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 rupture on the angiogram is an echo‐attenuated plaque (f and g); attenuation is defined as shadowing or attenuation of the ultrasound signal (loss of echoes) in the absence of calcification. Also note positive remodeling within the lesion (markedly from d to g) compared to the proximal (A) and distal (H) vessel reference.
Figure 8.7 An eccentric, calcific, and small plaque accumulation leading to negative remodeling. (a) and (c) refer to proximal and distal vessel references and their respective longitudinal views (white arrows in d). In (b) notice how the vessel cross‐sectional area (or EEM) is smaller than both the proximal and distal vessels. The longitudinal view depicts clearly the artery shrinkage at the lesion site.
Figure 8.8 Diagnostic IVUS was performed to assess this angiographic filling defect at the proximal right coronary artery (white arrow in the angiogram). The IVUS imaging run begins at the ostium a of the right coronary artery to beyond the filling defect b. Note the calcification (white arrow in the IVUS) without lumen compromise.
Source: Mintz 2005 [5]. Reproduced with permission of Taylor & Francis.
A number of definitions of remodeling have been proposed and published [4–6,13–16]. One definition compares the lesion EEM CSA to the average of the proximal + distal reference EEM CSA; positive remodeling is an index >1.0 and negative remodeling <1.0. A second definition defines positive remodeling as a lesion EEM greater than the proximal reference EEM, intermediate remodeling as a lesion EEM between the proximal and distal reference EEM, and negative remodeling as a lesion EEM less than the distal reference EEM. Using a third definition, arterial remodeling has been calculated by a remodeling index (lesion/reference EEM); positive remodeling is an index >1.05, intermediate remodeling is an index of 0.95–1.05, and negative remodeling is an index <0.95.
It is important to note that all of these remodeling definitions are based on a comparison of the reference EEM and lesion EEM. Accordingly, because both reference and lesion sites may have undergone quantitative changes in EEM during the atherosclerotic process, the evidence of remodeling derived from this index is relative and indirect. It depends on the definition of the reference, and the classification of an individual lesion depends on the definition used.
Inaba et al. [37], have reported a novel concept of remodeling, in which positive (RI >1.0) and negative (RI <0.88) lesion site remodeling was associated with unanticipated non‐culprit lesion major adverse cardiac events in the PROSPECT study.
Unstable lesions
In patients with acute coronary syndromes, culprit lesions more frequently exhibit positive remodeling and a large plaque area; conversely, patients with a stable clinical presentation more frequently show negative remodeling and a smaller plaque area [4–6]. Echolucent plaques are also more common in unstable than in stable patients. In addition, unstable lesions have less calcium than stable lesions; and when present, calcific deposits in unstable lesions are small, focal, and deep [6]. Plaque ruptures can occur with varying clinical presentations although they are more often associated with acute coronary syndromes [39]. Typical IVUS features of acute myocardial infarction include plaque rupture, thrombus, positive remodeling, attenuated plaque, spotty calcification, and thin‐cap fibroatheroma (Figure 8.6) [4–5].
Attenuated plaque is defined as hypoechoic or mixed atheroma with deep ultrasound attenuation without calcification or very dense fibrous plaque (Figure 8.6). Wu et al. [17] reported that 78% of the patients with acute myocardial infarction had attenuated plaques in the Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction (HORIZONS‐AMI) trial. Lee et al. [18] documented that attenuated plaque was observed in 39.6% of patients with ST‐segment elevation myocardial infarction (STEMI) and 17.6%
