Название | Interventional Cardiology |
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Автор произведения | Группа авторов |
Жанр | Медицина |
Серия | |
Издательство | Медицина |
Год выпуска | 0 |
isbn | 9781119697381 |
Other unusual lesion morphology
During coronary angiography it is common to encounter unusual appearing lesions that elude accurate characterization despite thorough examination using multiple radiographic projections. The use of IVUS allows accurate characterization of unusual morphology: filling defects, aneurysms, and spontaneous dissections. While most filling defects are true thrombi, a small percentage are highly calcified plaque (Figures 8.8 and 8.9) or even calcified nodules, an unusual form of vulnerable plaque.
Figure 8.9 This patient underwent a previous PCI with DES implantation of a lesion, in the diagonal artery, during which the artery was dissected. Follow‐up catheterization showed both restenosis and a large aneurysm on angiography. The IVUS shows from proximal to distal (a to h) the body of the aneurism (asterix in the longitudinal view and c to h) and the eccentric proximal restenotic lesion (b). Notice that the adventitia stops at the point of transition from the vessel to the aneurysm (c and d), indicating loss of vessel wall integrity and making this, in fact, a pseudoaneurysm. Notice the double lumen from e to g; and normal vessel with three‐layer aspect in h.
In an IVUS analysis of 77 angiographically diagnosed aneurysms, 27% were true aneurysms (Figure 8.10), 4% were pseudoaneurysms (Figure 8.10), 16% were complex plaques, and 53% were normal arterial segments adjacent to stenoses [6]. In‐stent neoatherosclerosis has been recently described as an important mechanism of late stent failure (i.e. restenosis and stent thrombosis).
Figure 8.10 This young, female patient presented with STEMI and type 4 SCAD by angiography in the mLAD. IVUS showed a normal three‐layer aspect to the proximal vessel (a and magnified image in b). Notice the crescent aspect of the hyperechoic hematoma comprising the true lumen from c to h (arrows in e). FL indicates false lumen and TL true lumen; note a septal branch within the FL in panel F.
Courtesy of Dr. José Mariani Jr.
Spontaneous coronary artery dissection (SCAD)
Both IVUS and OCT can be used to diagnosis of SCAD, and both modalities have strengths and weaknesses). IVUS can be preferred where there in evidence of false lumen (Type 1), and in small calibre and tortuous vessels, where the imaging probe risks being occlusive; and proximal vessel dissections, where the false lumen stretches the external elastic lamina, increasing the vessel size. However, IVUS resolution can be insufficient for the detection of intima‐media complex fenestrations as seen in OCT [5]. By IVUS, a spontaneous coronary artery dissection appears as a medial dissection with an intramural hematoma occupying some or all of the dissected false lumen without identifiable intimal tears and without a communication between the true and false lumens, typically in a non‐atherosclerotic artery (Figure 8.11).
Figure 8.11 This patient presented with restenosis at follow‐up after stent implantation in the right coronary artery (arrows on angiogram and telling angiotomography images, top panel). On IVUS, all stent struts are seen at proximal and distal references (e.g. 20 mm and 25 mm), whereas at the fracture site there is superficial calcification from 11 to 4 o’clock and no stent strut is seen (arrow).
Guidance for stent implantation
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