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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3592_Библиотеки_им_академика_М_И_Перельмана
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Vascular and Intravascular Imaging Trends, Analysis, and Challenges, Volume 1
https://t.me/medicina_free
edge of the struts, and in polymeric scaffolds is the area between the abluminal side
of the strut and the lumen contour [67]. They also quantified the area occupied by
the scaffold/stent struts, with exclusion of the strut and neointimal areas from the
flow area and usage of interpolated lumen contour to assess the degree of strut
embedment on the vessel wall. The authors emphasize that after the integration of
the BRS in the vessel wall, measurements of scaffold area, neointimal area and ISA
area can no longer be used and, at long-term follow-up, only the flow area is a
comparable parameter, between metallic and bioresorbable devices.
So far, limited data exist in the vascular healing process associated with
absorbable metal scaffolds. OCT analysis performed in a subgroup of patients in
BIOLSOVE-II showed that the minimal lumen area decreased significantly from
post-procedure to 6 months. However, between 6 and 12 months the difference was
not significant. In addition, maximum backscattered values also decreased significantly from the post-procedure to 6 months. At baseline, magnesium struts appear
as bright structures with shadowing, but over time they are resorbed and only
vestiges of struts are visible at 12 months. This process is evident through the
changes in the maximum values of backscattering and attenuation values. According
to this data, serial imaging of the magnesium scaffold appears to refl ect the
restoration of the vessel anatomy, with an almost complete reabsorption at 12
months [ 68].
2.5 Bioresorbable scaffolds in real-world clinical settings
The following cases depict the use of the bioresorbable technology in real-world
clinical cases, and the utility of OCT for pre-device assessment, scaffold optimization and evaluation of intravascular complications after scaffold implantation,
which are often not visible on coronary angiography.
2.5.1 Case 1—the need for state-of-the-art peri-procedural intravascular imaging
A 57 year old male, obese patient with a past medical history of hypertension,
dyslipidemia and past smoking was admitted to the intensive cardiac care unit with a
non-ST-elevation acute myocardial infarction. He underwent coronary angiography
that revealed three vessel diseases: occluded mid-right coronary artery (RCA) with
visible retrograde filling, occluded mid-circumflex artery (LCX) with visible retrograde filling, and left anterior descending artery (LAD) with a subocclusive lesion in
its mid portion. Left ventriculography revealed postero-basal hypokinesia. RCA
was considered the culprit and PCI was performed using a standard floppy 0.014″
guidewire, a 2.5/14 mm compliant balloon for predilation and an Absorb 3.5/18 mm
stent (slowly deflated). Postdilation was not performed due to the optimal angiographic result with apparent good apposition (figures 2.2 and 2.3).
Two days later, the patient was submitted to staged PCI of the LAD. After
predilation with a 2.5/20 mm compliant balloon, a second lesion (75% by QCA) was
evident in the mid/distal segment of the LAD and predilated with a 2.0/15 mm
compliant balloon. Subsequently, two Absorbs were implanted, 2.5/18 mm distally
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Figure 2.2. (a) LAD with a subocclusive lesion in its mid portion, (b) LCX occluded after the second obtuse
marginal branch (OM) and (c) RCA occluded in its mid segment.
Figure 2.3. (a) RCA after predilation with a 2.5/14 mm compliant balloon, (b) slow deflation of an Absorb
3.5/18 mm stent and (c) final result (arrow pointing at the Absorb site).
and 3.0/23 mm proximally without overlap, followed by postdilation of both
scaffolds with a non-compliant 3.0/12 mm balloon. The final angiographic result
was good, with no visible complications (figure 2.4).
One month after the procedures, the patient reported mild shortness of breath
during moderate effort which worsened throughout the following months, though
no chest pain was reported. The patient maintained dual antiplatelet therapy with
aspirin (100 mg per day) and ticagrelor (90 mg twice a day). Angiographic revision
was scheduled and performed six months after the index event, revealing an
occluded mid LAD with retrograde filling by the RCA, before the first implanted
BRS. OCT was performed in the RCA, which revealed malapposition in the mid
portion of the scaffold (figure 2.5). PCI of the LAD was performed with double
cannulation. After the guidewire was advanced into the LAD, dilation with a noncompliant 2.0/20 mm balloon was performed. OCT showed diffuse restenosis of
both the distal and proximal BRS and two significant additional lesions, one in the
gap between the scaffolds, and the other proximal to the first implanted BRS (edge
dissection during the first device implantation? A de novo lesion?). Dilation with
non-compliant balloons was accomplished, followed by the implantation of a DES
in the first lesion, overlapping the proximal scaffold. In the second lesion, a new
DES was implanted overlapping both BRS scaffolds. Afterwards, dilation of the
distal BRS with a drug-eluting balloon was performed. Final OCT showed no edge
dissections and good strut apposition (figures 2.6–2.8). This case illustrates the
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Figure 2.4. (a) LAD predilation with two compliant balloons (2.0/15 mm distally and 2.5/20 mm proximally),
(b) LAD after implantation of two Absorbs (one dot: 3.0/23 mm; two dots: 2.5/18 mm) and (c) final result,
after postdilation.
