A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association.

Abstract

The compositions of lesion types that precede and that may initiate the development of advanced atherosclerotic lesions are described and the possible mechanisms of their development are reviewed. While advanced lesions involve disorganization of the intima and deformity of the artery, such changes are absent or minimal in their precursors. Advanced lesions are either overtly clinical or they predispose to the complications that cause ischemic episodes; precursors are silent and do not lead directly to complications. The precursors are arranged in a temporal sequence of three characteristic lesion types. Types I and II are generally the only lesion types found in children, although they may also occur in adults. Type I lesions represent the very initial changes and are I n this report we characterize lesions that precede and may initiate the development of advanced atherosclerotic lesions. Advanced lesions are defined as those in which an accumulation of lipid in the intima is associated with intimal disorganization and thickening, deformity of the arterial wall, and often with complications such as fissure, hematoma, and thrombosis. Advanced lesions may produce symptoms, but the lesions that precede them are clinically silent.This report is the second in a series of three. The first 1 provided a definition of the arterial intima and its atherosclerosis-prone regions. The third report will describe the different types of advanced atherosclerotic lesions and will provide a histological classification of all human atherosclerotic lesion types. The precursors of advanced lesions are divided into three morphologically characteristic types. Both type I and II lesions represent small lipid deposits in the arterial intima, and type II includes those lesions generally referred to as fatty streaks. Type III represents the stage that links type II to advanced lesions. The term "early lesions" is sometimes used for type I and II lesions. "Early" implies that these lesions are followed by "later" (advanced) lesions. It also implies that they are found early in life. Neither implication is necessarily "A Definition of Initial, Fatty Streak, and Intermediate Lesions of Atherosclerosis" was approved by the American Heart Association SAC/Steering Committee on October 20, 1992.Requests for reprints should be sent to the Office of Scientific Affairs, American Heart Association, 7272 Greenville Ave, Dallas, TX 75231-4596. true, although types I and II are generally the only lesions present in children, and there is evidence that certain type II lesions are prone to proceed to type III and more advanced lesions.The distinctions that separate individual lesion types are based on consistent morphological characteristics, which indicate that each type may stabilize temporarily or permanently and that progression to the next type may require an additional stimulus. The morphological features of each type of lesion and the time at which each tends to occur and predominate in the course of a human life are strong presumptive evid...

Lipoprotein Lipase (LPL) Strongly Links Native and Oxidized Low Density Lipoprotein Particles to Decorin-coated Collagen

“…For this purpose we obtained samples of coronary arteries from four explanted human hearts and stained frozen sections immunohistochemically for apoB-100, MDA-lysines, LPL, decorin, and collagen type I. The samples were graded according to the AHA guidelines (37,38), and we found areas of type I lesion in all four samples, type II lesion in two samples, type III lesion in one sample, and type V lesion on two samples. ApoB-100, MDA-lysines, LPL, decorin, and collagen were present in distinct, characteristic, partially overlapping areas of the intima.…”

Modulation of Endosomal Cholesteryl Ester Metabolism by Membrane Cholesterol

“…We obtained egg yolk phosphatidylcholine (P-2772), dioleoylphosphatidylserine (P-1060), dicetyl phosphate, trioleoylglycerol (T-9275), cholesteryl oleate, 4-methylumbelliferyl N-acetyl-␤-D-glucosaminide dihydrate, the sodium salt of adenosine 5Ј-monophosphate (A-1752), imipramine (I-0899), and progesterone (P-8783) from Sigma; U18666A from Biomol; 25-hydroxycholesterol from Steraloids; pepstatin A, leupeptin and the sodium salt of ATP from Roche Applied Science; [1,2,6, (18), LDL (18), and acetylated LDL (19) were prepared as described. Anionic liposomes were prepared as described (20) …”

“…One of the major hallmarks of atherosclerosis is the progressive accumulation of intracellular and extracellular cholesterol (1)(2)(3). In early stages of atherosclerosis excess cholesterol is mainly deposited as cholesteryl fatty acyl esters ("cholesteryl ester").…”

Macrophage function in atherosclerosis

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