Interventional Cardiology Live Case
Study Series:
A Master Class in Procedural Techniques
Samin K. Sharma, MD
Annapoorna S. Kini, MD
Director
Cardiac Cath Lab and Intervention
Professor of Medicine
Co-Director
Cardiovascular Institute
Mount Sinai Medical Center
New York, NY
Associate Director
Cardiac Cath Lab
Mount Sinai Medical Center
New York, NY
Sameer K. Mehta, MD
Voluntary Associate Professor of Medicine
University of Miami - Miller School of
Medicine,
Miami, Florida
September 21, 2010: Case #1: NJ, 72-y-o man
Presentation:
Crescendo exertional angina and SOB for 2 months and stress
MPI revealed moderate-to-severe multivessel ischemia and TID
History:
Hypertension, hyperlipidemia, ex-smoker, colon ca s/p colectomy
& chemotherapy 2006 CRi
Medications:
ASA, clopidogrel, simvastatin, metoprolol, amlodipine
SOB = shortness of breath; MPI = myocardial perfusion imaging; TID = transient ischemic
dilation; Cri = incomplete blood cell count recovery; ASA = acetylsalicylic acid
Case #1 (cont)
Cardiac Cath: 8/6/2010:
SYNTAX Score
26
Three-vessel CAD with LVEF 65%
Left main: no obstruction
LAD: 80% long calcified lesion of proximal LAD (large) with 70% apical
lesion and mild diffuse first diagonal
LCx: 50% prox LCx, 80% OM1 & 50% distal LCx (Medina 1,1,1)
RCA: 70%-99% multiple lesions in RCA, fills via LAD
PCI 8/6/10:
PCI of RCA (XienceV® x 4, 3-3.5 mm size)
Plan Today:
PCI of calcified LAD lesion using RotaDES and LCx bifurcation
CAD = coronary artery disease; LVEF = left ventricular ejection fraction; LAD = left anterior descending; LCx = left
circumflex; OMI = first obtuse marginal; RCA = right coronary artery; PCI = percutaneous coronary intervention;
RotaDES = rotablation and drug-eluting stent implantation
® Abbott Laboratories, Abbott Park, Ill.
Issues Involving the Case
• Choice of Antithrombotic Therapy
• Treatment of Calcified Lesions
• Bifurcation Lesion Intervention
REPLACE-2 vs ACUITY PCI: 30-day Events
REPLACE-2 PCI
ACUITY PCI
Heparin + GP IIb/IIIa (n = 3008)
Bivalirudin alone (n = 2994)
Heparin + GP IIb/IIIa (n = 2619)
Bivalirudin alone (n = 2561)
P = .30
%
P = .40
7.0 7.6
10.0
%
P = .45
9.2
8.2
8.8
P < .001
P < .001
4.1
4.2
2.4
Ischemic
Composite
P = .49
11.1
10.5
Major
Bleeding
2.1
Net Clinical
Outcomes
Lincoff AM, et al. JAMA. 2003;289:853-863
Ischemic
Composite
Major
Bleeding
Net Clinical
Outcomes
Stone GW, et al. N Engl J Med. 2006;355:2203.
HORIZONS AMI Trial: 30-Day Mortality of PCI
Heparin + GPIIb/IIIa inhibitor (n = 1662)
Bivalirudin monotherapy (n = 1678)
Death (%)
HR = 0.63 [0.40, 0.99]
2.8%
P = .049
Cardiac
1.8%
Noncardiac
Number at risk
Bivalirudin
0.2%
0.1%
Time in days
1678
1647
1640
1632
1620
1563
Heparin + GPIIb/IIIa 1662
1631
1615
1598
1583
512
From Stone GW, et al. N Engl J Med .2008;358:2218. © 2008 Massachusetts
Medical Society. All rights reserved.
1635
1604
HORIZONS AMI Trial: 30-Day Mortality of PCI
Death (%)
This higher early events
Heparin + GPIIb/IIIa inhibitor (n = 1662)
in bivalirudin group were
due to
Bivalirudin monotherapy (n = 1678)
higher acute stent thrombosis
and can be eliminated by
HR = 0.63 [0.40, 0.99]
extended (1-3 hours) infusion
P = .049
after PCI or by prasugrel load
instead of clopidogrel load.
2.8%
Cardiac
1.8%
Noncardiac
Number at risk
Bivalirudin
0.2%
0.1%
Time in days
1678
1647
1640
1632
1620
1563
Heparin + GPIIb/IIIa 1662
1631
1615
1598
1583
512
From Stone GW, et al. N Engl J Med .2008;358:2218. © 2008 Massachusetts
Medical Society. All rights reserved.