Figure 2.5. (a) RCA at 6 months after the index event with a good angiographic result, (b) distal part of the
scaffold, with neointimal growth covering the polymeric struts, (c) and (d) mid portion of the scaffold with
malapposition between 5 and 10 o’clock, (e) proximal part of the scaffold with good apposition and luminal
area, and (f) proximal RCA with calcified plaques (*).
usefulness of OCT during PCI, both in type A and in more complex lesions. It is
unknown whether an edge dissection was present after implantation of the BRS in
the LAD or if any other mechanism was responsible for the subsequent proximal
vessel occlusion. Restenosis remains an important limitation of current generation
DESs, with reported rates of TLR ranging from 5%–10% [69]. Regarding BRS
restenosis, current data are very limited and treatment strategies remain to be
elucidated.
2.5.2 Case 2—a careful OCT interpretation
A 40-year-old male patient presented to the emergency department with an
oppressive and recurrent chest pain, and was diagnosed with a non-ST-elevation
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Figure 2.6. (a) Double cannulation of RCA and LAD showing occlusion of the mid segment of the LAD,
proximal to the previously implanted BRS, (b) LAD, after dilation with a 2.0/20 mm non-compliant balloon,
(c) restenosis of the distal BRS, with a mean luminal area of 1.45 mm
with a fibrotic plaque, (e) distal part of the proximal scaffold with good apposition and neointimal coverage of
the struts, (f) restenosis of the mid portion of the proximal scaffold, (g) proximal segment of the proximal
scaffold with good apposition and (h) lesion proximal to the scaffolds, fibrotic and calcified (*), with a mean
luminal area of 1.00 mm
2
.
2
, (d) a gap between the two scaffolds
Figure 2.7. (a) LAD after implantation of a DES 3.0/18 mm proximal to the first scaffold, overlapping the
proximal BRS, (b) and (c) implantation of a DES 2.75/12 mm in the gap between scaffolds followed by
prolonged drug-eluting balloon dilation in the distal scaffold and (d) final result.
acute myocardial infarction. He was a smoker with hypertension and uncontrolled
dyslipidemia. Coronary angiography showed a 75% lesion in the mid segment of the
LAD and LCX occluded proximally, filling distally by RCA collaterals. OCT was
performed in the LAD and revealed a 15 mm fibrolipid lesion, with a mean diameter
of 1.2 mm (mean reference diameter of 2.33 mm), absence of calcium and proper
plaque free landing zones (figure 2.9). According to these findings, predilation with a
2.0/12 mm compliant balloon was conducted and a BRS 2.5/18 mm was implanted
and postdilated with a 3.0/15 mm non-compliant balloon inflated at nominal
pressure. The final OCT confirmed good expansion and apposition and revealed
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Figure 2.8. (a) Dissection visible in the gap between the scaffolds, pre-DES implantation, (b) and (c) after
proximal DES implantation with scaffold overlap and good apposition, (d) distal scaffold after drug-eluting
balloon dilation, (e) and (f) after implantation of the second DES, overlapping both scaffolds, showing good
apposition and (g) long view, final pullback.
Figure 2.9. (a) LAD with a 75% lesion in its mid segment and (b)–(d) OCT revealing a fibrolipid lesion (# lipid
pools).
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the presence of a small distal edge dissection (3 mm), without flow compromise and
not visible angiographically, so no further measure was taken (figure 2.10).
PCI of the LCX CTO was performed 2 weeks later. After the guidewire
progressed to the distal vessel and the lesion was predilated with a 2.0/20 mm
compliant balloon, OCT was performed and revealed a long obstructive lesion, with
small amounts of calcium and abundant red thrombus (figure 2.11). Two Absorbs
were implanted, a 2.5/28 mm distally and a 3.0/18 proximally, with overlap. OCT
Figure 2.10. (a) A BRS 2.5/18 mm being slowly deflated, (b) and (c) small edge dissection without flow
limitation and not angiographically visible, (d) BVS struts (‘black box’ appearance) with good expansion and
apposition, (e) proximal edge of the scaffold, dissection free, and (f) final result.
Figure 2.11. (a) CTO of the proximal LCX, (b) progression of the guidewire to the distal vessel and predilation
with a compliant 2.0/20 mm balloon, (c) red thrombus (T) visible at the distal part of the lesion, (d) plaque with
abundant lipid pools (#) and (e) and (f) severe calcified (*) stenosis.
