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Fuster et al. (1992) observed small thrombi in only 11% when atherectomy for severe stenotic lesions was executed along with a histological study of derived fragments, though it was not focused either patient had unstable angina or any clinical features.11 Several published articles observed that there are no past documents about the presence of thrombus in unstable angina patients.5-9, 12 Restenosis after coronary endarterectomy has been associated to prompt arterial remodeling, mural thrombus formation and elastic recoil tendency of the arterial wall. However, advancement of coronary artery disease is not defined or anticipated.13 In a study, Villadsen et al. (2017) found that coronary artery disease is a typical phenomenon in the unstable angina patients who became stabilized by rapid treatment procedure.14 Moreover, chronic stable angina pectoris awaiting for coronary revascularization was also found in a state of progression of coronary stenosis which is also similar to other published articles.3-5, 9, 15Transfer of the smooth muscle cells from tunica media to the intima; along with propagation of the smooth muscle cells induced by the fragmentation of the internal elastic lamina plays a role in unstable angina.16 In the study by Ahmed et al. (2003) found a common phenomenon that, greater percentage of smooth muscle cells in the remnant of re-stenotic lesions achieved by endarterectomy.17 However, Marso et al. (2012) found that patient underwent percutaneous transluminal coronary angioplasty may develop total occlusion due to restenosis, and may also have only angina pectoris due to collateral circulation formation.18 All these come to a conclusion that there is a remarkable difference among the cases who develop unstable angina, and probable causes may due to re-stenotic lesions after coronary endarterectomy and those due to the formation of new arteriosclerotic lesions which is also similar to other published articles.7-10, 15-19

Following pathologic reports of atheroma material, there is an intimate relation between acute ischemic events like unstable angina and myocardial infarction and intracoronary thrombosis

DA, Antman EM, Braunwald E, Gibson CM. The independent and combined risk of diabetes and non-end stage renal impairment in non-ST-segment elevation acute coronary syndromes. J Natl Med Assoc. 2003; 95: 1042-47.

18. Marso SP, Mercado N, Maehara A, Weisz G, Mintz GS, McPherson J, Schiele F, Dudek D, Fahy M, Xu K, Lansky A, Templin B, Zhang Z, de Bruyne B, Serruys PW, Stone GW. Plaque composition and clinical outcomes in acute coronary syndrome patients with metabolic syndrome or diabetes. J Am Coll Cardiol Img. 2012; 5: 42–52.

19. Gaede P, Lund-Andersen H, Parving HH, Pedersen O. Effect of a multifactorial intervention on mortality in type 2 diabetes. N Engl J Med. 2008; 358: 580-59.

20. Kestenbaum BR, Adeney KL, de Boer IH, Ix JH, Shlipak MG, Siscovick DS. Incidence and progression of coronary calcification in chronic kidney disease: The multi-ethnic study of atherosclerosis. Kidney Int. 2009; 76: 991-98.

21. Lansky AJ, Ng VG, Maehara A, Weisz G, Lerman A, Mintz GS, De Bruyne B, Farhat N, Niess G, Jankovic I, Lazar D, Xu K, Fahy M, Serruys PW, Stone GW. Gender and the extent of coronary atherosclerosis, plaque composition, and clinical outcomes in acute coronary syndromes. J Am Coll Cardiol Img. 2012; 5: 62-72.

22. Ranjan R, Adhikary D, Saha H, Saha SK, Hasan K, Adhikary AB. Coronary atheroma [14 cm] extracted from the right coronary artery during off-pump coronary artery bypass grafting. Bangabandhu Sheikh Mujib Med Univ J. 2017; 10: 97-100.

23. Cutlip DE, Chhabra AG, Baim DS, Chauhan MS, Marulkar S, M