samin k. sharma, md director cardiac cath lab and intervention professor of medicine co-director...

Samin K. Sharma, MDDirector Cardiac Cath Lab and Intervention Professor of Medicine Co-Director Cardiovascular Institute Mount Sinai Medical Center New York, NY

Annapoorna S. Kini, MD Associate Director Cardiac Cath Lab Mount Sinai Medical Center New York, NY

Sameer K. Mehta, MD Voluntary Associate Professor of MedicineUniversity of Miami - Miller School of Medicine, Miami, Florida

Interventional Cardiology Live Case Study Series:

A Master Class in Procedural Techniques

Presentation: Crescendo exertional angina and SOB for 2 months and stressMPI 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

September 21, 2010: Case #1: NJ, 72-y-o man

SOB = shortness of breath; MPI = myocardial perfusion imaging; TID = transient ischemic dilation; Cri = incomplete blood cell count recovery; ASA = acetylsalicylic acid

Cardiac Cath: 8/6/2010:Three-vessel CAD with LVEF 65%

Left main: no obstructionLAD: 80% long calcified lesion of proximal LAD (large) with 70% apical lesion

and mild diffuse first diagonalLCx: 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

Case #1 (cont)

SYNTAX Score26

® Abbott Laboratories, Abbott Park, Ill.

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

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 PCIHeparin + GP IIb/IIIa (n = 3008)Bivalirudin alone (n = 2994)

Heparin + GP IIb/IIIa (n = 2619)Bivalirudin alone (n = 2561)

ACUITY PCI

%

7.0

Ischemic Major Net ClinicalComposite Bleeding Outcomes

P = .40%

P < .001

P = .30

7.6

4.1

2.4

10.09.2

8.28.8

4.2

2.1

11.110.5

P = .45

P < .001

P = .49

Ischemic Major Net ClinicalComposite Bleeding Outcomes

Stone GW, et al. N Engl J Med. 2006;355:2203.Lincoff AM, et al. JAMA. 2003;289:853-863

Number at riskBivalirudin 1678 1647 1640 16351632 1620 1563 Heparin + GPIIb/IIIa 1662 1631 1615 16041598 1583 512

Dea

th (%

)

Time in days

1.8%

Heparin + GPIIb/IIIa inhibitor (n = 1662)

Bivalirudin monotherapy (n = 1678)

0.2%0.1%

Cardiac

Noncardiac

HORIZONS AMI Trial: 30-Day Mortality of PCI

2.8%HR = 0.63 [0.40, 0.99]

P = .049

From Stone GW, et al. N Engl J Med .2008;358:2218. © 2008 Massachusetts Medical Society. All rights reserved.

Number at riskBivalirudin 1678 1647 1640 16351632 1620 1563 Heparin + GPIIb/IIIa 1662 1631 1615 16041598 1583 512

Dea

th (%

)

Time in days

1.8%

Heparin + GPIIb/IIIa inhibitor (n = 1662)

Bivalirudin monotherapy (n = 1678)

0.2%0.1%

Cardiac

Noncardiac

HORIZONS AMI Trial: 30-Day Mortality of PCI

2.8%HR = 0.63 [0.40, 0.99]

P = .049

From Stone GW, et al. N Engl J Med .2008;358:2218. © 2008 Massachusetts Medical Society. All rights reserved.

This higher early eventsin bivalirudin group were due to higher acute stent thrombosis and can be eliminated by extended (1-3 hours) infusion after PCI or by prasugrel load instead of clopidogrel load.

4.4

9.2

%

Data presented by Stone GW, Trans Catheter Cardiovascular Therapeutics, 2009, San Francisco, Calif.