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showed malapposition with plaque/thrombus protrusion (figure 2.12) and postdilation was achieved with non-compliant balloons, 2.5/20 and 3.0/20 mm for the distal
and proximal scaffolds, respectively. Final angiography and OCT confirmed a good
result (figure 2.13). The 2 week OCT revaluation of the LAD showed a sealed
coronary dissection (figure 2.14). Fourteen months later, the patient underwent an
angiographic/OCT follow-up showing no scaffold restenosis (figure 2.15).
2.5.3 Case 3—BRS in calcified vessels. Does OCT have a role?
A 50-year-old male patient with hypertension, dyslipidemia and current smoking
was referred to invasive risk stratification due to stable angina (class III of the
Canadian Cardiovascular Society) and documented myocardial ischemia in a
Figure 2.12. (a) Distal BRS 2.5/28 mm implantation, (b) distal edge with no dissection, (c) OM bifurcation, (d)
scaffolds struts with malapposition and plaque/thrombus protrusion (arrow), (e) overlap area with plaque
protrusion and (f) proximal edge.
Figure 2.13. (a) Distal edge, (b) previous malapposition area, (c) overlap of the two scaffolds, and (d) long
view showing good expansion and apposition.
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Figure 2.14. LAD follow-up after 2 weeks. (a) Previous dissection area (+) with no visible complications and
(b)–(d) good expansion and apposition, with some evident neointimal strut coverage.
Figure 2.15. LAD and LCX 14 month follow-up. (a) LAD with a patent scaffold, (b) and (c) struts with
neointimal coverage, no visible restenosis and maintained vessel architecture, (d) LCX in angiography with
patent scaffolds, and (e) and (f) no restenosis, visible neointimal growth, blood in the lumen (B).
non-invasive imaging stress test. Coronary angiography revealed a 75% stenosis in
the mid segment of the LAD (diffuse atherosclerosis) and two apparently significant
lesions in the RCA (non-dominant, small caliber vessel). OCT guided PCI of the
LAD was performed, revealing a long calcified lesion with a mean reference
diameter of 3.1 mm (figure 2.16). Predilation was executed with a 3.0/20 mm
compliant balloon followed by the implantation of a BRS 3.5/28 mm. OCT
disclosed an inadequate expansion on the most severe calcified segment (figure 2.17)
and postdilation with a non-compliant 3.5/15 mm balloon was achieved. Final
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Figure 2.16. (a) LAD with a 75% calcified lesion in its mid segment (red arrow), (b) lipid pool with
inflammatory activity and apparent macrophage accumulation (white arrow), (c) and (d) calcified lesion (*),
and (e) mixed plaque with fibrotic tissue, lipids (#) and calcium (mean luminal area of 1.49 mm
2
).
Figure 2.17. (a) Distal scaffold edge, no complications, (b) struts well apposed, over a calcific plaque, (c) and
(d) underexpansion of the scaffold due to calcified lesions, and (e) long view showing evident underexpansion
(white arrows).
OCT confirmed good scaffold expansion and apposition (figure 2.18). Angiographic
follow-up attained 14 months later showed mild intra-scaffold hyperplasia, with no
significant restenosis (figure 2.19).
2.5.4 Case 4—BRS in ST-elevation myocardial infarction and long-term evaluation
by OCT
A female patient, 66 years of age, presented to a non-primary-PCI-capable center
with typical angina symptoms. An anterior ST-elevation acute MI was diagnosed
and thrombolytic therapy was administered, with signs of reperfusion. She was
transferred to a PCI-capable center to perform coronary angiography which
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Figure 2.18. (a) Final LAD angiography, (b) and (c) struts well apposed and expanded over calcium.
Figure 2.19. (a) LAD follow-up (14 months), (b) and (c) struts with neointimal coverage, ‘black boxes’
perfectly discernible, calcium (*) visible.
revealed an occluded mid LAD, next to the bifurcation with the first diagonal, and a
75% stenosis in the mid segment of the RCA. Complete revascularization was
performed. The LAD and diagonal branch were wired, predilation of the LAD
was accomplished with a 2.0/20 mm compliant balloon and a 3.0/28 mm BRS was
implanted and postdilated with a 3.0/20 mm non-compliant balloon (figure 2.20). A
DES was implanted in the RCA, and no complications were observed. Follow-up
with angiography and OCT was performed 25 months later and revealed a patient
artery with neointimal growth and a mild degree of neoatherosclerosis. At this time
point, scaffold struts could still be identified, although their appearance corresponded mostly to remnants of struts covered by tissue and not exposed to
bloodstream (figure 2.21). In the proximal segment, a 50% lesion (QCA) was
identified and OCT revealed a mean lumen area of 1.79 mm
2
. The patient was
asymptomatic and, as such, evaluation with fractional flow reserve was performed
and showed a value of 0.84 (figure 2.22).
2.5.5 Case 5—different devices for different lesions
The patient was a 48-year-old male with two-vessel coronary artery disease with
repeated TVR. Different devices were implanted with different timings and in
different clinical settings, according to lesion characteristics and location
(figure 2.23).
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