Interventional Cardiology. Группа авторов

CSA and lumen CSA, the atheroma or plaque&media (P&M) complex is calculated.

      In stented vessels, the stent forms a third measurable structure (stent CSA). It appears as bright points along the circumference of the vessel. Complete quantification of a stented lesion is possible by tracing the EEM and lumen areas of the proximal and distal reference and the EEM, lumen, and stent areas of the stented lesion; calculating derived measures (minimum and maximum EEM, stent, and lumen diameters; peri‐stent P&M area and thickness; and intra‐stent intimal hyperplasia [IH, area and %IH); and measuring stent length. With the use of motorized pullback, area measurements can be added to calculate volumes using Simpson’s formula.

Qualitative analysis

Grayscale IVUS has some ability to differentiate plaque composition based on different echoreflectivity of the tissue. Atherosclerotic plaques are rarely homogeneous and contain a mixture of plaque components with different impedance (density). A standard approach is to compare the echointensity or “brightness” of the plaque to the surrounding adventitia that is used as a reference. Three basic types of lesions are distinguished according to plaque echogenicity: (i) “soft” or hypoechoic plaque does not reflect much ultrasound and appears dark with less echointensity compared to the adventitia (Figure 8.5), (ii) fibrous, and (iii) calcific plaques are characterized by equal or greater intensity than the adventitia. A plaque that is not so reflective as to cause shadowing is labeled “hard” or hyperechoic and is composed primarily of fibrous tissue. The presence of acoustic shadowing along with the brightest echoes and reverberations are characteristic of the presence of calcification (Figure 8.4). Extensive target lesion calcification may adversely impact the PCI procedure by affecting the ability for effective dilatation of a coronary stenosis and is associated with greater likelihood of stent underexpansion. In lesions with maximum circumferential extension of calcium >180 degree by IVUS, greater calcific burden was associated with a smaller stent area and greater stent eccentricity [4].

Figure 8.4 A pure soft or hypoechoic plaque is uncommon because atherosclerotic plaques are rarely homogeneous. (a) shows an example of a predominantly soft plaque – a thin fibrous cap (small arrows) and lipid core underlying it; the plaque is less bright than the adventitia a. In (b), fibrous plaque or hyperechoic plaque is shown. Hyperechoic plaque is as bright as or brighter than the adventitia a without shadowing. In this eccentric plaque, the thickness of the media behind the thickest part of the plaque b is an artifact caused by attenuation of the beam as it passes through the hyperechoic plaque. In reality, the media becomes thinner with increasing atherosclerosis. Note that the media behind the thinnest part of the plaque is also thinner – without artifacts. (c) shows superficial calcium – defined as calcium a that is closer to the intima than it is to the adventitia. Calcium shadows the deeper arterial structures; in this case, the arc of calcification is ~180°.

      Intimal hyperplasia due to in‐stent restenosis often appears to have low echogenecity depending, in part, on age and adjunct therapies (i.e. brachytherapy).

      The identification of thrombus is difficult by IVUS. It may appear as lobulated hypoechoic mass within the lumen, scintillating echoes, a distinct interface between the presumed thrombus imaging and underlying plaque, and blood flow through the thrombus (Figure 8.5j).

Figure 8.5 Diagnostic intravascular ultrasound was performed to assess the angiographic filling defect at the right coronary artery. The intravascular ultrasound images are shown from proximal (A) to distal (J). There is marked segmental positive remodeling (B to I) with severe malapposition and underexpansion throughout the entire length of the stent, which appear “sized” just to the smallest lumen (panel B). Notice the space between the stent strut and the intima and the blood speckle/thrombus behind the stent struts in the axial (B through I) as well as the longitudinal view (at the bottom). At the site of maximum stent malapposition (I), the stent area (4.99mm²) was smaller than lumen area (15.22mm²) and external elastic membrane (26.64mm²). The entire distal 20+mm of the stent was thrombus filled with additional thrombus on the abluminal side of the stent partly filling the area of malapposition and causing the linear filling defect on the angiogram. The small intraluminal mass on IVUS (J, small arrows) represented the tail of the thrombus with the bulk being proximal to that slice.

      Source: From Caixeta A et al. Einstein 2013;11: 364‐366.

Comparison of IVUS and angiography

Coronary angiography depicts the coronary anatomy as a longitudinal silhouette of the lumen. Conversely, IVUS with its tomographic perspective directly images the lumen, atheroma, and the vessel wall. Coronary angiography significantly underestimates the presence, severity, and extent of atherosclerosis compared to IVUS [4–6]. Furthermore, IVUS routinely shows significant atherosclerosis in angiographically “normal” segments in patients undergoing PCI [11]. This phenomenon may be explained by three major factors: (i) coronary atherosclerosis is often diffusely distributed involving long segments of the vessel containing no truly normal reference segment for comparison, (ii) complex atherosclerotic plaques are not appreciated by the two‐dimensional “silhouette”, and (iii), most importantly, the presence of arterial wall remodeling [4,5]. In some circumstances diffuse, concentric, and symmetrical coronary disease can affect the entire length of the vessel resulting in an angiographic appearance of a small artery with minimal luminal narrowing.

      Coronary artery remodeling

Arterial remodeling of the vessel wall at the site of coronary plaques was originally described from necropsy examinations by Glagov et al. [12] and later validated in vivo by IVUS imaging [30]. “Positive,” “outward,” or “expansive” remodeling is defined as an increase in arterial dimensions; and “negative,” “inward,” or “constrictive” remodeling is defined as a smaller arterial dimension. Positive remodeling occurs as a compensatory increase in local vessel size in response to increasing plaque burden, especially during early stages of atherosclerosis [4,5] (Figures 8.5 and 8.6). An absolute reduction in lumen dimensions typically does not occur until the lesion occupies, on average, an estimated 40–50% of the area within the EEM (40–50% plaque burden). Conversely, negative remodeling has been implicated in the development of native significant stenosis in the absence of plaque accumulation (Figure 8.7) [13–15].

Figure 8.6 This patient presented with a STEMI a complex left anterior (lesion between a to h) and disrupted plaque by IVUS. The IVUS imaging run shows the residual fibrous cap from b to e, the evacuated plaque cavity (asterix), and the true lumen containing the catheter. Note a severe lesion in the angiogram after fibrinolysis. Distal to the plaque