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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].