Normal intima
Single-layer appearance or three-layer appearance with intimal thickness < 0.3 mm
Minimal atherosclerotic burden
≤20% of VA occupied by plaque
Moderate atherosclerotic burden
>20%, ≤40% of VA occupied by plaque
Large atherosclerotic burden
>40%, ≤60% of VA occupied by plaque
Massive atherosclerotic burden
>60% of VA occupied by plaque
Atherosclerotic lesions are heterogeneous and include varying amounts of calcium, dense fibrous tissue, lipid, smooth muscle cells, thrombus, etc. By IVUS, imaging can grossly separate lesions into subtypes according to echodensity and the presence or absence of shadowing and reverberations (Table 4.2) [3].
Table 4.2
Intravascular ultrasound plaque characteristics
Homogeneousa | Mixedb | ||
|---|---|---|---|
Soft | Fibrous | Calcificc | Soft/fibrous |
Low echoreflective | High echoreflective | High echoreflective with shadowing | Soft/calcific |
Fibrocalcific | |||
4.1.1 Soft (Echolucent ) Plaque
The term “soft” refers not to the plaque’s structural characteristics but rather to the acoustic signal that arises from low echogenicity. Soft plaque is less bright compared with reference adventitia. Soft plaque contains varying amounts of fibrous and fatty tissue. Reduced echogenicity may also result from a necrotic zone within the plaque, an intramural hemorrhage, or a thrombus (Fig. 4.1a).
Fig. 4.1
Plaque morphology. (a) Soft (echolucent) plaque. Soft plaque is less bright compared with reference adventitia. Soft plaque contains varying amounts of fibrous and fatty tissue. (b) Fibrous plaque has an intermediate echogenicity between soft (echolucent) atheromas and highly echogenic calcific plaques. Fibrous plaque is as bright as or brighter than the adventitia without shadowing. (c, d) Calcified plaque is echodense (hyperechoic) plaque (brighter than the reference adventitia) that shadows using IVUS calcium can be localized and characterized as superficial [closer to tissue-lumen interface (c)] and deep [closer to the media-adventitia junction (d)]. (e) When there is no dominant plaque composition, the plaque was considered “mixed.” Mixed plaque is also called as “fibrocalcific,” “fibrofatty” plaque
4.1.2 Fibrous Plaque
Fibrous plaque has an intermediate echogenicity between soft (echolucent) atheromas and highly echogenic calcific plaques. Fibrous plaque represents the majority of atherosclerotic lesion. Fibrous plaque is as bright as or brighter than the adventitia without shadowing. Very dense fibrous plaques may produce sufficient attenuation to be misclassified as calcification with acoustic shadowing. Both calcified and fibrotic plaques are hyperechoic (Fig. 4.1b).
4.1.3 Calcified Plaque
Calcium is a powerful reflector of ultrasound. Calcific deposits appear as bright echoes that obstruct the penetration of ultrasound, a phenomenon known as “acoustic shadowing .” In practice calcium is echodense (hyperechoic) plaque (brighter than the reference adventitia) that shadows using IVUS calcium can be localized and characterized as superficial (closer to tissue-lumen interface) and deep (closer to the media-adventitia junction) and quantified according to its arc and length. The arc of calcium can be measured (in degrees) by using an electronic protractor centered on the lumen. Because of beam-spread variability at given depths within the transmitted beam, this measurement is usually valid only to ±15°. Semiquantitative grading has also been described, which classifies calcium as absent or subtending 1, 2, 3, or 4 quadrants. The length of the calcific deposit can be measured using motorized transducer pullback (Fig. 4.1c, d).
4.1.4 Mixed Plaque
Plaques frequently contain more than one acoustical subtype. When there is no dominant plaque composition, the plaque was considered “mixed.” Mixed plaque is also called as “fibrocalcific ,” “fibrofatty ” plaque (Fig. 4.1e).
4.2 Vulnerable Plaque
No definitive IVUS features define a plaque as vulnerable. However, necropsy studies demonstrated that unstable coronary lesions are usually lipid rich with a thin fibrous cap. Accordingly, hypoechoic plaques without a well-formed fibrous cap are presumed to represent potentially vulnerable atherosclerotic lesions. The important mechanisms leading to the development of acute coronary syndrome (ACS) are rupture of a vulnerable plaque and subsequent thrombus formation. The majority of ACS events are the result of sudden luminal thrombosis, with 55–60% due to plaque rupture, 30–35% caused by plaque erosion, and a small portion resulting from a calcified nodule.
4.2.1 Plaque Rupture
Rupture of vulnerable plaque and/or endothelial erosions with subsequent thrombus formation are considered the main mechanisms implicated in the pathogenesis of ACS. Ruptured plaque contains a cavity that communicated with the lumen with an overlying residual fibrous cap fragment [4] (Figs. 4.2 and 4.5). Rupture sites separated by a length of artery containing smooth lumen contours without cavities are considered to represent different plaque ruptures (multiple plaque ruptures) (Fig. 4.3). Plaque rupture is closely related to obstructive thrombus formation, and the longitudinal morphology of plaque rupture also affects the coronary flow. The presence of thrombi may obscure IVUS detection of plaque rupture.
Fig. 4.2
Plaque rupture . Ruptured plaque contains a cavity that communicated with the lumen with an overlying residual fibrous cap fragment
Fig. 4.3
Multiple plaque rupture . Rupture sites separated by a length of artery containing smooth lumen contours without cavities are considered to represent different plaque ruptures (multiple plaque ruptures)
4.2.2 Thrombus
The identification of thrombus is one of the most difficult aspects of IVUS imaging [5, 6] (Figs. 4.4 and 4.5).
