Letter by Chung and Kim Regarding Article, “Head-to-Head Comparison of Inflammation and Neovascularization in Human Carotid Plaques: Implications for the Imaging of Vulnerable Plaques”

HomeCirculation: Cardiovascular ImagingVol. 10, No. 10Letter by Chung and Kim Regarding Article, "Head-to-Head Comparison of Inflammation and Neovascularization in Human Carotid Plaques: Implications for the Imaging of Vulnerable Plaques" Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Chung and Kim Regarding Article, "Head-to-Head Comparison of Inflammation and Neovascularization in Human Carotid Plaques: Implications for the Imaging of Vulnerable Plaques" Hyemoon Chung, MD and Weon Kim, MD, PhD Hyemoon ChungHyemoon Chung Division of Cardiology, Department of Internal Medicine, Kyung Hee University Hospital, Seoul, Korea and Weon KimWeon Kim Division of Cardiology, Department of Internal Medicine, Kyung Hee University Hospital, Seoul, Korea Originally published26 Sep 2018https://doi.org/10.1161/CIRCIMAGING.117.006995Circulation: Cardiovascular Imaging. 2017;10:e006995To the Editor:We read with interest the recent published article by Demeure et al1 on the comparison of inflammation and neovascularization in carotid plaques. The authors had reported that inflammation and intraplaque neovascularization (IPN) confirmed by contrast echocardiography, known as 2 features of plaque vulnerability, were not systemically associated in carotid plaque. Furthermore, the presence of IPN was not related with patients' symptoms, whereas inflammation was associated. In their study, intensity of contrast enhancement was highly correlated with the amount of neovessels confirmed by histology, which means imaging study was well validated.Inflammation and angiogenesis influence each other; inflammation is known as a stimulator for angiogenesis—the main process of new vessel formation. Previous reports demonstrated that anti-inflammatory agents suppressed pathological angiogenesis. Angiogenic factors also amplify the process of inflammation. The association between neovascularization, inflammation, and plaque vulnerability had been already demonstrated by a previous study.2 What is the significant leading cause of plaque destabilization has been a major concern. Neovascularization, major criteria of vulnerable plaque, is a local process, whereas inflammation, major criteria of vulnerable plaque, is a systemic process affecting systemic coagulation pathway and local process on the plaque. There are various mechanisms of progression of vulnerable plaque and different types of vulnerable plaque, and neovascularization is one of contributors of plaque destabilization and subsequent cardiovascular event. Obviously, neovascularization is one of the crucial sources of intraplaque hemorrhage, which is associated with progression of plaque rupture. However, not all neovascularization might directly lead to vulnerable plaque, and that point might be related with conflicting data whether IPN might be associated with adverse clinical outcome or not. Plaque with neovascularization may be more vulnerable when combined with active inflammation. Previous reports demonstrated the association between IPN and patients' symptoms3 and future stroke events.4 However, there is a lack of large population-based data, and several conflicting conclusions had been demonstrated, as mentioned by Demeure et al. We had thought that neovascularization might be associated with clinical cardiovascular events. Therefore, we had evaluated the presence of IPN using contrast carotid echocardiography and investigated the association between IPN and clinical outcome. In our previous published study, the presence of IPN was not related with 1-year cardiovascular outcome, although it was related with matrix metalloproteinase-9; matrix metalloproteinase is one of the crucial proteases playing a key role in plaque rupture.5 We do not think that neovascularization has nothing to do with plaque vulnerability. Neovascularization is certainly one of the critical sources of plaque rupture and subsequent adverse cardio-cerebrovascular events. Further study is needed to identify what is the predictor of future vascular events in patients with neovascularization in carotid plaque. We agree with these results that neovascularization was not directly associated with inflammation and neurological symptoms.HyemoonChung, MDWeon Kim, MD, PhDDivision of CardiologyDepartment of Internal MedicineKyung Hee University HospitalSeoul, KoreaDisclosuresNone.References1. Demeure F, Bouzin C, Roelants V, Bol A, Verhelst R, Astarci P, Gerber BL, Pouleur AC, Pasquet A, de Meester C, Vanoverschelde JJ, Vancraeynest D. Head-to-head comparison of inflammation and neovascularization in human carotid plaques: implications for the imaging of vulnerable plaques.Circ Cardiovasc Imaging. 2017; 10:e005846. doi: 10.1161/CIRCIMAGING.116.005846.LinkGoogle Scholar2. Pelisek J, Well G, Reeps C, Rudelius M, Kuehnl A, Culmes M, Poppert H, Zimmermann A, Berger H, Eckstein HH. Neovascularization and angiogenic factors in advanced human carotid artery stenosis.Circ J. 2012; 76:1274–1282.CrossrefMedlineGoogle Scholar3. Owen DR, Shalhoub J, Miller S, Gauthier T, Doryforou O, Davies AH, Leen EL. Inflammation within carotid atherosclerotic plaque: assessment with late-phase contrast-enhanced US.Radiology. 2010; 255:638–644. doi: 10.1148/radiol.10091365.CrossrefMedlineGoogle Scholar4. Staub D, Patel MB, Tibrewala A, Ludden D, Johnson M, Espinosa P, Coll B, Jaeger KA, Feinstein SB. Vasa vasorum and plaque neovascularization on contrast-enhanced carotid ultrasound imaging correlates with cardiovascular disease and past cardiovascular events.Stroke. 2010; 41:41–47. doi: 10.1161/STROKEAHA.109.560342.LinkGoogle Scholar5. Kim HS, Woo JS, Kim BY, Jang HH, Hwang SJ, Kwon SJ, Choi EY, Kim JB, Cheng X, Jin E, Kim WS, Kim KS, Kim W. Biochemical and clinical correlation of intraplaque neovascularization using contrast-enhanced ultrasound of the carotid artery.Atherosclerosis. 2014; 233:579–583. doi: 10.1016/j.atherosclerosis.2014.01.042.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails October 2017Vol 10, Issue 10 Advertisement Article InformationMetrics © 2017 American Heart Association, Inc.https://doi.org/10.1161/CIRCIMAGING.117.006995PMID: 29021261 Originally publishedSeptember 26, 2018 PDF download Advertisement SubjectsVascular Disease