1635
1604
HORIZONS-AMI: Clinical Follow-Up
1-Year FU
%
2-Year FU
P = .98
%
Heparin+GP IIb/IIIa (n = 1802)
Bivalirudin group (n = 1800)
P = .98
20
Heparin+GP IIb/IIIa (n = 1802)
Bivalirudin group (n = 1800)
15
11.9 11.9
P < .001
9.2
P < .001
10
P = .22
5.8
P = .005
4.4
3.6
3.8
9.6
P = .04
P = .03
P = .03
6.4
6.9
P = .005
5.1
4.8
2.5
2.1
0
Major Reinfarction Cardiac All-Cause
Bleeding
Mortality Mortality
6.1
4.6
4.2
5
3.5
18.7 18.8
MACE
Mehran R, et al. Lancet. 2009:374:1149
Major
Bleeding
Reinfarction
Cardiac
Mortality
All-Cause MACE
Mortality
Data presented by Stone GW, Trans Catheter
Cardiovascular Therapeutics, 2009, San Francisco, Calif.
ACUITY Trial: Impact of MI and Major Bleeding
(non-CABG) in the First 30 Days on Risk for Death
Mortality at 390 Days
%
Both MI and Major
Bleed
(n = 94)
MI onlyMajor Bleed only Without Major Bleed
Without MI
(n = 611)
(n = 551)
Stone G, et al. N Engl J Med. 2006;355:2203-2216.
No MI
Major Bleed
(n = 12,557)
TRITON-TIMI 38 Trial: Net Clinical Benefit
Bleeding Risk Subgroups – Therapeutic Consideration
Reduced
maintenance dose
guided by PK
16%
Age ≥ 75 or
Wt < 60 kg
4%
Avoid Prasugrel
Prior CVA/TIA
Subgroups With Positive Benefit:
•
•
•
•
•
•
STEMI
Multivessel/diabetes
SAT on clopidogrel
Clopidogrel non-/hypo-responders
Clopidogrel allergy
Complex or high-risk lesions
CVA = cerebrovascular accident; TIA = transient ischemic attack;
SAT = subacute stent thrombosis
Wiviott S, et al. Circulation. 2007;116:2923.
Significant Net Clinical
Benefit with Prasugrel
80%
Maintenance
Dose 10 mg
Updated Dual Anti-Platelet Therapy (DAPT) Post
Stenting Incorporating Prasugrel:
Optimal DAPT post stenting continues to evolve with aspirin (81-325 mg PO
daily) lifelong and clopidogrel (600 mg load/75 mg PO daily) for 1-12 months
being used routinely.
Two new recommendations have emerged from the results of major
randomized trials:
1. Increasing clopidogrel dose to 150 mg for 1 week as per OASIS-7 trial.
2. Use of prasugrel (TRITON TIMI-38 trial): Prasugrel (60 mg load/10 mg PO daily for
1-15 months) is more effective than clopidogrel in reducing primary endpoints of
death, MI, stroke, and stent thrombosis. The relative benefit of prasugrel was
higher in patients with STEMI and in diabetes.
But prasugrel use was associated with higher fatal, major and minor bleeding vs
clopidogrel especially in patients with prior CVA (also less effective in this
subgroup), age > 75 years and weight < 60 kg.
Updated DAPT Post Stenting Incorporating Prasugrel
Therefore in following subgroups of PCI patients, prasugrel will be
preferred over clopidogrel:
•
•
•
•
•
STEMI
Multivessel patients with diabetes
Clopidogrel allergy
Clopidogrel nonresponders
Stent thrombosis in clopidogrel compliant pts
Even in these PCI patients, prasugrel should be absolutely avoided in those with prior
CVA and with history of major vascular or nonvascular bleeding (such as GI or GU
bleeding) and prasugrel maintenance dose should be decreased to 5 mg PO daily in
those > 75 years old or < 60 kg. Patients should be strictly monitored and instructed for
signs and symptoms of bleeding. Routine use of PPI for GI prophylaxis is indicated with
prasugrel.
For staged procedures in patients on maintenance dose of prasugrel, an extra loading
dose of 10 mg before PCI will suffice. To switch patients who are taking clopidogrel
maintenance dose, prasugrel loading dose of 30mg followed by 5-10 mg PO daily (as
indicated) maintenance is advised.
