ISSN 1671-5411 CN 11-5329/R
Volume 18 Issue 8
Aug.  2021
Turn off MathJax
Article Contents
Please cite this article as: YIN WJ, J JING, ZHANG YQ, TIAN F, ZHANG T, ZHOU SS, CHEN YD. Association between non-culprit healed plaque and plaque progression in acute coronary syndrome patients: an optical coherence tomography study. J Geriatr Cardiol 2021; 18(8): 631−644. DOI: 10.11909/j.issn.1671-5411.2021.08.001
Citation: Please cite this article as: YIN WJ, J JING, ZHANG YQ, TIAN F, ZHANG T, ZHOU SS, CHEN YD. Association between non-culprit healed plaque and plaque progression in acute coronary syndrome patients: an optical coherence tomography study. J Geriatr Cardiol 2021; 18(8): 631−644. DOI: 10.11909/j.issn.1671-5411.2021.08.001

Association between non-culprit healed plaque and plaque progression in acute coronary syndrome patients: an optical coherence tomography study

doi: 10.11909/j.issn.1671-5411.2021.08.001
More Information
  • Corresponding author: cyundai@vip.163.com
  • Available Online: 2021-07-28
  • Publish Date: 2021-08-28
  •  BACKGROUND Healed plaques are frequently found in patients with acute coronary syndrome, but the prognostic value is debatable. This study investigated the clinical features of non-culprit healed plaques detected by optical coherence tomography (OCT) with the aim of predicting plaque progression of healed plaques. METHODS This study retrospectively analyzed 113 non-culprit lesions from 85 patients who underwent baseline OCT imaging and follow-up angiography from January 2015 to December 2019. Plaque progression predictors were assessed by multivariate analysis. RESULTS Among 113 non-culprit lesions, 27 healed plaques (23.9%) were identified. Patients with non-culprit healed plaques had prior antiplatelet therapy (65.0% vs. 33.8%, P = 0.019), hypertension (85.0% vs. 50.7%, P = 0.009), and dyslipidemia (70.0% vs. 41.5%, P = 0.04) which were more frequently than those without healed plaques. The thickness (r = 0.674, P < 0.001), arc (r = 0.736, P < 0.001), and volume (r = 0.541, P = 0.004) of healed plaque were correlated with minimum lumen diameter changes. At a mean follow-up of 11.5 months, the non-culprit healed plaques had a lower minimum lumen diameter (1.61 ± 0.46 mm vs. 1.91 ± 0.73 mm, P = 0.016), lower average lumen diameter (1.86 mm vs. 2.10 mm, P = 0.033), and a higher degree of diameter stenosis (41.4% ± 11.9% vs. 35.5% ± 13.1%, P = 0.031) when compared to baseline measurements. The plaque progression rate was higher in the healed plaque group (33.3% vs. 8.1%, P = 0.002), and multivariate analysis identified healed plaques [odds ratio (OR) = 8.49, 95% CI: 1.71−42.13] and lumen thrombus (OR = 10.69, 95% CI: 2.21−51.71) as predictors of subsequent lesion progression. CONCLUSIONS Healed plaques were a predictor for rapid plaque progression. The quantitative parameters of healed plaque showed a good agreement with plaque progression. Patients with healed plaque were associated with prior antiplatelet therapy and high level of low-density lipoprotein cholesterol. Bifurcation lesions might be the predilection sites of healed plaques.
  • loading
  • [1]
    Partida RA, Libby P, Crea F, et al. Plaque erosion: a new in vivo diagnosis and a potential major shift in the management of patients with acute coronary syndromes. Eur Heart J 2018; 39: 2070−2076. doi: 10.1093/eurheartj/ehx786
    [2]
    Davies MJ. The contribution of thrombosis to the clinical expression of coronary atherosclerosis. Thromb Res 1996; 82: 1−32. doi: 10.1016/0049-3848(96)00035-7
    [3]
    Zhou J, Chew M, Ravn HB, et al. Plaque pathology and coronary thrombosis in the pathogenesis of acute coronary syndromes. Scand J Clin Lab Invest Suppl 1999; 230: 3−11.
    [4]
    Eisen A, Giugliano RP, Braunwald E. Updates on acute coronary syndrome: a review. JAMA Cardiol 2016; 1: 718−730. doi: 10.1001/jamacardio.2016.2049
    [5]
    Jang IK. Plaque progression: slow linear or rapid stepwise? Circ Cardiovasc Imaging 2017; 10: e006964. doi: 10.1161/CIRCIMAGING.117.006964
    [6]
    Crea F, Libby P. Acute coronary syndromes: the way forward from mechanisms to precision treatment. Circulation 2017; 136: 1155−1166. doi: 10.1161/CIRCULATIONAHA.117.029870
    [7]
    Jia H, Abtahian F, Aguirre AD, et al. In vivo diagnosis of plaque erosion and calcified nodule in patients with acute coronary syndrome by intravascular optical coherence tomography. J Am Coll Cardiol 2013; 62: 1748−1758. doi: 10.1016/j.jacc.2013.05.071
    [8]
    Dai J, Fang C, Zhang S, et al. Frequency, predictors, distribution, and morphological characteristics of layered culprit and nonculprit plaques of patients with acute myocardial infarction: in vivo 3-vessel optical coherence tomography study. Circ Cardiovasc Interv 2020; 13: e009125. doi: 10.1161/CIRCINTERVENTIONS.120.009125
    [9]
    Virmani R, Kolodgie FD, Burke AP, et al. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol 2000; 20: 1262−1275. doi: 10.1161/01.ATV.20.5.1262
    [10]
    Russo M, Kim HO, Kurihara O, et al. Characteristics of non-culprit plaques in acute coronary syndrome patients with layered culprit plaque. Eur Heart J Cardiovasc Imaging 2020; 21: 1421−1430. doi: 10.1093/ehjci/jez308
    [11]
    Burke AP, Kolodgie FD, Farb A, et al. Healed plaque ruptures and sudden coronary death: evidence that subclinical rupture has a role in plaque progression. Circulation 2001; 103: 934−940. doi: 10.1161/01.CIR.103.7.934
    [12]
    Shimokado A, Matsuo Y, Kubo T, et al. In vivo optical coherence tomography imaging and histopathology of healed coronary plaques. Atherosclerosis 2018; 275: 35−42. doi: 10.1016/j.atherosclerosis.2018.05.025
    [13]
    Okamoto H, Kume T, Yamada R, et al. Prevalence and clinical significance of layered plaque in patients with stable angina pectoris-evaluation with histopathology and optical coherence tomography. Circ J 2019; 83: 2452−2459. doi: 10.1253/circj.CJ-19-0640
    [14]
    Fracassi F, Crea F, Sugiyama T, et al. Healed culprit plaques in patients with acute coronary syndromes. J Am Coll Cardiol 2019; 73: 2253−2263. doi: 10.1016/j.jacc.2018.10.093
    [15]
    Tsuchiya H, Nakano A, Nakamura N, et al. Healed coronary plaque rupture as a cause of rapid lesion progression: a case demonstrated with in vivo histopathology by directional coronary atherectomy. Eur Heart J Cardiovasc Imaging 2019; 20: 1317. doi: 10.1093/ehjci/jez186
    [16]
    Araki M, Yonetsu T, Kurihara O, et al. Predictors of rapid plaque progression: an optical coherence tomography study. JACC Cardiovasc Imaging 2020; 29: S1936−878X(20)30736-1. doi: 10.1016/j.jcmg.2020.08.014
    [17]
    O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the American College of Emergency Physicians and Society for Cardiovascular Angiography and Interventions. Catheter Cardiovasc Interv 2013; 82: E1−E27. doi: 10.1002/ccd.24776
    [18]
    Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014; 64: e139−e228. doi: 10.1016/j.jacc.2014.09.017
    [19]
    Zeitouni M, Sabouret P, Kerneis M, et al. 2019 ESC/EAS guidelines for management of dyslipidaemia: strengths and limitations. Eur Heart J Cardiovasc Pharmacother 2020; 11: pvaa077. doi: 10.1093/ehjcvp/pvaa077
    [20]
    Li X, Wu C, Lu J, et al. Cardiovascular risk factors in China: a nationwide population-based cohort study. Lancet Public Health 2020; 5: e672−e681. doi: 10.1016/S2468-2667(20)30191-2
    [21]
    Suzuki N, Asano T, Nakazawa G, et al. Clinical expert consensus document on quantitative coronary angiography from the Japanese Association of Cardiovascular Intervention and Therapeutics. Cardiovasc Interv Ther 2020; 35: 105−116. doi: 10.1007/s12928-020-00653-7
    [22]
    Luo XJ, Wang W, Wang YT, et al. [Application of the descending branch of the lateral circumflex femoral artery in the coronary artery bypass grafting operation]. Zhonghua Wai Ke Za Zhi 2017; 55: 834−837. [In Chinese]. doi: 10.3760/cma.j.issn.0529-5815.2017.11.003
    [23]
    Uemura S, Ishigami K, Soeda T, et al. Thin-cap fibroatheroma and microchannel findings in optical coherence tomography correlate with subsequent progression of coronary atheromatous plaques. Eur Heart J 2012; 33: 78−85. doi: 10.1093/eurheartj/ehr284
    [24]
    Berry C, L’Allier PL, Grégoire J, et al. Comparison of intravascular ultrasound and quantitative coronary angiography for the assessment of coronary artery disease progression. Circulation 2007; 115: 1851−1857. doi: 10.1161/CIRCULATIONAHA.106.655654
    [25]
    Waters D, Craven TE, Lespérance J. Prognostic significance of progression of coronary atherosclerosis. Circulation 1993; 87: 1067−1075. doi: 10.1161/01.CIR.87.4.1067
    [26]
    Di Vito L, Yoon JH, Kato K, et al. Comprehensive overview of definitions for optical coherence tomography-based plaque and stent analyses. Coron Artery Dis 2014; 25: 172−185. doi: 10.1097/MCA.0000000000000072
    [27]
    Yabushita H, Bouma BE, Houser SL, et al. Characterization of human atherosclerosis by optical coherence tomography. Circulation 2002; 106: 1640−1645. doi: 10.1161/01.CIR.0000029927.92825.F6
    [28]
    Vergallo R, Porto I, D’Amario D, et al. Coronary atherosclerotic phenotype and plaque healing in patients with recurrent acute coronary syndromes compared with patients with long-term clinical stability: an in vivo optical coherence tomography study. JAMA Cardiol 2019; 4: 321−329. doi: 10.1001/jamacardio.2019.0275
    [29]
    Kato K, Yonetsu T, Kim SJ, et al. Nonculprit plaques in patients with acute coronary syndromes have more vulnerable features compared with those with non-acute coronary syndromes: a 3-vessel optical coherence tomography study. Circ Cardiovasc Imaging 2012; 5: 433−440. doi: 10.1161/CIRCIMAGING.112.973701
    [30]
    Kang SJ, Mintz GS, Oh JH, et al. Intravascular ultrasound assessment of distal left main bifurcation disease: the importance of the polygon of confluence of the left main, left anterior descending, and left circumflex arteries. Catheter Cardiovasc Interv 2013; 82: 737−745. doi: 10.1002/ccd.23263
    [31]
    Tearney GJ, Regar E, Akasaka T, et al. Consensus standards for acquisition, measurement, and reporting of intravascular optical coherence tomography studies: a report from the International Working Group for Intravascular Optical Coherence Tomography Standardization and Validation. J Am Coll Cardiol 2012; 59: 1058−1072. doi: 10.1016/j.jacc.2011.09.079
    [32]
    DeVore GR, Klas B, Satou G, et al. Evaluation of fetal left ventricular size and function using speckle-tracking and the simpson rule. J Ultrasound Med 2019; 38: 1209−1221. doi: 10.1002/jum.14799
    [33]
    Pinilla-Echeverri N, Mehta SR, Wang J, et al. Nonculprit lesion plaque morphology in patients with ST-segment-elevation myocardial infarction: results from the COMPLETE trial optical coherence tomography substudys. Circ Cardiovasc Interv 2020; 13: e008768. doi: 10.1161/CIRCINTERVENTIONS.119.008768
    [34]
    Sato T, Minami Y, Asakura K, et al. Age- and gender-related differences in coronary lesion plaque composition on optical coherence tomography. Circ J 2020; 84: 463−470. doi: 10.1253/circj.CJ-19-0859
    [35]
    Zhu J, Bernucci MT, Merkle CW, et al. Visibility of microvessels in optical coherence tomography angiography depends on angular orientation. J Biophotonics 2020; 13: e202000090. doi: 10.1002/jbio.202000090
    [36]
    Jang IK, Tearney GJ, MacNeill B, et al. In vivo characterization of coronary atherosclerotic plaque by use of optical coherence tomography. Circulation 2005; 111: 1551−1555. doi: 10.1161/01.CIR.0000159354.43778.69
    [37]
    Usui E, Mintz GS, Lee T, et al. Prognostic impact of healed coronary plaque in non-culprit lesions assessed by optical coherence tomography. Atherosclerosis 2020; 309: 1−7. doi: 10.1016/j.atherosclerosis.2020.07.005
    [38]
    Alenazy FO, Thomas MR. Novel antiplatelet targets in the treatment of acute coronary syndromes. Platelets 2021; 32: 15−28. doi: 10.1080/09537104.2020.1763731
    [39]
    Kedhi E, Fabris E, van der Ent M, et al. Six months versus 12 months dual antiplatelet therapy after drug-eluting stent implantation in ST-elevation myocardial infarction (DAPT-STEMI): randomised, multicentre, non-inferiority trial. BMJ 2018; 363: k3793. doi: 10.1136/bmj.k3793
    [40]
    Watanabe H, Domei T, Morimoto T, et al. Effect of 1-month dual antiplatelet therapy followed by clopidogrel vs 12-month dual antiplatelet therapy on cardiovascular and bleeding events in patients receiving PCI: the STOPDAPT-2 randomized clinical trial. JAMA 2019; 321: 2414−2427. doi: 10.1001/jama.2019.8145
    [41]
    Räber L, Mintz GS, Koskinas KC, et al. Clinical use of intracoronary imaging. Part 1: guidance and optimization of coronary interventions. An expert consensus document of the European Association of Percutaneous Cardiovascular Interventions. Eur Heart J 2018; 39: 3281−3300. doi: 10.1093/eurheartj/ehy285
    [42]
    Finn AV, Nakano M, Narula J, et al. Concept of vulnerable/unstable plaque. Arterioscler Thromb Vasc Biol 2010; 30: 1282−1292. doi: 10.1161/ATVBAHA.108.179739
    [43]
    Li Y, Gutiérrez-Chico JL, Holm NR, et al. Impact of side branch modeling on computation of endothelial shear stress in coronary artery disease: coronary tree reconstruction by fusion of 3D angiography and OCT. J Am Coll Cardiol 2015; 66: 125−135. doi: 10.1016/j.jacc.2015.05.008
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Figures(5)  / Tables(4)

    Article Metrics

    Article views (309) PDF downloads(34) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return