1. Conquering the Complex Coronary Intervention… Lesions, Drugs, Devices and Stress
William O. Suddath, M. D.
Director, Interventional Cardiology Training
Georgetown University
Washington Hospital Center

2. I have no real or apparent conflicts of interest to report.
William O. Suddath, MD
I have no real or apparent conflicts of interest to report.

3. Evolution of Percutaneous Coronary Reperfusion
FDA Approval DES
CMS Approval DES
Cypher
FDA Approval
Cook Stent-bail out
JJIS stent-elective
Introduction of
Thrombolytic Therapy
HFICA Approval
Stent
Brachytherapy
1st PTCA
DES Thrombosis
Introduction of IV NTG
ACEI
Statins
Approval of PCI for AMI
GUSTO, PACT trials
Clinical Trials
-Dir Atherectomy
-Stent
-Rotablator
-Excimer Laser
PCI for AMI
BSC Approval
TAXUS 3

5. Complex Lesions / Complex Disease
AMI
Calcification
Multistenting
Ostium
Thrombus
Long lesions
CTO
Unstable angina
Multivessel
Saphenous graft
Bifurcation
Diabetes
Chronic renal failure
Left main
Diffuse disease
“REAL WORLD”

6. Pathophysiology of ST-Elevation Myocardial Infarction
Generally caused by a completely occlusive thrombus in a coronary artery
Results from stabilization of a platelet aggregate at site of plaque rupture by fibrin mesh
Review pathophysiology for STEMI. Contrast this with other ACS presentations (UA and non-STEMI).
platelet
RBC
fibrin mesh
GP IIb-IIIa 6

7. 1. Time is Myocardium 2. Infarct Size is Outcome
100 D 80 60
Mortality Reduction (%) C 40 20 B A
Extent of
Myocardial Salvage 4 8 12 16 20 24
Time From Symptom Onset to Reperfusion Therapy, h
Critical Time-dependent Period
Goal: Myocardial Salvage
Time-independent Period
Goal: Open Infarct-Related Artery
Gersh BJ, et al. JAMA. 2005;293:979.

8. MedSTAR Transport Washington Hospital Center Washington, DC8 8

9. America’s Aging Society
-- Over 65: 72 million, represents 20% of populace in next twenty years --Over 85: 18 million by Only 20% are fully mobile % have some degree of dementia

15. Approach Understand, It’s a team effort…
Know your teams strengths and weakness
Anesthesia
Surgery
Recruit advice and opinion… it’s not a sign of weakness
Put away your ego…

16. Anatomical Considerations
Rational
Anatomical Considerations
Radial
Cannulation
Superficial artery
Easy compression
Early ambulation

17. Angiography
2D Longitudinal
Lumen Imaging

18. New Technologies

23. IVUS Imaging
2D Cross-Sectional
Imaging

24. IVUS Imaging: Plaque Surface and Volume
Transverse
Plane
Longitudinal
Plane

26. Pharmacology ASA Anticoagulation… bivalrudin, oral Xa
Antiplatelet Therapy… which one?
Adjunctive Therapy… vasodilators
Lytic Therapy
II B, III A Inhibition

27. Indirect vs Direct Thrombin Inhibition
Indirect inhibition by heparin requires the presence of antithrombin (AT), the actual inhibitor.
Heparin (long yellow strand) binds to AT, causing a shape change that increases the ability of AT to inhibit thrombin.
Direct inhibition with Angiomax® (bivalirudin) inhibits thrombin directly with high affinity and specificity.
It requires no cofactor, and acts alone.
Bivalirudin’s effectiveness is not affected by variability in the concentration of a co-factor like AT.
Key Message: Angiomax inhibits thrombin directly; therefore, it does not promote coagulation.
On the left panel, heparin is not labeled but is represented by the long strand.
Several “antithrombin” agents have been developed to prevent coagulation for many clinical circumstances. Heparin is a ubiquitous agent in the hospital and outpatient settings that is an imprecise and inefficient anticlotting agent.
Indirect inhibition by heparin requires the presence of antithrombin (AT), the actual inhibitor in the clotting cascade. The panel on the left shows heparin (see the long strand) binding to AT and causing a shape change that increases the ability of AT to inhibit thrombin.
Angiomax inhibits thrombin directly with high affinity and specificity. The panel on the right shows Angiomax binding to thrombin. Angiomax provides rapid, effective thrombin inhibition to prevent thrombosis and platelet effects.
Hirsh J et al. Chest. 2001;119(1 suppl):64S-94S.
Weitz JI et al. Thromb Res. 2002;106:V275-V284.
Gibson CM, 2006