Issues Involving the Case
• Choice of Antithrombotic Therapy
• Treatment of Calcified Lesions
• Bifurcation Lesion Intervention
Treatment of Calcified Lesions
Interventional Techniques
• Noncompliant (NC) balloon (high pressure inflation up to
20-24 atm)
• NC balloon with another side-by-side wire in the vessel
and high pressure inflation
• Cutting balloon (up to 8-12 atm)
• AngioSculpt® balloon (up to 16-20 atm)
• Rotational atherectomy (heavily calcified)
® AngioScore Inc., Fremont, Calif
Atherectomy: Rotablator®
Diamond
microchips
Differential cutting
PTCA
Rotablator®; Boston Scientific, Inc., Natick, Mass.
PRCA
Rotational Atherectomy (RA, PRCA, PTRCA)
Indications:
•
•
•
•
•
•
•
•
Calcified lesion
Undilatable/chronic lesion
Diffuse long lesion
Small vessels (< 2.5 mm)
In-stent restenosis
Bifurcation lesion
Ostial lesion
Rotastent (SPORT trial)
Limitations:
•
•
•
•
•
Slow flow / No flow
Perforation
CK-MB release
Wire bias and dissection
Technically challenging
PRCA = percutaneous rotational coronary atherectomy; PTCRA = percutaneous
transluminal coronary rotational ablation; CK-MB = creatine kinase-MB isoenzyme
Rotational Atherectomy: Current Issues
• Slow / no-flow
• CPK, CK-MB release
• Coronary spasm
• Intimal dissections and acute closure
• Perforation
• Wire bias problems
• Heat generation
CPK = creatine phosphokinase
Rotational Atherectomy: Complications
Mechanism of No/Slow-flow
•
•
•
•
•
•
•
•
•
•
Atheromatous debris embolism
Platelet and microthrombi
Platelet activation, aggregation, lysis (by rota burr)
Microcirculatory (vasculature) spasm
Heightened microvasculature reactivity / tone
Microcavitation
Impaired local synthesis of EDRF
Neuro-humoral reflex
Lower epicardial vessel pressure and higher LVEDP
Extreme cases: free radical injury, local edema, microvascular
plugging, no-reflow
EDRF = endothelium-derived relaxing factor; LVEDP = left ventricular end-diastolic pressure
Rotational Atherectomy: Complications
Slow-flow
Settings:
•
•
•
•
•
Long calcified lesions
Total occlusion and right coronary artery
Poor LV function and hemodynamic instability
Thrombotic lesions (also post-MI)
? on -blockers
Technical modifications:
•
•
•
•
•
Small initial burr size and small upsizing
Short ablation runs and avoid RPM drops ?Slow-speed
Avoid hypotension and bradycardia
Rota flush & GP IIb/IIIa inhibitors
Treatment: verapamil, nitro, adenosine, nitroprusside, IABP
Best treatment to prevent slow flow is to avoid it from happening.
IABP = intra-aortic balloon pump
Rotational Atherectomy and GPIIb/IIIa Inhibitors
Activation of Platelets by Rotablation Is Speed-Dependent
Transmission electron micrography:
• Platelet-rich plasma through chamber with
rota burr held stationary (0 rpm) and stirred
in an aggregometer for 5 minutes:
Intact platelet membrane, intracellular
granules, and clear background.
• Platelet-rich plasma was subjected to
rotablation at 180,000 rpm and stirred in an
aggregometer for 5 minutes:
Ruptured platelet membranes, depletion of
intracellular organelles (“ghost platelets”),
and cloudy background.
From Williams MS. Circulation. 1998;98:742-748.
Rotational Atherectomy and Platelets
Initial Aggregation Slope
(units/min)
Effect of Rotablation on Platelet Aggregation
Rotablation Speed (rpm x 10-3)
From Williams MS, et al. Circulation. 1998;98:742-748.
Rotational Atherectomy
Activation of Platelets by Rotablation Is Speed-Dependent
Rotational
Speed (rpm)
Platelet Aggregates
(> 20 m)/mL blood
180,000
7434  2193
140,000
2269  627
Control
633  258
P < .0001 for all groups
Porcine blood exposed to a rotating
burr resulted in: Platelet aggregation
and red blood cell crenation.
From Reisman M, et al. Cathet Cardiovasc Diagn. 1998;45:208-214.
Slower rotational speed results
in a significantly lower number
of platelet aggregates.
