Interventional Cardiology. Группа авторов

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% of those with non‐ST‐segment elevation myocardial infarction (NSTEMI). Plaque ruptures and attenuated plaques are considered to be unstable and have been identified in both culprit and non‐culprit lesions of patients with (STEMI) [4–5]. Histopathologically, the vast majority of attenuated plaques correspond to either a fibroatheroma with a necrotic core or pathologic intimal thickening with a lipid pool; almost all segments with superficial echo attenuation indicated the presence of an fibroatheroma with an advanced necrotic core [19]. Most importantly, attenuated plaque has been associated with the occurrence of microvascular obstruction after primary PCI no‐reflow phenomenon, and with late acquired stent malapposition in patients with STEMI [4–6,20,21].

      Detection of Vunerable Plaque

PROSPECT and VIVA were the first prospective studies that used three‐vessel IVUS imaging to examine it is efficacy in detecting nonculprit lesions that are likely to progress and cause cardiovascular ischemi events [5] In PROSPECT [22], a minimum lumen area≤4mm², plaque burden ≥ 70%, and the presence of a TCFA phenotype, derived by virtual histology (VH)‐IVUS, were predictors of subsequent non‐culprit MACE. Lesions with these high risk plaque characteristics were eleven times more likely to cause events within a 3.4‐year follow‐up than simple lesions [hazard ratio (HR): 11.05, P < 0.001]; however, the positive predictive value of these three high‐risk plaque features for subsequent events was low (18.2%). In the light of IVUS limitations in detecting vulnerable plaque [22–25] other imaging modalities including NIR and OCT has the potential value of vulnerable plaque detection (e.g. COMBINE OCT‐FFR; PROSPECT II [26,27] and plaque sealing are promising (PROSPECT II ABSORB; PREVENT Trial NCT02316886 [28].

      Role of intravascular imaging for assessment of lesion severity

Coronary angiography may underestimate stenosis severity most markedly in arteries with a 50–75% plaque burden and in patients with multivessel disease [6]. In patients with stable coronary artery disease, fractional flow reserve (FFR) or instantaneous flow reserve (iFR) is the well‐established physiologic index to assess the functional significance of a coronary stenosis. Studies have used FFR ≤0.80 as the optimal cut‐off point to guide revascularization [29,30], and have reported correlation between FFR values and anatomic parameters (especially minimum lumen area; MLA) derived from IVUS or optical coherence tomography (OCT) [31]. Of the IVUS‐derived measurements, MLA cut‐off values to predict FFR had been widely reported. The correlation between MLA cut‐off points and ischemic FFR threshold ranged from 2.0 to 3.9 mm² in non‐left main coronary artery (LMCA) intermediate stenosis and from 4.5 to 5.9 mm² in LMCA stenosis [4–5,32]. The FIRST (Fractional Flow Reserve and Intravascular Ultrasound Relationship) study, based on a multicenter, prospective registry in the USA and Europe proposed 3.07 mm² as a best cut‐off value to define the presence of myocardial ischemia [33]. In the largest sample‐size and international multicenter study with 822 patients (881 lesions), Han et al. [31] found that best cut‐off value of IVUS‐MLA to define the functional significance (FFR <0.8) to be 2.75 mm². A meta‐analysis of 11 studies comparing IVUS‐MLA with FFR for assessment of intermediate lesions showed that the weighted overall mean MLA cut‐off was 2.61 mm² in non‐LMCA and 5.35 mm² in LMCA to predict a functional stenosis [34].

      Atherosclerotic obstruction of the LMCA is present in approximately 4% of all coronary angiograms [35] and is often underestimated by coronary angiography. The main reasons for the discrepancy between angiography and IVUS are the following: (i) diffuse atherosclerotic plaque involvement may lead to a lack of a “true normal” reference segment, (ii) a short LMCA makes identification of a normal reference