Table 2.

Comparison of American Heart Association’s histopathological classification^,20,64,65 and proposed endovascular SFA classification of atherosclerosis.

Atherosclerosis Grade	Modified AHA Classification	Histology findings	Endovascular SFA Classification	Endoluminal description
Normal artery	Normal artery	Three concentrically oriented layers: 1) TI formed by endothelium overlying a thin connective tissue with a prominent internal elastic membrane; 2) TM with abundant smooth muscle cells in a wavy matrix of elastic fibers and collagen; 3) TE with collagen fibers and fibroblasts.	Normal endoluminal surface	Delicate smooth endoluminal surfaces with homogeneous reflectance, blue and green AF.
Grade I	Intimal thickening	Proliferation of smooth muscle cells underlying the intima, in a proteoglycan-rich matrix. It does not contain macrophages.
Grade II	Intimal xanthomata	Focal accumulations of fat-laden macrophages at the intima. Predominantly contain macrophages and few T-cells and smooth muscle cells.	Early lesion	Slightly raised, small dot-like or streak-like endoluminal lesions with preserved reflectance and slightly lower AF in blue and green channels compared to surrounding surface.
Grade III	Pathologic intimal thickening or intermediate lesion	True necrosis is not apparent, and there is no evidence of cellular debris; some lipid may be present deep in the lesion, but it is dispersed. The fibrous cap overlying the areas of lipid is rich in smooth muscle cells and proteoglycans. Some scattered macrophages and lymphocytes may also be present, but these are usually sparse.	Intermediate lesion	Longitudinal elevated lesions with preserved reflectance and low blue and green AF compared to surrounding surface.
Grade IV	Fibrous cap atheroma	Thick layer of connective tissue covering the lipid or necrotic core. The cap consists purely of smooth muscle cells in a collagenous proteoglycan matrix, with varying degrees of infiltration by macrophages and lymphocytes.	Advanced lesion	Large lesions protruding into the lumen or causing circumferential stenosis. Lesions have smooth homogeneous surfaces with preserved reflectance, with reduction of luminal AF proportional to the thickness of the fibrous cap.
Grade V	Thin fibrous cap atheroma	Thin fibrous cap (mean cap thickness of 74μm±24μm) heavily infiltrated by macrophages with loss of smooth muscle cells, overlying a large necrotic core (approximately 25% of plaque area).
Grade VI	Complicated plaque	Surface defects include: Ulcer: excavation in the endoluminal surface of a plaque caused by embolization of thrombus with a portion of the necrotic core after exposure to lumen surface; Erosion: identified when serial sectioning of a thrombosed arterial segment fails to reveal fibrous cap rupture. Typically, the endothelium is absent at the erosion site. The exposed intima consists predominantly of smooth muscle cells and proteoglycans, and surprisingly, the eroded site contains minimal inflammation; Fissure or rupture: clear communication between the lipid core and the lumen with a break in the fibrous cap.	Ulcerated plaque	Ulcers appear as punched-out lesions with slightly raised, irregular bead-like borders and a central dark grey crater with reflectance and “starry sky” speckled pattern in blue and green channels.
		Intraplaque hemorrhage is an area of the plaque with fresh or organized erythrocytes causing disruption of plaque architecture.	Hemorrhagic plaque	Distinct dark grey area in the dome of plaques with low reflectance and negligible AF.
		Thrombus is a mass formed by erythrocytes, fibrin, and platelets in the luminal side of a plaque.	Plaque with intraluminal thrombus	Occlusive or sub-occlusive intraluminal lesion with variable reflectance (preserved in chronic clots and diminished in acute clots) and negligible AF.