Post-Procedure; Brachytherapy; Magnetic Resonance Imaging (Mri); 3.0 Tesla Temperature Information - Boston Scientific SYNERGY Mode D'emploi

• If greater than usual resistance is felt during delivery system withdrawal into the guide
catheter, the stent system and guide catheter should be removed as a single unit (see
note in above section).
table 3. representative system Deflation times (seconds)
balloon Length / 8 12
Diameter mm mm
2.25 mm
2.50 mm
2.75 mm
≤ 16 ≤ 16
3.00 mm
3.50 mm
4.00 mm

post-procedure

• Care must be exercised when crossing a newly deployed stent with ancillary devices to
avoid disrupting the stent placement, apposition, geometry, and/or coating.
If the patient requires Magnetic Resonance Imaging (MRI), see Magnetic resonance Imaging.

brachytherapy

The safety and effectiveness of the SYNERGY™ stent in patients with prior brachytherapy of
the target lesion have not been established.
The safety and effectiveness of the use of brachytherapy to treat in-stent restenosis in the
SYNERGY stent has not been established.
Both vascular brachytherapy and the SYNERGY stent alter arterial remodeling. The interaction,
if any, between these two treatments has not been determined.

Magnetic resonance Imaging (MrI)

Through non-clinical testing, the SYNERGY stent has been shown to be MR Conditional (poses
no known hazards under specified conditions). The conditions are as follows:
• Field strengths of 3.0 and 1.5 Tesla with
- Static magnetic field gradient < 11 T/m (extrapolated).
- Product of static magnetic field and static magnetic field gradient < 25 T²/m
(extrapolated).
• A calculated rate of change of magnetic field (dB/dt) of 60 T/s or less.
• A maximum whole body averaged specific absorption rate (SAR) of lower than 2.0 W/kg
for a total active MR scan time (with RF exposure) of 15 minutes or less. The SYNERGY
stent should not migrate in this MRI environment. MR imaging within these conditions may
be performed immediately following the implantation of the stent. This stent has not been
evaluated to determine if it is MR Conditional beyond these conditions.

3.0 tesla temperature Information

Non-clinical testing of RF-induced heating was performed at 123 MHz in a 3.0 Tesla Magnetom
Trio™, Siemens Medical Solutions MR system, software version Numaris/4, syngo™ MR
A30A. The stents were in a location and orientation in the phantom that produced the
worst case Radio Frequency (RF) heating. RF power was applied for 15 minutes and the
measured conductivity of the phantom material was about 0.49 S/m. The phantom average
SAR calculated using calorimetry was 2.3 W/kg. The maximal in-vitro temperature rise was
calculated as 2.6°C when the local SAR was scaled to 2.0 W/kg for a measured stent length up
to 74 mm. Predicted in-vivo heating based on these non-clinical tests and computer simulation
of the patient exposure to the electromagnetic fields in MRI yielded to the following maximal
in vivo rises: for landmarks at the chest level, the calculated temperature rise was 2.6°C with a
calculated uncertainty upper bound temperature of 4.7°C for a whole body average SAR value
of 2.0 W/kg and a continuous scan time of 15 minutes.
The actual in vivo rise is expected to be less than these values as the calculations did not
include the cooling effects due to blood flow in the lumen of the stent and blood perfusion in
the tissue outside the stent.
Black (K) ∆E ≤5.0
16 20 24 28 32
mm mm mm mm mm
≤ 16
≤ 16 ≤ 16
≤ 16
≤ 16
≤ 21
≤ 21 ≤ 21
≤ 21
1.5 tesla temperature Information
Non-clinical testing of RF-induced heating was performed at 64 MHz in a 1.5 Tesla Intera™ Philips
Medical Systems, software version Release 12.6.1.3, 2010-12-02 whole body coil MR scanner.
The stents were in a location and orientation in the phantom that produced the worst case RF
heating. RF power was applied for 15 minutes and the measured conductivity of the phantom
material was about 0.50 S/m. The phantom average SAR calculated using calorimetry was 2.3
38
W/kg. The maximal in-vitro temperature rise was calculated as 2.6°C when the local SAR was
mm
scaled to 2.0 W/kg for a measured stent length up to 74 mm. Predicted in-vivo heating based on
these non-clinical tests and computer simulation of the patient exposure to the electromagnetic
≤ 21 fields in MRI yielded to the following maximal in vivo rises: for landmarks at the chest level, the
calculated temperature rise was 2.6°C with an uncertainty upper bound temperature of 4.8°C for
a whole body average SAR value of 2.0 W/kg and a continuous scan time of 15 minutes.
The actual in vivo rise is expected to be less than these values as the calculations did not
include the cooling effects due to blood flow in the lumen of the stent and blood perfusion in
≤ 30
the tissue outside the stent.
In vivo, local SAR depends on MR Field strength and may be different than the estimated
whole body averaged SAR, due to body composition, stent position within the imaging
field, and scanner used, thereby affecting the actual temperature rise. No tests have been
performed on possible nerve or other tissue stimulation possible to be activated by strong
gradient magnetic fields and resulting induced voltages.