STRATAS Trial
Technique Matters: Incidence of Slow-Flow
• Predictors of CK-MB release:
– deceleration > 5000 rpm > 5 sec
P = .008
%
• Predictors of restenosis:
– deceleration > 5000 rpm
– LAD location
Current optimal Burr-to-Artery
Ratio (BA): 0.3-0.5
Aggressive
strategy
Routine
strategy
(n = 249)
BA: > 0.9
(n = 248)
BA: < 0.8
Whitlow PL, et al. Am J Cardiol. 2001;87:699-705.
Rotational Atherectomy: Complications
Perforation
Settings:
•
•
•
•
•
Lesion in a bend > 90
Calcified lesion
Large burr-to-artery ratio
Total occlusion
Wire - bias situations
Technical modifications:
•
•
•
•
•
Smaller initial burr size (start with 1.25 mm burr)
Bending the wire technique
Rota extra support wire
?Predilatation with a smaller balloon
Avoid abciximab before rotablation
Rotational Atherectomy
Mount Sinai Hospital Experience (6%-9% of PCI)
%
Complications
---DES---
short burr runs, rota-flush,
abciximab, stent, experience
slow speed (140-150,000 rpm)
rotational atherectomy, BA: 0.4-0.5
STEPS for Rotational Atherectomy
Mechanism of action: Plaque ablation and pulverization
by the abrasive diamond-coated burr:
Physical principles:
1. Differential cutting is defined as the ability to ablate one
material selectively while sparing and maintaining the integrity
of another, based on differences in substrate composition,
resulting in a polished smooth lumen compared with multiple
intimal tears/dissections with balloon angioplasty; ie, able to
ablate inelastic tissue selectively (ie, plaque) while maintaining
the integrity of elastic tissue (ie, the normal vessel wall) due to
the principle of differential cutting.
STEPS for Rotational Atherectomy (cont)
Physical principles:
2. Orthogonal displacement of friction at rotational speeds
> 60,000 rpm; the friction, which occurs when sliding surfaces
are in contact, is virtually eliminated. As a result, there is
reduced surface drag and unimpeded advancement and
withdrawal of the burr, allowing the rotating burr to pass
through tortuous and diseased segments of the coronary tree.
The abraded plaque is pulverized into microparticles (size of
RBCs), which are 5–10 μm in diameter. These particles are small
enough to pass through the coronary microcirculation and
ultimately undergo phagocytosis in the liver, spleen, and lung.
STEPS for Rotational Atherectomy (cont)
Indications:
1. Severely calcified lesions
2. Undilatable/inelastic lesions
3. Diffuse recurrent In-stent restenosis with multiple jailed side
branches
Contraindications:
1. Acute myocardial infarction
2. Saphenous vein graft/thrombotic lesions
3. Presence of dissection
STEPS for Rotational Atherectomy (cont)
Preparation for procedure:
1. Proper burr size selection (~0.5:1 burr-to-artery ratio).
2. Proper guide catheter size selection (6F for up to 1.75 mm burr and 7F for 2.0 mm or
bigger burr).
3. Additional guidewire (Runthrough NS®/Fielder®) with J-tip prepped.
4. Noncompliant balloon (1:1 balloon size-to-artery ratio) prepped.
5. Temporary pacemaker for RCA/dominant LCx lesions (optional at attending
discretion).
6. Make connections to tachometer, NO tank, and flush solution (use the 3-way
stopcock for flush).
7. Gently remove the rota-floppy wire from the packing (first remove distal wire tip
from the back-stopper), and wipe with generously wet 4x4. It is a very delicate wire,
so handle with care and loop the wire making only 3 loops.
Runthrough NS®; Terumo Interventional Systems, Somerset, NJ .
Fielder®; Abbott Vascular, Redwood City, Calif.
STEPS for Rotational Atherectomy (cont)
Steps for operator:
1. Place the rota-floppy guidewire beyond lesion (direct wire placement/wire
exchange with over-the-wire 1.5 mm balloon / fine cross).
2. Backload and advance the burr over the guidewire to the co-pilot.
3. Place the wire-clip at the end of rota-wire, and reconfirm verbally that wire
clip is in place.
4. Turn on the flush solution and do RPM check while holding the co-pilot in
the hand (to prevent entanglement of rota burr and blue drape/4x4
gauze).
5. Press foot pedal to activate dynaglide mode.
STEPS for Rotational Atherectomy (cont)
Steps for operator: (cont)
6. Advance the burr inside the guiding catheter to the ostium of the coronary
artery.