1-Year FU

5.8

3.6 3.8

2.1

P < .001 11.9

HORIZONS-AMI: Clinical Follow-Up

Heparin+GP IIb/IIIa (n = 1802)Bivalirudin group (n = 1800)

11.9

4.83.5

P = .22P = .005

P = .03

P = .98

0

5

10

15

20

2-Year FU

Heparin+GP IIb/IIIa (n = 1802)Bivalirudin group (n = 1800)

6.9

9.6

6.45.1

4.2

2.5

P < .001

18.7 18.8

6.1

4.6

P = .03

P = .005

P = .04

P = .98

Major Reinfarction Cardiac All-Cause MACE Bleeding Mortality Mortality

%

Mehran R, et al. Lancet. 2009:374:1149

Major Bleeding

Reinfarction Cardiac Mortality

All-Cause Mortality

MACE

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)

%

Major Bleed only -Without MI

(n = 551)

MI only- Without Major Bleed

(n = 611)

No MI Major Bleed (n = 12,557)

Stone G, et al. N Engl J Med. 2006;355:2203-2216.

TRITON-TIMI 38 Trial: Net Clinical BenefitBleeding Risk Subgroups – Therapeutic Consideration

Significant Net Clinical Benefit with Prasugrel

80%

4%

16%

Maintenance Dose 10 mg

Reduced maintenance dose guided by PKAge ≥ 75 or Wt < 60 kg

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 thrombosisWiviott S, et al. Circulation. 2007;116:2923.

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.

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.

Updated DAPT Post Stenting Incorporating Prasugrel

Interventional Techniques

Treatment of Calcified Lesions

• 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®

Differential cutting

PTCA PRCA

Diamondmicrochips

Rotablator®; Boston Scientific, Inc., Natick, Mass.

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

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

Rotational Atherectomy: Complications

EDRF = endothelium-derived relaxing factor; LVEDP = left ventricular end-diastolic pressure

Slow-flowSettings: •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

From Williams MS. Circulation. 1998;98:742-748.

Activation of Platelets by Rotablation Is Speed-Dependent

Rotational Atherectomy and GPIIb/IIIa Inhibitors

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, et al. Circulation. 1998;98:742-748.

Rotational Atherectomy and Platelets

Effect of Rotablation on Platelet Aggregation

Initi

al A

ggre

gatio

n Sl

ope

(uni

ts/m

in)

Rotablation Speed (rpm x 10-3)

Porcine blood exposed to a rotating burr resulted in: Platelet

aggregation and red blood cell crenation.

RotationalSpeed (rpm)

Platelet Aggregates(> 20 m)/mL blood

180,000 7434 2193

140,000 2269 627

Control 633 258

P < .0001 for all groups

Slower rotational speed results in a significantly lower number of platelet aggregates.

From Reisman M, et al. Cathet Cardiovasc Diagn. 1998;45:208-214.

Rotational AtherectomyActivation of Platelets by Rotablation Is Speed-Dependent

• Predictors of CK-MB release:– deceleration > 5000 rpm > 5 sec • Predictors of restenosis: – deceleration > 5000 rpm– LAD location

STRATAS Trial

Whitlow PL, et al. Am J Cardiol. 2001;87:699-705.

%P = .008

Technique Matters: Incidence of Slow-Flow

Current optimal Burr-to-ArteryRatio (BA): 0.3-0.5

Aggressive strategy (n = 249) BA: > 0.9

Routine strategy (n = 248) BA: < 0.8

PerforationSettings:•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


Complications

Mount Sinai Hospital Experience (6%-9% of PCI)

slow speed (140-150,000 rpm)rotational atherectomy, BA: 0.4-0.5

short burr runs, rota-flush, abciximab, stent, experience

---DES---

Rotational Atherectomy

%

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.

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


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 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 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:

• Move advancer knob back and forth to remove tension between drive shaft and Teflon® sleeve.

• Open copilot and move burr back and forth under fluoroscopic guidance to remove tension between guidewire and rota burr.

• 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.


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).


