Abstract

<p class="Abstract">This study aims to evaluate the histopathological analysis as well as the effect of coronary endarterectomy with severe calcified coronary artery disease. During the year of 2015 to 2017, a total of 135 patients (56 patients of stable angina and 79 patients of unstable angina) underwent atherectomy in adjunct to off-pump coronary artery bypass graft surgery. Histopathological study of atheroma specimen demonstrates the presence of calcification, foam cell, cholesterol clefts, thrombus, smooth muscle cell, and also necrotic tissue using standard hematoxylin and eosin stain techniques. However, smooth muscle cells and foam cell were identified with plaque using the monoclonal antibodies. Thrombus was more common in unstable angina group of patients (64.4%) in comparison to the patients with stable angina (23.2%). An accelerated progression pattern of smooth muscle cell proliferation and calcification were observed which was also common and significantly higher in unstable angina group of patients. The presence of thrombus and accelerated progressive pattern of smooth muscle cell proliferation in unstable angina patients imply the episodic disruption of atheromatous plaque followed by subsequent healing and may play a vital role in the pathophysiology of underlying angina pectoris.</p>

Highlights

  • A condition named unstable angina is differentiated by the symptoms severity and how it is progressed to infarction or may be sudden death, which has been into different clinical series.[1]

  • Though the necropsy material is solely taken in case of the severe end of disease, the atheroma plaque material is taken from the live patient along with the stable and unstable angina.[7]

  • The aim of this study was to correlate the relationship among unstable angina and morphological features of atheroma extracted during off-pump coronary artery bypass graft surgery

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Summary

Introduction

A condition named unstable angina is differentiated by the symptoms severity and how it is progressed to infarction or may be sudden death, which has been into different clinical series.[1]. In some percentage of cases in the culprit plaque, an intraluminal filling defect is found with a non-occlusive thrombus.[2, 3] From the pathological findings, it is identified that the plaque disruption occurs where the thrombus is projected into the lumen. Ante-grade blood flow is kept in procession. The activated platelet giving a layer cover the projecting thrombi, which forms the emboli in the intra-myocardial vascular bed.[3,4,5] According to the clinical spectrum, the crescendo type of unstable angina is severe which is clear by the pathological process.[6] Though the necropsy material is solely taken in case of the severe end of disease, the atheroma plaque material is taken from the live patient along with the stable and unstable angina.[7] The common facts in the studies that the thrombus comes from the plaque which is responsible for unstable angina rather than from stable angina

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