Abstract
Acute coronary syndrome results from the intimal injury of an epicardial coronary artery. Plaque erosion is intimal injury which does not exhibit plaque rupture.
Pathological studies have shown that plaque erosion often develops on intimal thickening or a fibroatheroma, with few lipid core and calcification. The exposed intima at the eroded site is predominantly comprised of vascular smooth muscle cells and proteoglycans. Plaque erosions are more often observed in younger individuals and smokers compared with plaque ruptures.
There have been few angioscopic investigations of plaque erosion. Because the injured intima hides behind a thrombus, the plaque morphology is often overlooked by angioscopy. The combination of angioscopy and an intravascular imaging device visualizing cross-sectional images of an artery is thought to be helpful for identifying plaque erosion. A recent study using both angioscopy and intravascular ultrasound demonstrated that the morphologies of culprit lesions are associated with the clinical features of the patients with acute myocardial infarction. Identifying the morphology of intimal injury may help to determine the optimal management of acute coronary syndrome.
Access provided by Autonomous University of Puebla. Download chapter PDF
Similar content being viewed by others
Keywords
1 What Is Plaque Erosion?
Acute coronary syndrome (ACS) is caused by the formation or presence of a thrombus in an epicardial coronary artery. The formation of a thrombus results from intimal injury, which has a variety of morphologies. Pathological studies have shown that plaque rupture is the main morphology observed in the culprit lesions of ACS patients. Plaque rupture is defined as a perforation of a fibrous cap overlying a lipid core. Plaque rupture is not observed in approximately one-fourth of the patients with acute events. Plaque erosion is an intimal injury which does not exhibit plaque rupture. The ruptured site is characterized by a thin fibrous cap, large lipid core, and numerous activated inflammatory cells. On one hand, erosion often develops on intimal thickening or a fibroatheroma with few lipid core and calcification. The exposed intima at the eroded site is predominantly comprised of vascular smooth muscle cells and proteoglycans [1]. According to pathological studies, plaque erosions are more often observed in younger individuals and smokers compared with plaque ruptures [2, 3].
2 Angioscopic Findings of Plaque Erosion
Angioscopy can visualize the luminal surface of the intima and thrombus. The injured intima hides behind the intraluminal and mural thrombus, so the plaque morphology is often overlooked. Just after the thrombus has disappeared or decreased in size, the injured intima becomes visible. Typically, plaque erosion is diagnosed if there is only reddening and a rough surface, with no evidence of trans-cap ruptures, such as a dissection, cleft, or depressed ulceration (Fig. 8.1). Kubo et al. analyzedthe culprit lesions in patients with myocardial infarction by optical coherence tomography (OCT), angioscopy, and intravascular ultrasound (IVUS). There was a significant difference in the incidence of plaque erosion diagnosed by these intravascular imaging devices (23 %, 3 %, and 0 % by OCT, angioscopy, and IVUS, respectively; p = 0.003). The difference in the incidence of erosion was significant between OCT and CAS (p = 0.026) or between OCT and IVUS (p = 0.005), but not between CAS and IVUS (p = 0.500) [4]. The combination of angioscopy and an intravascular imaging device visualizing the cross-sectional images of an artery is thought to be helpful in identifying plaque erosion (Fig. 8.2). Ozaki et al. assessed coronary CT angiographic characteristics of culprit lesions in acute coronary syndromes not related to plaque rupture as defined by optical coherence tomography and angioscopy. CT angiography revealed that a low-attenuation plaque, positive remodeling, and spotty calcification were significantly less common in the ACS not related to plaque rupture than ACS related to plaque rupture, but similar to stable angina [5].
