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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3919_Библиотеки_им_академика_М_И_Перельмана
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Case 2. Stent thrombosis
61-year-old man. High cholesterol; NIDDM.
Stable angina. Angioplasty 3 days previously
with two 3.5 mm ⫻ 18 mm AVE GFX stents in the
LAD.
Presentation with anterior ST elevation and pain.
Procedure:
JL4 8F guide; 0.014⬙ high torque inter-
mediate wire with 3.5 mm monorail balloon.
Extensive dilatation in stents and between.
Further Cordis CrossFlex™ 3.0 mm ⫻ 15 mm
deployed overlapping distal end of lower stent
where a dissection could be seen. Abciximab
(ReoPro
®
) given.
Nick Curz e n :
It again appears that the culprit lesion responsible
for this thrombosis is an edge dissection. This
time a slightly stiffer wire is used to disobliterate
the vessel. I favour this type of wire as its
increased stiffness allows it a greater chance of
finding a way through the thrombus. On the other
hand, stiffer wires are more likely to pick up stent
struts or intimal flaps, especially in this ‘blind’
situation. After the wire has passed through into
the distal vessel it is a good idea to push the
deflated balloon through the occlusion into the
vessel beyond the stent in order to check that no
stent strut has been picked up, before going back
to dilate. The aim of the balloon dilatations that
are then performed is not completely clear.
Obviously the primary aim is to disrupt the throm-
bus so that the IIb/IIIa inhibitor can gain adequate
access. This could be achieved with a smaller-
diameter balloon than the stent or a balloon of the
same diameter at low pressure. Usually, however,
the balloon chosen is of the same diameter as the
stent and is then inflated to high pressure. What
is the logic of this? Is there evidence that stent
thrombosis occurs because stents are not fully
deployed? Is there any evidence that higher infla-
tion pressures make the thrombus dissolution
more efficient? If the balloon is not contained
completely within the stent then presumably there
is a chance of exacerbating or creating dissection
at this location? My current strategy is therefore
to use a low pressure inflation with a reference
diameter-sized balloon within the stent to
166 STENT THROMBOSIS
a b
Figure 13.2a–e
LCA angiogram. a) Total occlusion of LAD, in stent. b) Stent seen with ‘cut-off’ LAD, an appearance often
consistent with thrombosis.
https://t.me/med1917
completely disrupt the clot but not to keep inflat-
ing to higher and higher pressures if bits of
thrombus can still be seen attached within the
stent. If there is a clear edge dissection then I
would deploy an overlapping stent, as in this case,
in order to cover it.
In any case of stent thrombosis it is important
to document the degree of myocardial damage
that has resulted from it. This should be done by
both cardiac enzymes and echo assessment of LV
function. Patients who had gone home and are
transferred back into hospital are likely to have
already sustained significant myocardial damage
and need to be treated appropriately for this with
ACE inhibitors. I would not routinely anticoagulate
patients because they had had a stent thrombosis.
CASE 2. STENT THROMBOSIS 167
c d
e
Figure 13.2
continued
c) After wire passage and inflation a ‘flap-like’ lesion
is seen across LAD. d) Hazy appearance at site seen
in c. e) After new stent deployed, resultant
angiogram.
https://t.me/med1917
https://t.me/med1917
Restenosis represents a major challenge to the
interventional community. We cause it, and even
with the best results ever published the angio-
graphic restenosis rate for stented vessels is still
at least 10%! This chapter inevitably focuses on
mechanisms for treating restenotic lesions,
although perhaps it is more appropriate for the
long term that we dedicate our resources
towards understanding why some patients are
susceptible to intimal proliferation, so that we
may develop prophylactic strategies to prevent
it.
Current treatment options are diverse and each
interventionist has their own bias. Without
doubt, further high quality randomized studies
are required to help provide unequivocal
guidance as to the correct therapy for this diffi-
cult patient group.
We invited Patrick Serruys and co-workers
Manel Sabaté and Jurgen MR Ligthart to
discuss the options for the management of
restenosis, including the role of brachytherapy.
Case 1. Restenosis
55-year-old man. Ex-smoker; high cholesterol.
Inferior MI 1997 treated with streptokinase.
Recurrent angina since then with abnormal ETT.
Catheter findings:
Good LV; single-vessel disease
in dominant RCA with proximal occlusion.
