Abstract

BackgroundTo analyse histological composition and progression of carotid plaque.MethodsThirty-one patients (22 males, mean age 68.03 ± 7.3 years) admitted for carotid endarterectomy for extracranial high-grade internal carotid artery stenosis (≥ 70% luminal narrowing) were enrolled. The patients were divided into 2 groups according to symptomatology (group I, 17 symptomatic patients; and group II, 14 asymptomatic patients). A histological analysis and inflammatory cell quantification of each excised carotid plaque was made. Nine carotid arteries were removed from human cadavers that were not preselected for carotid artery disease. These specimens were used as a control tissue without any macroscopic signs of atherosclerotic plaques.ResultsFifty eight percent of all carotid plaques were classified as complex plaque with possible surface defect, hemorrhage or thrombus. The inflammatory cells concentration did not differ between the two groups. All specimens from human cadavers were classified as preatheroma with extracellular lipid pools.ConclusionAsymptomatic and symptomatic patients could have the same histological components on their carotid plaques. Fibrotic and calcific plaques could become vulnerable as complex plaques with surface defect, hemorrhage and thrombus could remain silent. Asymptomatic carotid stenosis should be followed close with no invasive diagnostic methods and clinical evaluation.

Highlights

  • To analyse histological composition and progression of carotid plaque

  • Patients Thirty-six nonconsecutive surgical inpatients admitted for carotid endarterectomy for extracranial high-grade (≥ 70%) internal carotid artery stenosis were entered into this study between February 2003 and July 2005 from 3 participating hospitals

  • Focal cerebral ischemic events were defined as transient ischemic attack (TIA), amaurosis fugax (AF), central retinal artery occlusion (CRAO), or cerebrovascular accident

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Summary

Introduction

To analyse histological composition and progression of carotid plaque. In 1995, a report from the Committee on Vascular Lesions of the Council on Atherosclerosis, American Heart Association (AHA), had described the characteristic components and pathogenic mechanisms of the various advanced atherosclerotic lesions [1]. This report provides a classification of human atherosclerotic lesions based on their histological composition and structure and reflects the temporal natural history of disease. Thrombosis Journal 2007, 5:4 http://www.thrombosisjournal.com/content/5/1/4 sequence of lesion progression, grading from type I (initial lesions) to type VIII (fibrotic plaque). The present study was designed to characterize the progression and composition of carotid plaque, according with patient symptomatology, based on the American Heart Association (AHA) classification for human atherosclerotic lesions [1,4].

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