7. Three steps to remove tension/inertia from the system:
a. Move advancer knob back and forth to remove tension between drive shaft
and Teflon® sleeve.
b. Open copilot and move burr back and forth under fluoroscopic guidance to
remove tension between guidewire and rota burr.
c. Brief Dyna-tap under fluoroscopic guidance. If there is residual
tension/inertia and there is sudden burr advancement/jump – it occurs at
low speed and therefore is safer; ie, prevents dissection.
8. For distal lesions: advance the burr manually/at dynaglide mode to just
proximal to lesion.
STEPS for Rotational Atherectomy (cont)
Technique of rotablation:
1. Slow burr advancement
2. To-and-fro pecking motion of the burr
3. Shorter burr run times (15–20 sec)
4. Low burr speeds (140,000–150,000 RPM)
5. Strict avoidance of significant drops in rpm (> 5000 RPM for > 5 sec)
6. Flush the system with diluted contrast (1:10 dye-to-saline ratio) during the
ablation runs.
7. Keep systolic blood pressure > 100 mm Hg during the procedure, use 1-2
cc of diluted IV neosynephrine 100-200 ug as needed (neosynephrine may
cause reflex bradycardia).
STEPS for Rotational Atherectomy (cont)
After completion of rotablation:
1. Activate the dynaglide mode and remove the burr from the guiding catheter on
dynaglide mode, while pressing brake release (the black button on the Rotablator®
console), and advancing the wire as the burr is withdrawn.
2. Three steps after completion of procedure:
a. Remove wire clip
b. Turn off the flush solution
c. Remove the burr from the wire
3. Take a cine image to rule out complications
4. Advance another guidewire (Runthrough NS®/Fielder®) across the lesion, parallel to
rota-floppy wire
5. Use NC balloon for post-rota PTCA (modified CB-PTCA with rota-floppy wire in-situ)
to prepare lesion for stent delivery.
6. Remove rota-floppy after stent placement, and before deploying the stent.
Rota+BMS vs Rota+DES
Procedural and Clinical Results
Rota + BMS (n = 284)
P = NS
Rota + DES (n = 130)
P = NS
P < .01
P = .62
P = .09
%
%
P = NS
Procedural
Success
Clinical
Success
CK-MB 30-day
Stent
TVR
>3x
MACE Thrombosis
MACE = major adverse cardiac events; TVR = target vessel revascularization
Data presented by Sharma S, et al. American College of Cardiology Scientific Sessions,
Chicago, Ill, 2008
RotaDES Issues
• Procedural and clinical results — as restenosis will be
determined by stent expansion
• What should be DES length post-rotablation? All ablated
areas or lesion coverage only
• No randomized trial yet — ongoing ROTAXUS Trial
Issues Involving the Case
• Choice of Antithrombotic Therapy
• Treatment of Calcified Lesions
• Bifurcation Lesion Intervention
Bifurcation Lesion Classification
Duke’s Classification
Medina Classification
A
B
Prebranch
Medina: 1,0,0
< 5%
C
Pre- and
postbranch
Postbranch
Medina: 0,1,0
< 5%
Medina: 1,1,0
5%-10%
D
E
True
Bifurcation
Medina: 1,1,1
15%-20%
Causes:
Plaque shift
Spasm
Dissection
Most common = 45%
F
Ostial
Medina: 0,0,1
< 5%
Prebranch
and Ostial
Medina: 1,0,1
10%-15%
MADS (Main, Across, Distal, Side) Classification of Techniques
Based on the Manner in which First Stent Is Implanted With
Multiple Final Stent Strategy
M
Main prox. first
A
Main Across side first
D
Distal first
Reprinted from EuroIntervention Vol 5(1), 39-49, Stankovic G, et al. © 2009, with
permission from Europa Edition.
