© 2000 American Heart Association, Inc.
Commentary |
Natural History and Histological Classification of Atherosclerotic Lesions
An Update
From the Louisiana State University Medical Center, New Orleans.
Correspondence to Herbert C. Stary, MD, Professor of Pathology, LSU Medical Center, 1901 Perdido St, New Orleans, LA 70112. E-mail hstary{at}lsumc.edu (Arterioscler Thromb Vasc Biol. 2000;20:1177-1178.)
Key Words: atherosclerosis development • lipid core • fibrous cap • histological classification
Some years ago, this journal published three Scientific Statements, in which the American Heart Association’s (AHA’s) Committee on Vascular Lesions had compiled much of what is known about the composition and structure of human atherosclerotic lesions and about arterial sites at which they develop.1 2 3 The statements had concluded by recommending a numerical classification of histologically defined lesion types. The recommendation was thought to be timely and appropriate. Several autopsy studies in which state-of-the-art histological methods were used had just thrown new light on the compositions of lesions and on the diversity of mechanisms whereby they developed. After reviewing the new data, the Committee felt obligated to recommend use of a standard numerical nomenclature of precisely defined lesion types to replace a variety of duplicate and vague terms. The provision of an up-to-date histological classification of lesions was perceived as a priority, not least because of the urgent need for histological "templates" for images of lesions that were being obtained with a variety of invasive and noninvasive techniques that had become available in clinical practice.
The AHA-recommended classification had been originally developed and used to convey the results of an inquiry into the compositions of atherosclerotic lesions as they silently develop over much of a lifetime in a population. In the accompanying article in this issue, Virmani and colleagues4 suggest terms for lesions that, in their studies of sudden death, they found preferable to a numerical classification.
In this Commentary, some issues that regard the numerical classification are addressed and, it is hoped, clarified. The issues include the relation between specific numbered lesion types and the development of clinical manifestations, the nature of the difference between lesion types IV and V, and the existence of more than one sequence in lesion progression and provision for this in the numerical classification.
Except for lesion types I through III, which are always small and clinically silent, there is no certain correlation between a lesion’s composition and size on one hand and the degree of lumen obstruction and clinical manifestations on the other. Thus, either of lesion types IV through VI may obstruct the lumen of a medium-size artery to the point of producing a clinical event, even a fatal one, or lesions of the same histologies may exist without significantly obstructing the lumen.
Numerous pathological studies indicate that clinical manifestations and fatal outcomes are most often associated with processes included under the type VI lesion (although even these processes may remain silent). The criteria for the type VI histology include one or more of surface defect, hematoma, and thrombosis. The three processes are often interrelated, although sometimes only one or two are present. For example, a fissure may produce hematoma but little or no superimposed thrombus; occlusive thrombi may form on a surface lacking an apparent defect; ulcerated lesions without much of either hematoma or thrombus may be present.
Clinical manifestations may emerge and fatal outcomes occur in the presence of lesions of type IV or V when these reach a size that is sufficiently obstructive. Lesions at the type IV or type V stage contain a lipid core, but they differ from each other in the derivation and thus, the nature of the fibromuscular layer that faces the lumen above the lipid core (the "cap" of the lesion).
In type IV lesions, the cap still constitutes only preexisting intima, which at highly susceptible artery sites is relatively thick (adaptive intimal thickening). Thus, depending on location in the vascular tree, the thickness of the cap of type IV lesions varies somewhat. However, cap composition is like that of normal intima.1 3 Because in type IV lesions the lesion cap represents the thickness of the intima at the affected intimal site, it is primarily the amount of lipid that is segregated at the core that determines the degree to which the lumen will be narrowed at this stage of development. In most people, a type IV lesion will not obstruct the lumen much, in part because of the vessel wall’s ability, at this stage, for outward expansion. However, when blood lipid levels are very high and a large amount of lipid accumulates quickly, this lesion type, too, may narrow a lumen.
Type V lesions, on the other hand, are defined as those in which
major parts of the fibromuscular cap represent replacement of
tissue disrupted by accumulated lipid and hematoma or organized
thrombotic deposits. Cap portions or layers generated by disease and
added to the preexisting part have a greater proportion of rough
endoplasmic reticulum–rich smooth muscle cells. These cells do not
follow the alignments usual of the normal intima (including adaptive
thickening), and the caps contain a greater proportion of collagen
fibers. The new layers oppose outward expansion of the vessel wall, and
narrowing (loss) of the lumen is a prominent feature of type V lesions.
