Читать книгу Interventional Cardiology - Группа авторов - Страница 224

IVUS studies have shown that lumen enlargement after stent implantation is a combination of vessel expansion and plaque redistribution/embolization, not plaque compression [36–38]. Plaque reduction in patients with acute coronary syndromes is attributed to plaque or thrombus embolization [38]. Intrusion or prolapse of plaque through the stent mesh into the lumen is more common in acute coronary syndromes and in saphenous vein graft lesions. Importantly, after stent implantation there is a significant residual plaque burden behind the stent struts that almost always measures 50–75% at the center of the lesion. Thus, the stent CSA always looks smaller than the EEM even when the stent is fully expanded. Stent expansion describes the minimum stent CSA either as an absolute measure (absolute expansion), or compared with the predefined reference area – proximal, distal, largest, or average reference area – (relative expansion). Greater absolute stent expansion has been associated with better long‐term stent patency, better clinical outcomes and a lower risk of stent failure [4–5, 39]. Intravascular ultrasound studies have been relatively consistent in showing that a stent cross‐sectional area of 5.5 mm² best discriminates subsequent events in non‐left main lesions. For LM lesions, cut‐offs values are higher (e.g. >7 mm² for distal LM and >8 mm² for proximal LM by IVUS) [4–5, 40,41].

The recent expert consensus suggests that the cut‐off >80% for the MSA (relative to average reference lumen area) appears to be a reasonable approach to adopt in clinical practice [4,5].

Apposition refers to the contact between the stent struts to the arterial wall. Incomplete stent apposition is defined as one or more struts clearly separated from vessel wall with evidence of blood speckles behind the strut. There is no conclusive evidence suggesting that isolated acute incomplete stent apposition (in the absence of concomitant underexpansion) is associated with adverse clinical outcomes. Identifiable causes of restenosis other than intimal hyperplasia include chronic underexpansion (18–40%) stent fracture (<5%) and neoatherosclerosis [4,5].