A definition of the intima of human arteries and of its atherosclerosis-prone regions. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association.

Abstract

T his report is a concise review of current knowledge of the structure and function of the intima of the aorta and the major distributing arteries. The main purpose of the review is to delineate normal arterial intima from atherosclerotic lesions and, in particular, to distinguish physiological adaptations from atherosclerotic increases in intimal thickness. To characterize normal intima, including the adaptive intimal thickenings, some of which represent locations in which atherosclerotic lesions are prone to develop, the structure, composition, and functions of the arterial intima in young people as well as in laboratory animals not subjected to known atherogenic stimuli are reviewed.This report on arterial intima is the first in a series of four. The second report will review and define initial, fatty streak, and intermediate types of atherosclerotic lesions, and the third report will review all types of advanced (i.e., potentially clinical and clinical) lesions. The overall objective is to define arterial intima and all types of atherosclerotic lesions, and then to postulate, in a fourth and final report, a valid and up-to-date pathobiological nomenclature and classification of atherosclerotic lesions.

Enzymatically Modified Low‐Density Lipoprotein Is Present in All Stages of Aortic Valve Sclerosis: Implications for Pathogenesis of the Disease

“…If we may assume that enzymatic degradation and fusion of lipid particles are essentially synonymous,10 our findings are in perfect accordance with the recently published electron micrographs of isolated extracellular lipid particles from aortic valves 26. Compared with the histological structure of adaptive intimal thickening of human arteries prone to atherosclerotic lesion development,27 the composition of the human aortic valve cusp with the fibrosa suffused with insudated lipoproteins is quite different. This dense matrix might favor entrapment of insudated lipoproteins counteracting sufficient statin effects.…”

Highly glycated oxyhaemoglobin impairs nitric oxide relaxations in human mesenteric microvessels

“…Nevertheless, haemoglobin possesses some properties that make it a good candidate for being a cause of diabetic endothelial dysfunction by this mechanism. It is sensitive to changes in glycaemic concentrations [27], it circulates freely in plasma in nanomolar concentrations [7] and it can penetrate into the vascular wall in non-pathological circumstances [30,31]. Very recently it has been shown that endothelial cells are able to incorporate cell-free haemoglobin, creating a new way for circulating haemoglobin to be in close contact with NO [32].…”

Carotid artery wall hypertrophy in children with metabolic syndrome

“…1,2 Five to ten per cent of coronary arteries of children aged 2-15 years show fibrous plaques, and it is generally believed that they evolve from an initial fatty streak. 3 Over the last 20 years, the development of noninvasive methods has allowed to assess in vivo abnormalities in vascular structure and function of young subjects at cardiovascular risk. [4][5][6] In particular, carotid intima-media thickness (IMT) is commonly used as a measure of preclinical atherosclerosis.…”