In the Figure
, the arrow from lesion type
VI to type V illustrates the transformation of hematoma and/or thrombus
to fibromuscular tissue and the formation of or increase in the
thickness of the cap portion of the type V lesion. A lesion may become
increasingly obstructive by repeatedly but only temporarily passing
through a type VI stage. Lesions containing fissures, small hematoma,
and thrombotic deposits are found in young adults.5 Thus,
increases in lesion thickness through processes additional to lipid
accumulation begin relatively early in life.
|
In the Figure
, the AHA-recommended classification is shown
in an updated arrangement. Lesion morphologies that had been listed as
types Vb and Vc in the 1995 statement3 are placed at the
end of the sequence as lesion types VII and VIII. This position better
reflects the directions in which lesion types may change
morphologically. It is, in part, the consequence of observations by
several groups of investigators of changes in lesions when high blood
lipid levels are drastically reduced in experimental
animals.5 These studies indicated that regression of lipid
from lesions comparable to human types IV and V (type VI had not been
produced in the animals) led to morphologies like those designated in
the Figure as types VII and VIII. It must be added that
histological compositions designated as types VII and
VIII might also be produced by processes other than lipid
regression.5
In the original classification, minimal changes (type II lesions)
are subdivided into those at highly susceptible sites of arteries and
prone to further development (type IIa) and those at moderately
susceptible sites that develop slowly, late, or not at all (type IIb).
A lesion’s position within the vascular tree and thus, the mechanical
forces and the nature of the vessel wall at that point, determine, in
large part, how a lesion is constituted. The characteristics of early
lesions at highly susceptible sites lie in their greater content of
lipid and macrophages and in the greater thickness of the
intima at these sites. In the Figure , the type II changes are
not subdivided into a and b types. Instead, the influence of highly
versus moderately susceptible arterial sites is emphasized,
and the propensity to development and progression is differentiated
with the use of either thick or thin arrows.
Atherosclerotic lesions result from a variety of pathogenetic
processes, including macrophage foam cell formation and death,
accumulation of extracellular lipid, displacement and reduction of
structural intercellular matrix and smooth muscle cells, generation of
mineral deposits, chronic inflammation, neovascularization, disruptions
of the lesion surface, and formation and transformation of hematoma and
thrombus to fibromuscular tissue. One or the other process may dominate
(or be lacking) in lesion development and progression. Some may
continue for the duration of the disease while others are added at
various stages. At later stages of lesion progression, many of the
processes may run synchronously. But despite lesion diversity, the
framework of principal morphologies and sequences shown in the Figure
has been documented.
In the AHA-recommended classification including the updated form
shown in the Figure, the preferred temporal sequence of typical
histological morphologies is denoted with roman
numerals. Steps in the development and progression of a disease are
normally designated with numerals in medical writing. The AHA Committee
had agreed that numerals that stood for strictly defined lesion types
were preferable to the continued use of the large variety of
traditional terms. To facilitate transition from existing gross
pathological nomenclatures to the numerical one, frequently used terms
that, though imprecise, seemed closest were appended to the precisely
defined roman numerals.
Because preferred sequences do exist, the use of consecutive
numerals is not only justified but, indeed, mandated. The arrows in the
Figure indicate that after type IV has developed, the pathways
to clinical disease vary. For example, a type IV lesion may develop
type VI changes without first gaining much fibromuscular tissue (thus,
not passing first through a type V stage), or a type IV or type V
lesion may calcify (ie, become a type VII lesion) without first (or
ever) developing type VI changes. Should additional developmental
sequences be revealed, for example as the resolution of clinical
imaging is perfected, a numerical scaffold would allow for additions
and rearrangement.
Received February 21, 2000; accepted February 21, 2000.
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M. Van Eck, I. S. T. Bos, W. E. Kaminski, E. Orso, G. Rothe, J. Twisk, A. Bottcher, E. S. Van Amersfoort, T. A. Christiansen-Weber, W.-P. Fung-Leung, et al. Leukocyte ABCA1 controls susceptibility to atherosclerosis and macrophage recruitment into tissues PNAS, April 30, 2002; 99(9): 6298 - 6303. [Abstract] [Full Text] [PDF]
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