Procedure:
JR4 8F; 0.014⬙ high torque floppy
wire. Extensive area dilated with 2.5 mm
monorail balloon. Magic Wallstent
®
(48 mm)
then deployed from proximal to mid-vessel and
more distal lesion stented with Cordis CrossFlex
®
3.0 mm ⫻ 25 mm.
Represented with limiting angina 5 months later
when angiogram showed diffuse restenosis
within the stents.
Procedure:
JR4 8F; 0.014⬙ high torque floppy
wire. Whole stented area dilated with 3.5 mm
Chubby™ balloon to 16 atm.
14
Restenosis
https://t.me/med1917
170 RESTENOSIS
a b
c
Figure 14.1
RCA angiogram. a) Acquisition of image, without
contrast, to visualize Wallstent
®
in RCA. b) Diffuse
in-stent restenosis with tight proximal segment.
c) Result after extensive balloon dilatation.
https://t.me/med1917
Case 2. Restenosis
55-year-old man. Hypertension; hypercholesterol-
aemia; ex-smoker; family history.
8/96 PTCA plus Cordis CrossFlex™ 3.5 mm ⫻
15 mm to proximal LAD.
5/97 recurrent limiting angina.
Catheter findings:
Significant stenosis in stent.
Procedure:
JL4 8F guide; 0.014⬙ high torque
floppy wire; 3.5 mm monorail balloon inflated
within stent and above it. Then two ACS MULTI-
LINK
®
stents as follows: (a) 3.5 mm ⫻ 35 mm to
12 atm deployed overlapping and extending
distally from the original Cordis CrossFlex™; (b)
3.5 mm ⫻ 15 mm ACS MULTI-LINK
®
overlapping
(a) proximally.
CASE 2. RESTENOSIS 171
a b
c d
Figure 14.2
LCA angiogram. a) In-stent restenosis in LAD, PA projection. b) In-stent restenosis in LAD, LAO projection. c)
After balloon dilatation and stent placed in stented territory, result in PA projection. d) Result in LAO projection.
https://t.me/med1917
Case 3. Restenosis
62-year-old man. Ex-smoker; hypertension. 7/96
PTCA plus stent to LAD. 5/97 recurrent limiting
angina.
Catheter findings:
Stenosis within stent.
Procedure:
JL4 8F guide; 0.014⬙ high torque
floppy wire; 3.5 mm monorail balloon inflated
within stent and above it. The ACS MULTI-LINK
®
3.5 mm ⫻ 25 mm overlapping whole of old stent.
172 RESTENOSIS
a b
Figure 14.3
LCA angiogram. a) In-stent mid-LAD lesion. b) Dilated and restented.
https://t.me/med1917
Case 4. Restenosis
54-year-old man. High cholesterol; hypertension;
ex-smoker. Acute anterior MI treated with strep-
tokinase resulting in no Q wave. Stented, with
recurrent symptoms at 6 months.
Catheter findings:
Tight restenosis at site of stent
with poor downstream run-off.
Procedure:
LC4 8F, 0.014⬙ high torque floppy
wire; 3.0 mm monorail balloon at high pressure,
18 atm, with excellent angiographic result.
CASE 4. RESTENOSIS 173
a b
Figure 14.4
LCA angiogram. a) Mid-LAD lesion within stent at 6 months. b) Result after in-stent redilatation with 3.0 mm
balloon at high pressure.
https://t.me/med1917
Case 5. Restenosis
76-year-old man. Ex-smoker. CABG surgery 1992
(vein grafts to LAD and RCA). Presented in 1996
with angina: underwent PTCA plus Medtronic
Wiktor
®
3.5 mm ⫻ 15 mm to AV circumflex.
Presents again 9 months later with unstable
angina.
Catheter findings:
LV function poor with extensive
174 RESTENOSIS
a b
c d
Figure 14.5
LCA angiogram. a) Selective circumflex injection: OM tight proximal stenosis. b) Guidewire to each limb and balloon
to origin of OM, stent to Cx/OM. c) Stent through Cx/OM stent, into distal OM. d) Final result of true Y stent.
https://t.me/med1917
inferoapical hypokinesis; LAD occluded after first
diagonal; in-stent stenosis involving origin of OM;
severe proximal RCA disease; both vein grafts
patent with good run off.
