE) data of KD patients in our hospital and measured the distances from the left coronary ostium to the proximal point of the aneurysm in the left MCA (D1) and to the MCA bifurcation (D2). We found that the ratio of the distances (D1/D2) was negatively correlated with the patients’ age of KD onset, indicating that longitudinal extension of the left MCA aneurysms coincided with the development of Type 1 VV externa. We performed a literature review of KD cases with extracardiac aneurysms and found that 15 patients also had giant aneurysms in the MCA. Also, 8 of 9 extracardiac aneurysm cases whose clear 2DE images were available in the reports, the giant MCA aneurysms seemed to have developed at positions immediately adjacent to the ostium. We assume that the giant coronary aneurysms might be a consequence of the coincidence of aneurysms in the MCA segments perfused by Type 1 and 2 VV externas and reflect a severe inflammation where Type 2 VV externa which is less susceptible to blood flow reduction than Type 1 VV externa is affected. Conclusions. Vasculitis in VV externa with the unique structure originating from and distributing most richly across coronary arteries might induce a vicious circle of hypoperfusion of VV externa and reduced coronary blood flow.
VL  - 5
IS  - 1
ER  -

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Author Information

Zenshiro Onouchi

Department of Pediatrics, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Kyoto, Japan
Akiko Hamaoka-Okamoto

Department of Pediatrics, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Kyoto, Japan
Chinatsu Suzuki

Department of Pediatrics, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Kyoto, Japan
Kenji Hamaoka

Department of Pediatrics, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Kyoto, Japan

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APA Style

Zenshiro Onouchi, Akiko Hamaoka-Okamoto, Chinatsu Suzuki, Kenji Hamaoka. (2021). Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions. Cardiology and Cardiovascular Research, 5(1), 7-15. https://doi.org/10.11648/j.ccr.20210501.12

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ACS Style

Zenshiro Onouchi; Akiko Hamaoka-Okamoto; Chinatsu Suzuki; Kenji Hamaoka. Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions. Cardiol. Cardiovasc. Res. 2021, 5(1), 7-15. doi: 10.11648/j.ccr.20210501.12

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AMA Style

Zenshiro Onouchi, Akiko Hamaoka-Okamoto, Chinatsu Suzuki, Kenji Hamaoka. Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions. Cardiol Cardiovasc Res. 2021;5(1):7-15. doi: 10.11648/j.ccr.20210501.12

Copy | Download

@article{10.11648/j.ccr.20210501.12,
  author = {Zenshiro Onouchi and Akiko Hamaoka-Okamoto and Chinatsu Suzuki and Kenji Hamaoka},
  title = {Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions},
  journal = {Cardiology and Cardiovascular Research},
  volume = {5},
  number = {1},
  pages = {7-15},
  doi = {10.11648/j.ccr.20210501.12},
  url = {https://doi.org/10.11648/j.ccr.20210501.12},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ccr.20210501.12},
  abstract = {Backgrounds. The mechanism causing coronary artery lesions in Kawasaki disease (KD) has not yet been fully clarified. Objective. We hypothesized that the main coronary artery (MCA) segment perfused by the vasa vasorum (VV) arose from the atrial and ventricular branches of peripheral coronary arteries in the myocardium (Type 1 VV externa) is more prone to aneurysm formation than that perfused by Type 2 VV originated from the ostium. Methods and Results. We reviewed the coronary angiography and two-dimensional echocardiogram (2DE) data of KD patients in our hospital and measured the distances from the left coronary ostium to the proximal point of the aneurysm in the left MCA (D1) and to the MCA bifurcation (D2). We found that the ratio of the distances (D1/D2) was negatively correlated with the patients’ age of KD onset, indicating that longitudinal extension of the left MCA aneurysms coincided with the development of Type 1 VV externa. We performed a literature review of KD cases with extracardiac aneurysms and found that 15 patients also had giant aneurysms in the MCA. Also, 8 of 9 extracardiac aneurysm cases whose clear 2DE images were available in the reports, the giant MCA aneurysms seemed to have developed at positions immediately adjacent to the ostium. We assume that the giant coronary aneurysms might be a consequence of the coincidence of aneurysms in the MCA segments perfused by Type 1 and 2 VV externas and reflect a severe inflammation where Type 2 VV externa which is less susceptible to blood flow reduction than Type 1 VV externa is affected. Conclusions. Vasculitis in VV externa with the unique structure originating from and distributing most richly across coronary arteries might induce a vicious circle of hypoperfusion of VV externa and reduced coronary blood flow.},
 year = {2021}
}

Copy | Download

TY  - JOUR
T1  - Vasculitis of Vasa Vasorum and Aneurysm Formation in Kawasaki Disease: Predilection for Coronary Arteries Lesions
AU  - Zenshiro Onouchi
AU  - Akiko Hamaoka-Okamoto
AU  - Chinatsu Suzuki
AU  - Kenji Hamaoka
Y1  - 2021/01/15
PY  - 2021
N1  - https://doi.org/10.11648/j.ccr.20210501.12
DO  - 10.11648/j.ccr.20210501.12
T2  - Cardiology and Cardiovascular Research
JF  - Cardiology and Cardiovascular Research
JO  - Cardiology and Cardiovascular Research
SP  - 7
EP  - 15
PB  - Science Publishing Group
SN  - 2578-8914
UR  - https://doi.org/10.11648/j.ccr.20210501.12
AB  - Backgrounds. The mechanism causing coronary artery lesions in Kawasaki disease (KD) has not yet been fully clarified. Objective. We hypothesized that the main coronary artery (MCA) segment perfused by the vasa vasorum (VV) arose from the atrial and ventricular branches of peripheral coronary arteries in the myocardium (Type 1 VV externa) is more prone to aneurysm formation than that perfused by Type 2 VV originated from the ostium. Methods and Results. We reviewed the coronary angiography and two-dimensional echocardiogram (2DE) data of KD patients in our hospital and measured the distances from the left coronary ostium to the proximal point of the aneurysm in the left MCA (D1) and to the MCA bifurcation (D2). We found that the ratio of the distances (D1/D2) was negatively correlated with the patients’ age of KD onset, indicating that longitudinal extension of the left MCA aneurysms coincided with the development of Type 1 VV externa. We performed a literature review of KD cases with extracardiac aneurysms and found that 15 patients also had giant aneurysms in the MCA. Also, 8 of 9 extracardiac aneurysm cases whose clear 2DE images were available in the reports, the giant MCA aneurysms seemed to have developed at positions immediately adjacent to the ostium. We assume that the giant coronary aneurysms might be a consequence of the coincidence of aneurysms in the MCA segments perfused by Type 1 and 2 VV externas and reflect a severe inflammation where Type 2 VV externa which is less susceptible to blood flow reduction than Type 1 VV externa is affected. Conclusions. Vasculitis in VV externa with the unique structure originating from and distributing most richly across coronary arteries might induce a vicious circle of hypoperfusion of VV externa and reduced coronary blood flow.
VL  - 5
IS  - 1
ER  -

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