Image artifact Information

The calculated image artifact extends approximately 7 mm from the perimeter of the device
diameter and 5 mm beyond each end of the length of the stent when scanned in non-clinical
testing using a Spin Echo sequence. With a Gradient Echo sequence the calculated image
artifact extends 7 mm beyond the perimeter of the diameter and 6 mm beyond each end of the
length with both sequences partially shielding the lumen in a 3.0 Tesla Intera (Achieva Upgrade),
Philips Medical Solutions, software version Release 2.6.3.5 2009-10-12 MR system with a
transmit/receive head coil. This testing was completed using ASTM F2119-07 test method.

pre- and post-procedure antiplatelet regimen

The device carries an associated risk of acute, subacute, or late thrombosis, vascular
complications, and/or bleeding events. Therefore, the patient should be carefully selected,
and a P2Y inhibitor (i.e., clopidogrel, ticlopidine, prasugrel, or ticagrelor) must be prescribed
12
post procedure to reduce risk of thrombosis. Aspirin must be administered concomitantly with
P2Y inhibitor, and then continued indefinitely to reduce the risk of thrombosis. SYNERGY is
12
designed with a low initial polymer load, abluminal coating and bioabsorbable polymer which
may reduce the risk of thrombosis and the need for prolonged dual antiplatelet therapy. It
is strongly advised that the treating physician consider the European Society of Cardiology
recommendations (or other applicable country guidelines) for antiplatelet therapy pre– and
post–procedure to reduce the risk of thrombosis. In selected patients, it may be reasonable to
interrupt or discontinue P2Y
12
It is very important that the patient be compliant with the post-procedural antiplatelet
recommendations. Premature discontinuation of prescribed antiplatelet medication could
result in a higher risk of thrombosis, myocardial infarction, or death. This should be carefully
considered by the treating physicians prior to Percutaneous Coronary Intervention (PCI) for
patients who may require premature cessation of antiplatelet therapy, e.g., for surgical or
dental procedures. Patients who require premature discontinuation of antiplatelet therapy
due to significant active bleeding or the expectation of significant active bleeding should be
monitored carefully for cardiac events and once stabilised have their antiplatelet therapy
restarted without unnecessary delay.

Drug Interactions

When taken orally, everolimus is extensively metabolized by the cytochrome P4503A4
(CYP3A4) in the gut wall and liver and is a substrate for the countertransporter P-glycoprotein.
Therefore, absorption and subsequent elimination of everolimus may be influenced by drugs
that affect these pathways. Concurrent treatment with strong 3A4 inhibitors and inducers
is not recommended unless the benefits outweigh the risk. Inhibitors of P-glycoprotein
may decrease the efflux of everolimus from intestinal cells and increase everolimus blood
concentrations. In vitro, everolimus was a competitive inhibitor of CYP3A4 and of CYP2D6,
potentially increasing the concentrations of drugs eliminated by these enzymes. Thus, caution
should be exercised when coadministering everolimus with 3A4 and 2D6 substrates with a
6
inhibitor therapy after 3 months.