Скачать книгу

the correlation between angiography and necropsy or IVUS appears to be better in non‐LMCA lesions possibly because of unique geometric and angulation issues in the LMCA [66], and (v) significant inter‐ and intraobserver variability in the angiographic assessment of LMCA disease, especially in ostium location [4–6]. Hence, comparable to LMCA limitations of FFR, IVUS interrogation of the LMCA has multiple shortcomings. Imaging pullback from 2 directions (i.e. from each of its 2 branch arteries) can be helpful.

      Other unusual lesion morphology

Schematic illustration of patient underwent a previous PCI with DES implantation of a lesion, in the diagonal artery, during which the artery was dissected. Schematic illustration of young, female patient presented with STEMI and type 4 SCAD by angiography in the mLAD.

      Courtesy of Dr. José Mariani Jr.

      Spontaneous coronary artery dissection (SCAD)

Schematic illustration of patient presented with restenosis at follow-up after stent implantation in the right coronary artery.

      Stent sizing

      Pre‐interventional IVUS is performed to assess stenosis severity and plaque composition and distribution, measure reference vessel size, and measure lesion length. As a result, stent size can be chosen more accurately than solely by angiography. There are a number of paradigms that can be used. Stent size can be selected by identifying the maximum reference lumen diameter (proximal or distal to the lesion); it results in stent upsizing without an increase in complications. At the other extreme, stents can be sized to the “true vessel,” “media‐to‐media,” or mid‐wall dimensions to reflect the amount of angiographically silent disease and, in most cases, the extent of positive remodeling, not just vessel size. Typically, this measurement will be larger than reference lumen reference and, thus, should be used only by experienced operators who understand its limitations.

      IVUS measures lesion length more accurately than angiography because IVUS eliminates foreshortening, vessel tortuosity, or bend points.

      Stent expansion and malapposition

      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].

      Clinical

Скачать книгу