S
Side branch first
Complex Bifurcation Lesion Interventions
Technical Issues
1. How big is the sidebranch(es). Ready to lose the sidebranch (SB)?
2. Wire both branches. Difficult wiring?
3. Jailing the sidebranch wire(s). Hydrophilic?
4. Good back-up support guide catheter: 6, 7, or 8Fr?
5. Optimal views. Orthogonal projections?
6. Provisional or systematic SB stenting (1 vs 2 stents?)
7. Dedicated 2/3 stent technique (T, Culotte, Crush, SKS, V or W?)
Various Techniques for Stenting Trifurcation/Bifurcation
Lesions
Stent the MV +
Bifurcation Lesion balloon or debulk SB
MV
..and stent the SB only if
suboptimal results:
CP, EKG , < TIMI III flow,
> 90% stenosis
SB
Provisional/
Conventional
Stent Technique
Stent + stent
(“T stenting”)
MV = main vessel; CP = chest pain
Stent + stent
(“reverse-T”)
Various Techniques for Stenting Bifurcation Lesions
Bifurcation Lesion Stent + PTCA
Stent + stent
(“T stenting”)
Stent + stent
(“reverse-T”)
SB
MV
Stent + stent
(“Culotte”)
Stent + stent
(“Y” or “V”)
2
1
2
“V”
1
1
Stent + stent
(“Crush”)
2
1
Stent + stent
(“Kissing”)
Bifurcation Lesion Intervention Using DES
“Simultaneous Kissing Stent” (SKS) Technique
Pre
Post
Clinical Outcomes in Trials Comparing 1 DES (1S) vs
2 DES (2S) Strategy in Treating Coronary Bifurcations
MACE
%
TLR
1S 2S
1S 2S
Colombo A, et al.
SES stents
(n = 85)
Pan M, et al.
SES stents
(n = 91)
1S 2S
1S
2S
1S 2S
Ferenc M, et al. Steigen TK, et al. Colombo A, et al.
T-stenting
NORDIC Trial
CACTUS trial
(n = 202)
(n = 413)
(n = 85)
1S 2S
1S
2S
Hildick-Smith D, Sharma SK, et al.
PRECISE-SKS
et al. BBC ONE
(n = 100)
(n = 500)
Clinical Outcomes in Trials Comparing 1 DES (1S) vs 2 DES
(2S) Strategy in Treating Coronary Bifurcations (cont)
Incidence of Reported Stent Thrombosis
1S group
2S group
%
1S 2S
1S 2S
Colombo A, et al.
SES stents
(n = 85)
Pan M, et al.
SES stents
(n = 91)
1S
2S
1S
2S
1S 2S
Ferenc M, et al. Steigen TK, et al. Colombo A, et al.
T-stenting
NORDIC Trial
CACTUS trial
(n = 202)
(n = 413)
(n = 85)
1S 2S
1S
2S
Hildick-Smith D, Sharma SK, et al.
PRECISE-SKS
et al. BBC ONE
(n = 100)
(n = 500)
Clinical Outcomes in Trials Comparing 1 DES (1S) vs 2 DES
(2S) Strategy in Treating Coronary Bifurcations (cont)
Incidence of Reported Stent Thrombosis
1S group
2S group
%
Therefore while simple approach of one stent in the main
vessel may suffice in most bifurcation lesions,
a complex strategy (done correctly)
of 2 stents by one’s preferred technique may be required
especially if SBr is large size (>3mm) or lesion is
long/angulated
1S 2S
1S 2S
Colombo A, et al.
SES stents
(n = 85)
Pan M, et al.
SES stents
(n = 91)
1S
2S
1S
2S
1S 2S
Ferenc M, et al. Steigen TK, et al. Colombo A, et al.
T-stenting
NORDIC Trial
CACTUS trial
(n = 202)
(n = 413)
(n = 85)
1S 2S
1S
2S
Hildick-Smith D, Sharma SK, et al.
PRECISE-SKS
et al. BBC ONE
(n = 100)
(n = 500)
Newer Interventions and Stents in 2010
Bifurcation Stents
B
A
E
D
G
C
H
I
F
J
Interventional Cardiology Live Case
Study Series:
A Master Class in Procedural Techniques
Samin K. Sharma, MD
Annapoorna S. Kini, MD
Director
Cardiac Cath Lab and Intervention
Professor of Medicine
Co-Director
Cardiovascular Institute
Mount Sinai Medical Center
New York, NY
Associate Director
Cardiac Cath Lab
Mount Sinai Medical Center
New York, NY
Sameer K. Mehta, MD
Voluntary Associate Professor of Medicine
University of Miami - Miller School of
Medicine,
Miami, Florida
Take-Home Message:
Techniques of Rotational Atherectomy in DES Era
 Rotational atherectomy is a useful adjunctive device in
interventional treatment of heavily calcified lesions
 Optimal technique and strategy are crucial to avoid any
potential complications
 Properly performed rotational atherectomy followed by
DES implantation (RotaDES) may translate into excellent
long-term results and will broaden our scope of lesions
we can take care of safely
Interventional Cardiology Live Case Study Series:
A Master Class in Procedural Techniques
Please join us for our next live case:
Tuesday October
at 8:00 AM EST
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