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C HAPTER 5 / Atherosclerosis, Inflammation, and Acute Coronary Syndrome 115
transmigration from the plasma, encouraged by the areas of de- Type Va lesions can form larger compound lesions, composed
creased local blood flow (called eddies) at lesion-prone sites. Ini- of irregular intercalating lipid cores separated by thick layers of fi-
tially, these lesions colocalize with adaptive intimal thickenings. brous connective tissue (variably termed multilayered fi-
Lipid cores thicken the artery wall and are clearly visible when the broatheroma). Both hemodynamic and tensile forces may con-
luminal surface of the lesion is examined, although thickening tribute to the formation of such compound lesions; as lesions
usually occurs at the external boundary and contributes little to impinge on the circulation, alterations in blood flow promote
narrowing of the vessel lumen at this stage. 39 asymmetric vascular narrowing and a redistribution of the regions
This lesion type is characterized by the displacement of the inti- of predisposition to lesion formation. 39 An alternate explanation
mal smooth muscle cells and the intercellular matrix of the deep in- may be the serial rupture of the lesion surface, hematoma forma-
tima by accumulating pools of extracellular lipid. The dispersed tion, and thrombosis followed by fibrious organization.
cells appear attenuated and elongated with thickening of the base- Although type Vb lesions are primarily differentiated by calci-
ment membranes. Calcium particles are often found within the fication, they tend to possess greater fibrous connective tissue
lipid cores and even within the organelles of some of the smooth compared to earlier lesion types. Mineral deposits may eventually
muscle cells. In addition, capillaries may be readily identified replace a lesion’s core (an accumulation of dead cells and extracel-
around the lipid core and are most common at the lateral margins lular lipid). Such calcified lesions are variably also termed a type
and facing the lumen. Macrophages, smooth muscle cells, and even VII lesion. 28,31
mast cells and lymphocytes, populate the region between the lipid The type Vc lesions, being fibrotic and largely devoid of lipid
core and the endothelial surface. Coalescence of the lipid core leads core, often occur in the arteries in the lower extremities 24 and
to a subsequent increase in fibrous tissue (mainly collagen), which have been referred to as a type VIII lesion by some investiga-
will in turn alter the intima above the lipid core. When the fibrous tors. 28,33 These lesions may form by one of several mechanisms
tissue enrichment of the intima covering the lipid core occurs, the including thrombus organization, extension of the fibrous com-
lesion is classified as type V. In either conventional histological sec- ponent of an adjacent fibroatheroma, or resorption of lipid cores.
tions, or by examination by the unaided eye, the upper intimal layer Although fibrotic lesions rarely possess a lipid core, a positive stain
of a type IV lesion is indistinguishable from the fibrotic cover (also for lipids is not uncommon in this lesion type. It is noteworthy
known as the fibrous cap) of a type V lesion. This explains why both that wall shear stress caused by increased hydrostatic pressure is
types IV and V lesions are referred to as fibrous plaques. common in the lower extremities and could conceivably provide
Although this lesion class only minimally contributes to lumi- another mechanism for this lesion formation.
nal narrowing, type IV lesions have important clinical significance.
Enrichment of the region between the lipid core and the lesion sur- Type VI Lesions
face with proteoglycans, foam cells, and dispersed smooth muscle Lesion types V and VI may undergo disruption of the lesion sur-
cells with decreased collagen content renders the lesion susceptible face or develop hematoma, hemorrhage, or thrombotic deposits.
to fissures or ulceration. Ominously, localization and accumulation They account for the majority of atherosclerotic morbidity and
of macrophages in the periphery of advanced lesions, particularly mortality. Any one of these complications is sufficient to recate-
type IV, makes them vulnerable to sudden rupture. gorize type IV or V lesions as type VI lesions; they are also referred
to as complicated lesions. Moreover, the particular complicating
Type V Lesions event permits subdivision of type VI lesions into three subtypes
This stage in lesion progression is referred to as a fibroatheroma, be- according to (a) disruption, (b) hemorrhage, or (c) thrombosis;
cause of the intimal accumulation of abundant fibrous connective although practically, lesions are often complex and rarely conform
tissue adjacent to a lipid core. When a type V lesion has both a lipid perfectly to the lesion classification criteria. Indeed, instances of
core and calcification within the lesion, it is referred to as a type Vb surface disruptions, hematoma, and thrombosis superimposed on
lesion. Type Vc lesions are devoid of a lipid core and contain mini- other lesions types or even on intima without a noticeable lesion
mal lipid deposition. Type V lesions tend to cause a more noticeable are not uncommon. The composition of blood, the integrity of
narrowing of arteries than type IV lesions and are particularly clin- the intima, the sensitivity of the inflammatory response, and the
ically relevant given their susceptibility to fissure, hemorrhage, and dynamic range of shear and tensile forces to which the lesion or
rupture with hematoma and/or thrombus formation. intima is exposed varies greatly between persons. While physio-
Population studies of advanced lesion histology reveal that logical and biochemical studies aimed at characterizing both the
reparative smooth muscle cells infiltrate regions of the intima in determinants and mechanisms resulting in the spectrum of lesion
which lipid cores disturb or disrupt the cell and intercellular ma- types is ongoing, continued innovation in clinical imaging of le-
trix structure. This fibrous tissue often accounts for more of the sions has contributed much to the more accurate identification of
thickness of the lesion than its underlying lipid core. The new tis- lesion types and their associated clinical syndromes.
sue is composed of both collagen and smooth muscle cells. These In the past, clinical assessment of atherosclerotic lesions was con-
new smooth muscle cells are distinct from their older counterparts fined to advanced, gross vascular abnormalities, including
in that they are enriched in rough-surfaced endoplasmic reticu- aneurysms and vascular stenoses. But the integration of newer and
lum. Previous thrombi appear to result in thicker lesions and sur- emerging technologies has permitted more accurate depiction of le-
rounding tissue as they are incorporated into the growing lesion. sion morphology, which in turn informs more specific interventions
Type V lesions also contain large, numerous, and newly formed (Table 5-1). Targeting of treatment has been honed further by the
vessel capillaries at the periphery of the lipid core. The media ad- growing understanding of the pathophysiology of lesion progres-
jacent to the intima of type V lesions are characterized by deple- sion and associated clinical events. This has permitted clinicians to
tion and disorganization of smooth muscle cells. The surrounding move beyond simple diagnosis to proactive prevention of compli-
media and adjacent adventitia are enriched in lymphocytes, cated lesions through detection of earlier lesions and more accurate
macrophages, and macrophage foam cells. lesion characterization. Morphological, immunohistochemical, and