28. Bivalirudin is Cleaved by Thrombin, a Rapid Return to Hemostasis, a Safety Advantage
Heparin’s effects on platelets and its reappearance as it dissociates from cells and proteins may explain the prolonged bleeding risk following discontinuation of heparin, when a return to normal hemostasis is essential.
Angiomax® (bivalirudin) is cleaved by thrombin, allowing thrombin to quickly recover hemostatic activity upon discontinuation of Angiomax.
The natural reversibility and the short, 25-minute half-life may explain the significantly lower bleeding rates seen in clinical trials.
Key Message: The natural reversibility and the short, 25-minute half-life of Angiomax may explain the significantly lower bleeding rates seen in clinical trials.
Heparin’s effects on platelets and its reappearance as it dissociates from cells and proteins may explain the prolonged bleeding risk following discontinuation of heparin, when a return to normal hemostasis is essential.
Angiomax has a short half-life. It is actually cleaved by thrombin, allowing thrombin to quickly recover hemostatic activity upon discontinuation of Angiomax.
Angiomax Prescribing Information, June
Maraganore JM et al. Biochemistry. 1990;29:
Hirsh J et al. Chest. 2001;119(1 suppl):64S-94S.

29. Dual Antiplatelet Rx for PCI
Circ 102: 624,2000
Dual Antiplatelet Rx for PCI
% MACE
1.5
1.2
0.9
ISAR
FANTASTIC
STARS
MATTIS
CLASSICS

30. 85% Inactive Metabolites Esterases
Considerations N S O Cl
CH3 C N S O C H 3 F
Pro-drug
Clopidogrel
Prasugrel
Hydrolysis
(Esterases)
85% Inactive Metabolites Esterases N S O Cl
CH3 C N S O F
Oxidation
(Cytochrome P450)
HOOC
* HS N O F
Active Metabolite O N S Cl
CH3 C
Active Metabolite
HOOC
* HS N O Cl
OCH3

31. Devices

39. Support Systems

40. Shock Categories Ventricular Septal Rupture 4.6% “Isolated” RV Shock
3.4%
Tamponade/
Rupture
1.7%
Acute Severe MR
8.3%
Other
7.5%
Predominant
LV Failure
74.5%
Shock Registry
Hochman, JACC 36: 1063, 2000

43. Impella Axial flow pump Much simpler to use
Increases cardiac output & unloads LV
LP 2.5
12 F percutaneous approach; Maximum 2.5 L flow
LP 5.0
21 F surgical cutdown; Maximum 5L flow
Cost: 3-5K
Blood Inlet
Blood outlet
Motor
Pressure Lumen 43

44. ECMO

45. The Future
This is not your standard Cath Lab….

47. CAD and Intervention… the Future
Age
Prior PCI / CABG
Calcium
Sex
PVD… access
LV dysfunction LM
Valvular disease

54. Education / Preparation

55. Cath Lab VRTM Simulator
Percutaneous Coronary Interventions (PCI)
PTCA
Percutaneous Peripheral Interventions (PPI)
SFA
Cardiac Rhythm Management (CRM)
Heart Failure
Bradycardia

56. The full Vascular simulation set-up

57. Summary
A… