Intravascular ultrasound insights into the unstable features of the coronary atherosclerotic plaques: A systematic review and meta-analysis.
acute coronary syndrome
intravascular ultrasound
non-culprit lesion
plaque morphology
vessel remodeling
Journal
European journal of clinical investigation
ISSN: 1365-2362
Titre abrégé: Eur J Clin Invest
Pays: England
ID NLM: 0245331
Informations de publication
Date de publication:
Jan 2022
Jan 2022
Historique:
revised:
07
08
2021
received:
23
05
2021
accepted:
16
08
2021
pubmed:
20
8
2021
medline:
18
3
2022
entrez:
19
8
2021
Statut:
ppublish
Résumé
There is a lack of a comprehensive picture of plaque geometry and composition of unstable atherosclerotic lesions as observed with intravascular ultrasound techniques. We analysed through a systematic review with meta-analysis 39 characteristics of atherosclerotic plaques in three scenarios involving culprit and non-culprit lesions from acute coronary syndromes vs stable angina pectoris patients, and culprit vs non-culprit lesions in acute coronary syndromes patients. A systematic search of PubMed and EMBASE, from inception to April 2020 was performed. The combined odds ratios or mean differences of all IVUS characteristics were calculated with random-effects models. Twenty-eight studies involving 5434 subjects, and 5618 lesions were included. Culprit lesions in acute coronary syndromes have larger plaque areas and remodeling indexes (MD = 0.13 [0.08; 0.17], p < 0.001) and contained larger necrotic cores (MD = 0.67 (95% CI 0.19;1.15), p = 0.006) that stable angina culprit lesions. In acute patients, culprit plaques were also more remodeled, had larger necrotic cores and had more frequently a Thin-Cap Fibroatheroma morphology (OR = 1.79 (95% CI 1.21; 2.65), p = 0.004) than non-culprit lesions. Non-culprit lesions in acute syndromes were more often ruptured (OR = 2.25 (95% CI:1.05; 4.82), p = 0.037) or Thin-Cap Fibroatheromas than in stable angina. Culprit lesions from acute coronary patients are larger, more positively remodeled and contained more lipids as compared to stable angina lesions or non-culprit in acute patients. Non culprit lesions are also more often complicated or vulnerable in acute than stable patients.
Sections du résumé
BACKGROUND
BACKGROUND
There is a lack of a comprehensive picture of plaque geometry and composition of unstable atherosclerotic lesions as observed with intravascular ultrasound techniques. We analysed through a systematic review with meta-analysis 39 characteristics of atherosclerotic plaques in three scenarios involving culprit and non-culprit lesions from acute coronary syndromes vs stable angina pectoris patients, and culprit vs non-culprit lesions in acute coronary syndromes patients.
METHODS
METHODS
A systematic search of PubMed and EMBASE, from inception to April 2020 was performed. The combined odds ratios or mean differences of all IVUS characteristics were calculated with random-effects models.
RESULTS
RESULTS
Twenty-eight studies involving 5434 subjects, and 5618 lesions were included. Culprit lesions in acute coronary syndromes have larger plaque areas and remodeling indexes (MD = 0.13 [0.08; 0.17], p < 0.001) and contained larger necrotic cores (MD = 0.67 (95% CI 0.19;1.15), p = 0.006) that stable angina culprit lesions. In acute patients, culprit plaques were also more remodeled, had larger necrotic cores and had more frequently a Thin-Cap Fibroatheroma morphology (OR = 1.79 (95% CI 1.21; 2.65), p = 0.004) than non-culprit lesions. Non-culprit lesions in acute syndromes were more often ruptured (OR = 2.25 (95% CI:1.05; 4.82), p = 0.037) or Thin-Cap Fibroatheromas than in stable angina.
CONCLUSION
CONCLUSIONS
Culprit lesions from acute coronary patients are larger, more positively remodeled and contained more lipids as compared to stable angina lesions or non-culprit in acute patients. Non culprit lesions are also more often complicated or vulnerable in acute than stable patients.
Types de publication
Journal Article
Meta-Analysis
Systematic Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13671Subventions
Organisme : Unitatea Executiva pentru Finantarea Invatamantului Superior, a Cercetarii, Dezvoltarii si Inovarii
ID : PN-III-P2-2.1-PED-2019-2404
Informations de copyright
© 2021 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.
Références
Ambrose JA, Tannenbaum MA, Alexopoulos D, et al. Angiographic progression of coronary artery disease and the development of myocardial infarction. J Am Coll Cardiol. 1988;12:56-62.
Davies MJ, Thomas A. Thrombosis and acute coronary -artery lesions in sudden cardiac ischemic death. N Engl J Med. 1984;3101137-3101140.
Schoenhagen P, Zaida KM, Kapadia SR, Crowe TD, Nissen SE, Tuzcu EM. Extent and direction of arterial remodeling in stable versus unstable coronary syndromes. Circulation. 2000;101:598-603.
Fernandez-Ortiz A, Badimon JJ, Fark E, et al. Characterization of the relative thrombogenicity of atherosclerotic plaque components: implications for consequences of plaque rupture. J Am Coll Cardiol. 1994;23:1562-1569.
Falk E, Wilensky RL. Prediction of coronary events by intravascular imaging. J Am Coll Cardiol. 2012;5(Suppl. 5):S38-S41.
Libby P, Schoenbeck U, Mach F, Selwyn AP, Ganz P. Current concepts in cardiovascular pathology: the role of LDL cholesterol in plaque rupture and stabilization. Am J Med. 1998;104(2A):14S-18S.
Virmani R, Kolodgie FD, Burke AP, et al. Lesson from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000;20:1262-1275.
Smits PC, Pasterkamp G, de Jaegere PP, et al. Angioscopic complex lesions are predominantly compensatory enlarged: an angioscopy and intracoronary ultrasound study. Cardiovasc Res. 1999;41:458-464.
Konig A, Bleie O, Dudek D, Marso S, Rogers JH, et al. Coronary plaque dimensions and composition by intravascular ultrasound radio frequency lesion segment analysis in stable and unstable angina patients. Coron Artery Dis. 2009;20(5):309-316.
Hernando L, Corros C, Gonzalo N, et al. Morphological characteristics of culprit coronary lesions according to clinical presentation: insights from a multimodality imaging approach. Int J Cardiovasc Imaging. 2013;29(1):13-21.
Surmely JF, Nasu K, Fujita H, et al. Coronary plaque composition of culprit/target lesions according to the clinical presentation: a virtual histology intravascular ultrasound analysis. Eur Heart J. 2006;27(24):2939-2944.
Fujii K, Kobayashi Y, Minz GS, et al. Intravascular ultrasound assessment of ulcerated ruptured plaques. a comparison of culprit and nonculprit lesions of patients with acute coronary syndromes and lesions in patients without acute coronary syndromes. Circulation. 2003;108:2473-2478.
Souza CF, Maehara A, Mintz GS, et al. Tissue characterization and phenotype classification in patients presenting with acute myocardial infarction: Insights from the iWonder study. Catheter Cardiovasc Interv. 2017;90(7):1107-1114.
Wan X, Wang W, Liu J, Tong T. Estimating the sample mean and standard deviation from the sample size, median, range and/or interquartile range. BMC Med Res Methodol. 2014;14:135.
Higgins JPT, Thomas J, Chandler J, Cumpston M, Li T, Page MJ, Welch VA (Editors). Cochrane Handbook for Systematic Reviews of Interventions (2nd ed). John Wiley & Sons: Chichester (UK). 2019:167-168.