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 Clinical Success Success

%

MACE = major adverse cardiac events; TVR = target vessel revascularizationData presented by Sharma S, et al. American College of Cardiology Scientific Sessions, Chicago, Ill, 2008

CK-MB 30-day Stent TVR >3x MACE Thrombosis

Procedural and Clinical Results

P = NS

P = .09P = .62

P = NS

%P = NS

P < .01

Rota + BMS (n = 284)

Rota + DES (n = 130)

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

Prebranch Postbranch Pre- and postbranch

Ostial Prebranchand Ostial

TrueBifurcation

Bifurcation Lesion ClassificationDuke’s Classification

A

FED

B C

Medina: 1,0,0

Medina: 1,1,1 Medina: 0,0,1

Medina: 1,0,1

Medina: 1,1,0Medina: 0,1,0

Medina Classification

Most common = 45%

< 5% < 5%5%-10%

10%-15%

15%-20% < 5%Causes:Plaque shiftSpasmDissection

MADS (Main, Across, Distal, Side) Classification of Techniques Based on the Manner in which First Stent Is Implanted With Multiple Final Stent Strategy

Reprinted from EuroIntervention Vol 5(1), 39-49, Stankovic G, et al. © 2009, with permission from Europa Edition.

AMain Across side first

M Main prox. first

DDistal first

SSide branch first

Complex Bifurcation Lesion Interventions

Technical Issues

Various Techniques for Stenting Trifurcation/Bifurcation Lesions

Bifurcation Lesion

MV

Stent the MV +balloon or debulk SB ..and stent the SB only if

suboptimal results: CP, EKG , < TIMI III flow,

> 90% stenosis

Provisional/Conventional

Stent TechniqueStent + stent(“T stenting”)

Stent + stent(“reverse-T”)

SB

MV = main vessel; CP = chest pain

Various Techniques for Stenting Bifurcation Lesions

Bifurcation Lesion

MVSB

Stent + PTCAStent + stent(“T stenting”)

Stent + stent(“Y” or “V”)

“V”2

1

1

Stent + stent(“Culotte”)

1 2

Stent + stent(“reverse-T”)

Stent + stent(“Crush”)

2 1

Stent + stent(“Kissing”)

Bifurcation Lesion Intervention Using DES

“Simultaneous Kissing Stent” (SKS) Technique

PostPre

MACE

TLR

1SColombo A, et al.

SES stents(n = 85)

1S 1S 1S 1S 1S 1S2S 2S 2S 2S 2S 2S 2SPan M, et al.

SES stents(n = 91)

Steigen TK, et al.NORDIC Trial

(n = 413)

Ferenc M, et al.T-stenting(n = 202)

Colombo A, et al.CACTUS trial

(n = 85)

Hildick-Smith D, et al. BBC ONE

(n = 500)

Sharma SK, et al.PRECISE-SKS

(n = 100)

%

Clinical Outcomes in Trials Comparing 1 DES (1S) vs 2 DES (2S) Strategy in Treating Coronary Bifurcations

1S group2S group

%

Incidence of Reported Stent Thrombosis

1SColombo A, et al.

SES stents(n = 85)


SES stents(n = 91)


(n = 413)



(n = 85)


(n = 500)


(n = 100)

Clinical Outcomes in Trials Comparing 1 DES (1S) vs 2 DES (2S) Strategy in Treating Coronary Bifurcations (cont)

1SColombo A, et al.

SES stents(n = 85)


SES stents(n = 91)


(n = 413)



(n = 85)


(n = 500)


(n = 100)

1S group2S group

%

Incidence of Reported Stent Thrombosis

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 requiredespecially if SBr is large size (>3mm) or lesion is

long/angulated

Clinical Outcomes in Trials Comparing 1 DES (1S) vs 2 DES (2S) Strategy in Treating Coronary Bifurcations (cont)

A B C

D

G I

FE

JH

Bifurcation StentsNewer Interventions and Stents in 2010

Samin K. Sharma, MDDirector Cardiac Cath Lab and Intervention Professor of Medicine Co-Director Cardiovascular Institute Mount Sinai Medical Center New York, NY

Annapoorna S. Kini, MD Associate Director Cardiac Cath Lab Mount Sinai Medical Center New York, NY

Sameer K. Mehta, MD Voluntary Associate Professor of MedicineUniversity of Miami - Miller School of Medicine, Miami, Florida

Interventional Cardiology Live Case Study Series:

A Master Class in Procedural Techniques

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 19th at 8:00 AM EST

samin k. sharma, md director cardiac cath lab and intervention professor of medicine co-director...

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