3 Clinical Implications of Plaque Erosions Observed by Angioscopy
Angioscopy, which shows gross pathological findings in vivo, has the potential to clarify the differences in the pathogenic mechanisms between an erosion and rupture. Hayashi et al. examined the relationship between the morphologies of culprit lesions and the clinical features of the patients with acute myocardial infarction using coronary angioscopy and intravascular ultrasound [7]. These studies were performed immediately before percutaneous coronary intervention was undertaken. They found that the patients with eroded plaque lesions had smaller infarctions than those with ruptured plaque lesions. Furthermore, distal embolization was less frequent in the erosion group compared with the rupture group (rupture group 37.0 % vs. erosion group 0.0 %; P = 0.0026). These results also suggest that the morphology of the intimal injury may help to determine the optimal management of ACS. The mechanical stress caused by coronary spasm is suspected to contribute to the formation of erosion. The angioscopic findings of coronary spasm are discussed in detail in the next section.
4 Summary
There have been few angioscopic investigations of plaque erosion. Because a thrombus attaches to the injured intima, the morphology of the intima is often overlooked by angioscopy. The combination of angioscopy and an intravascular imaging device visualizing the cross-sectional images of the artery is thought to be helpful in identifying a plaque erosion. Identifying the morphology of the intimal injury may help to determine the optimal management of ACS.
References
Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000;20:1262–75. doi: 10.1161/01.ATV.20.5.1262.
Burke AP, Farb A, Malcom GT, Liang YH, Smialek J, Virmani R. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med. 1997;336:1276–82. doi: 10.1056/NEJM199705013361802.
Farb A, Burke AP, Tang AL, Liang TY, Mannan P, Smialek J, Virmani R. Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death. Circulation. 1996;93:1354–63. doi: 10.1161/01.CIR.93.7.1354.
Kubo T, Imanishi T, Takarada S, Kuroi A, Ueno S, Yamano T, Tanimoto T, Matsuo Y, Masho T, Kitabata H, Tsuda K, Tomobuchi Y, Akasaka T. Assessment of culprit lesion morphology in acute myocardial infarction: ability of optical coherence tomography compared with intravascular ultrasound and coronary angioscopy. J Am Coll Cardiol. 2007;50:933–9. doi: 10.1016/j.jacc.2007.04.082.
Ozaki Y, Okumura M, Ismail TF, Motoyama S, Naruse H, Hattori K, Kawai H, Sarai M, Takagi Y, Ishii J, Anno H, Virmani R, Serruys PW, Narula J. Coronary CT angiographic characteristics of culprit lesions in acute coronary syndromes not related to plaque rupture as defined by optical coherence tomography and angioscopy. Eur Heart J. 2011;32:2814–23. doi: 10.1093/eurheartj/ehr189. Epub 2011 June 30.
Prati F, Uemura S, Souteyrand G, Virmani R, Motreff P, Di Vito L, Biondi-Zoccai G, Halperin J, Fuster V, Ozaki Y, Narula J. OCT-based diagnosis and management of STEMI associated with intact fibrous cap. JACC Cardiovasc Imaging. 2013;6:283–7. doi: 10.1016/j.jcmg.2012.12.007.
Hayashi T, Kiyoshima T, Matsuura M, Ueno M, Kobayashi N, Yabushita H, Kurooka A, Taniguchi M, Miyataka M, Kimura A, Ishikawa K. Plaque erosion in the culprit lesion is prone to develop a smaller myocardial infarction size compared with plaque rupture. Am Heart J. 2005;149:284–90. doi: 10.1016/j.ahj.2004.06.020.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2015 Springer Japan
About this chapter
Cite this chapter
Inami, S. (2015). Plaque Erosion. In: Mizuno, K., Takano, M. (eds) Coronary Angioscopy. Springer, Tokyo. https://doi.org/10.1007/978-4-431-55546-9_8
Download citation
DOI: https://doi.org/10.1007/978-4-431-55546-9_8
Publisher Name: Springer, Tokyo
Print ISBN: 978-4-431-55545-2
Online ISBN: 978-4-431-55546-9
eBook Packages: MedicineMedicine (R0)