Procedure:
Amplatz left 8F guide; 0.014⬙ high
torque floppy wire to AVCx and OM. IVUS
confirmed very tight stenosis at OM origin and
significant stenosis within body of Medtronic
Wiktor
®
. Both AVCx and OM origin pre-dilated
with 3.0 mm monorail balloon. Then
3.0 mm ⫻ 15 mm ACS MULTI-LINK
®
into OM1
from AVCx and 4.0 mm ⫻ 15 mm ACS MULTI-
LINK
®
in AVCx across origin of OM (as a true ‘Y’
stent). Further 3.5 mm ⫻ 15 mm ACS MULTI-
LINK
®
overlapping distal end of Cx stent.
Comments of Patrick Serruys, Manel
Sabaté and Jurgen MR Ligthart :
This chapter addresses the controversial topic of
the treatment of in-stent restenosis. Although
restenosis is less frequent than after balloon
angioplasty, the rate after stent implantation
involves 15–20% in the best selected cases.
1,2
The
mechanism of in-stent restenosis is basically
neointimal proliferation, since the recoil and late
vessel constriction is prevented by the mechani-
cal properties of the stent.
The treatment of this complication involves
various techniques, including balloon angio-
plasty in-stent, stent implantation in-stent,
debulking techniques and more recently intra-
coronary radiation therapy. This variety of
approaches illustrates that the problem is far
from being solved. In the cases selected, the
operators chose either treatment with balloon
angioplasty or stent implantation within the
restenosed stent, showing satisfactory angio-
graphic results. However, the long-term follow-
up of these patients is not presented. In fact,
the recurrence rate appears to increase with the
number of re-interventions performed on the
lesion.
Debulking techniques appear to provide
additional value to balloon angioplasty for the
treatment of in-stent restenosis. For example,
when compared to balloon angioplasty alone,
laser debulking followed by balloon angioplasty
demonstrated a greater lumen gain, more intimal
hyperplasia ablation/extrusion, larger lumen
cross-sectional area and a tendency for less
frequent need for subsequent target vessel
revascularization.
3
In the same way, rotational
atherectomy showed a lower clinical recurrence
rate and a higher long-term angina-free survival
when used concomitantly with balloon angio-
plasty as compared to balloon angioplasty
alone.
4
Finally, treatment with atherectomy plus
adjunctive balloon angioplasty resulted in higher
acute gain and a trend towards a lower need for
repeat target vessel revascularization.
5
A
comparison of balloon angioplasty, laser and
rotational atherectomy has recently been
reported (oral presentation in the American Heart
Association, 1998), showing better results by the
use of adjunctive rotational atherectomy as
compared to the other two approaches.
The recent introduction of intracoronary radia-
tion in the therapeutic arsenal has provided the
interventional cardiologist with a new approach
to treat restenotic coronary lesions. The theoret-
ical benefit of radiation in preventing neointimal
proliferation resides in its ability to kill the more
rapidly dividing smooth muscle cells. To date,
two randomized placebo-controlled trials have
been carried out to evaluate the efficacy of
gamma-radiation in patients with in-stent
restenosis.
6,7
Teirstein et al.
6
randomized 55
patients to receive a 0.030⬙ ribbon containing
192
Ir
sealed sources or a ribbon containing placebo
seeds (Best Industries, Springfield, VA). Thirty-
five patients were treated with in-stent resteno-
sis. The dosimetry was calculated from the
intravascular ultrasound measurement in a range
of 8–30 Gray to the internal elastic membrane.
The placebo group showed a restenosis rate of
70% as compared to 14% in the irradiated group
(
p
= 0.0006). This beneficial effect was sustained
at 2-year follow-up. Waksman et al.
7
evaluated
130 patients who had developed in-stent resteno-
sis up to 47 mm long in the Washington
Radiation for In-stent Restenosis Trial (WRIST).
These patients were randomized to radiation
using a
192
Ir ribbon versus a non-radioactive
ribbon delivered into a non-centred closed-end
lumen catheter (Medtronic, San Diego, CA). The
prescribed dose was 15 Gray to a distance of
2 mm from the centre of the source for a vessel
size of 3.0–4.0 mm and to a distance of 2.4 mm
from the centre of the source for vessel diame-
ter of 4.0–5.0 mm. At 6-month follow-up, the
CASE 5. RESTENOSIS 175
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