Wells GA, Shea B, O’Connell D, Peterson J, Welch V, Losos M, Tugwell P. The Newcastle-Ottawa Scale (NOS) for Assessing the Quality in Nonrandomized Studies in Meta-Analyses. 2012. http://www.ohri.ca/programs/clinical_epidemiology/oxford.asp
R Core Team. R: A Language and Environment for Statistical Computing. Viena, Austria: R Foundation for Statistical Computing. 2020. https://www.R-project.org/
Balduzzi S, Rücker G, Schwarzer G. How to perform a meta-analysis with R: a practical tutorial. Evidence-Based Mental Health. 2019;153-160.
Simera I, Moher D, Hoey J, Schulz KF, Altman DG. A catalogue of reporting guidelines for health research. Eur J Clin Invest. 2010;40(1):35-53.
Moher D, Liberati A, Tetzlaff J, Altman DG. PRISMA Group. Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. Ann Intern Med. 2009;151:264-269.
Jeremias A, Spies C, Herity NA, et al. Coronary artery compliance and adaptive vessel remodelling in patients with stable and unstable coronary artery disease. Heart. 2000;84:314-319.
Bae JH, Kwon TG, Kim KH, Hyun DW, Kim KY, Kim DS. In-vivo coronary plaque composition in patients with acute coronary syndrome: a virtual histology intravascular ultrasound study. Korean Circ J. 2007;37(9):437-442.
Uemura R, Tanabe J, Yokoyama H, Ohaki M. Impact of histological plaque characteristics on intravascular ultrasound parameters at culprit lesions in coronary artery disease. Int Heart J. 2006;47(5):683-693.
Hong MK, Minz GS, Lee CW, et al. Comparison of virtual histology to intravascular ultrasound of culprit coronary lesions in acute coronary syndrome and target coronary lesions in stable angina pectoris. Am J Cardiol. 2007;100:953-959.
Hong MK, Minz GS, Lee CW, et al. A three-vessel virtual histology intravascular ultrasound analysis of frequency and distribution of thin-cap fibroatheromas in patients with acute coronary syndrome or stable angina pectoris. Am J Cardiol. 2008;101:568-572.
Hong MK, Minz GM, Lee CW, et al. Comparison of coronary plaque rupture between stable angina and acute myocardial infarction a three-vessel intravascular ultrasound study in 235 patients. Circulation. 2004;110:928-933.
Toutouzas K, Synetos A, Stefanadi E, et al. Correlation between morphologic characteristics and local temperature differences in culprit lesions of patients with symptomatic coronary artery disease. J Am Coll Cardiol. 2007;49(23):2264-2271.
Ko YG, Son JW, Park SM, et al. Effect of vessel size on lipid content of coronary plaques assessed by integrated backscatter intravascular ultrasound. Circ J. 2010;74(4):754-759.
Cascón-Pérez JD, de la Torre-Hernández JM, Ruiz-Abellón MC, et al. Characteristics of culprit atheromatous plaques obtained in vivo by intravascular ultrasound radiofrequency analysis: results from the CULPLAC study. Am Heart J. 2013;165(3):400-407.
Ivanovíc M, Rancić M, Rdzanek A, Filipjak KJ, Opolski G, Cvetanović J. Virtual histology study of atherosclerotic plaque composition in patients with stable angina and acute phase of acute coronary syndromes without ST segment elevation. Srp Arh Celok Lek. 2013;141:308-314.
Li XM, Huang CX, Wang T, Zhuang SW, Zhou H, Tian B. Comparison of coronary plaque composition among patients with acute coronary syndrome and stable coronary artery diseases. Chin Med J. 2008;121:534-539.
Kozuki A, Shinke T, Otake H, et al. Feasibility of a novel radiofrequency signal analysis for in-vivo plaque characterization in humans: comparison of plaque components between patients with and without acute coronary syndrome. Int J Cardiol. 2013;167:1591-1596.
Lee CW, Hwang I, Park CS, et al. Differences in intravascular ultrasound and histological findings in culprit coronary plaques between ST-segment elevation myocardial infarction and stable angina. J Thromb Thrombolysis. 2014;37(4):443-449.
Murray SW, Stables RH, Garcia-Garcia HM, et al. Construction and validation of a plaque discrimination score from the anatomical and histological differences in coronary atherosclerosis: the Liverpool IVUS-V-HEART (intra vascular ultrasound-virtual-histology evaluation of atherosclerosis requiring treatment) study. EuroIntervention. 2014;10(7):815-823.
Dong L, Mintz GS, Witzenbichler B, et al. Comparison of plaque characteristics in narrowings with ST-elevation myocardial infarction (STEMI), non-STEMI/unstable angina pectoris and stable coronary artery disease (from the ADAPT-DES IVUS Substudy). Am J Cardiol. 2015;115(7):860-866.
Ando H, Amano T, Matsubara T, et al. Comparison of tissue characteristics between acute coronary syndrome and stable angina pectoris-an integrated backscatter intravascular ultrasound analysis of culprit and non-culprit lesions. Circ J. 2011;75:383-390.
Kotani J, Mintz GS, Castagna MT, et al. Intravascular ultrasound analysis of infarct-related and non-infarct-related arteries in patients who presented with an acute myocardial infarction. Circulation. 2003;107:2889-2893.
Rodriguez-Granillo GA, Garcia-Garcia HM, McFadden EP, et al. In vivo intravascular ultrasound-derived thin-cap fibroatheroma detection using ultrasound radiofrequency data analysis. J Am Coll Cardiol. 2005;46:2038-2042.
Nakamura T, Kubo N, Funayama H, Sugawara Y, Ako J, Momomura S. Plaque characteristics of the coronary segment proximal to the culprit lesion in stable and unstable patients. Clin Cardiol. 2009;32(8):E9-E12.
Rdzanek A, Kochman J, Pietrasik A, Wilczynska J, Rancic M, Opolski G. The prevalence of potentially unstable coronary lesions in patients with coronary artery disease-virtual histology study. Kardiol Pol. 2008;66(3):244-250.
Liu HL, Zhang J, Ma DX, et al. Coronary plaque characterization of nonculprit or nontarget lesions assessed by analysis of in vivo intracoronary ultrasound radio-frequency data. Chin Med J (Engl). 2009;122(6):622-626.
Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med. 1987;316:1371-1375.
Davies MJ, Richardson PD, Woolf N, Katz D r, Mann J. Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. Br Heart J. 1993;69:377-381.
Pasterkamp G, Schoneveld AH, van der Wal AC, et al. Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodeling paradox. J Am Coll Cardiol. 1998;32:655-662.
Marc MC, Iancu AC, Ober CD, et al. Pre-revascularization coronary wedge pressure as marker of adverse long-term left ventricular remodelling in patients with acute ST-segment elevation myocardial infarction. Sci Rep. 2018;8(1):1897.
Yamada R, Okura H, Kume T, et al. Relationship between arterial and fibrous cap remodeling: a serial three-vessel intravascular ultrasound and optical coherence tomography study. Circ Cardiovasc Interv. 2010;3(5):484-490.
Langille BL, O'Donnell F. Reductions in arterial diameter produced by chronic decreases in blood flow are endothelium-dependent. Science. 1986;231(4736):405-407. 10.1126/science.3941904
Stone PH, Saito S, Takahashi S, et al. Prediction of progression of coronary artery disease and clinical outcomes using vascular profiling of endothelial shear stress and arterial plaque characteristics: the PREDICTION Study. Circulation. 2012;126(2):172-181. 10.1161/CIRCULATIONAHA.112.096438
Richardson PD, Davies MJ, Born GV. Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques. Lancet. 1989;2(8669):941-944. 10.1016/s0140-6736(89)90953-7
Maehara A, Mintz GS, Bui AB, et al. Morphologic and angiographic features of coronary plaque rupture detected by intravascular ultrasound. J Am Coll Cardiol. 2002;40:904-910.
Rodriguez-Granillo GA, Garcia-Garcia HM, Valgimigli M, et al. Global characterization of coronary plaque rupture phenotype using three-vessel intravascular ultrasound radiofrequency data analysis. Eur Heart J. 2006;27:1921-1927.
de Graaf MA, van Velzen JE, de Graaf FR, et al. The maximum necrotic core area is most often located proximally to the site of most severe narrowing: a virtual histology intravascular ultrasound study. Heart Vessels. 2013;28(2):166-172.
Konig A, Bleie O, Rieber J, et al. Intravascular ultrasound radiofrequency analysis of the lesion segment profile in ACS patients. Clin Res Cardiol. 2010;99:83-91.
Mintz GS. Intravascular imaging of coronary calcification and its clinical implications. JACC Cardiovasc Imaging. 2015;8(4):461-471. 10.1016/j.jcmg.2015.02.003
Inaba S, Okayama H, Funada JI, et al. Relationship between smaller calcifications and lipid-rich plaques on integrated backscatter-intravascular ultrasound. Int J Cardiol. 2010;145(2):347-348. 10.1016/j.ijcard.2009.12.011
Mori H, Torii S, Kutyna M, Sakamoto A, Finn AV, Virmani R. Coronary artery calcification and its progression: what does it really mean? JACC Cardiovasc Imaging. 2018;11(1):127-142. 10.1016/j.jcmg.2017.10.012
Asakura M, Ueda Y, Yamaguchi O, et al. Extensive development of vulnerable plaques as a pan-coronary process in patients with myocardial infarction: an angioscopic study. J Am Coll Cardiol. 2001;37:1284-1288.
Tanaka A, Shimada K, Sano T, et al. Multiple plaque rupture and C-reactive protein in acute myocardial infarction. J Am Coll Cardiol. 2005;45:1594-1599.
Rioufol G, Finet G, Andre-Fouet X, et al. Multiple ruptures of atherosclerotic plaques in acute coronary syndrome. endocoronary ultrasonography study of three arteries. Arch Mal Coeur Vaiss. 2002;95:157-165.
von Birgelen C, Klinkhart W, Minz GS, et al. Plaque Distribution and Vascular Remodeling of Ruptured and Nonruptured Coronary Plaques in the Same Vessel: An Intravascular Ultrasound Study In Vivo. J Am Coll Cardiol. 2001;37:1864-1870.
Goldstein JA, Demetriou D, Grines CL, Pica M, Shoukfeh M, O'Neill WW. Multiple complex coronary plaques in patients with acute myocardial infarction. N Engl J Med. 2000;28:915-922.
Mann J, Davies MJ. Mechanisms of progression in native coronary artery disease: role of healed plaque disruption. Heart. 1999;82:265-268.
Levin DC, Fallon JT. Significance of the angiographic morphology of localized coronary stenoses: histopathologic correlations. Circulation. 1982;66:316-320.
Finn AV, Nakano M, Narula J, Kolodgie FD, Virmani R. Concept of vulnerable/unstable plaque. Arterioscler Thromb Vasc Biol. 2010;30(7):1282-1292. 10.1161/ATVBAHA.108.179739
Spinu M, Olinic DM, Olinic M, Homorodean C. In vivo imaging of complicated atherosclerotic plaque-role of optical coherence tomography (OCT). Rom J Morphol Embryol. 2018;59(2):469-478.
Kubo T, Maehara A, Mintz GS, et al. The dynamic nature of coronary artery lesion morphology assessed by serial virtual histology intravascular ultrasound tissue characterization. J Am Coll Cardiol. 2010;55(15):1590-1597. 10.1016/j.jacc.2009.07.078
Stone GW, Maehara A, Lansky AJ. A prospective natural-history study of coronary atherosclerosis. N Engl J Med. 2011;364(3):226-235. 10.1056/NEJMoa1002358
Hong YJ, Jeong MH, Choi YH, et al. Impact of plaque components on no-reflow phenomenon after stent deployment in patients with acute coronary syndrome: a virtual histology-intravascular ultrasound analysis. Eur Heart J. 2011;32(16):2059-2066.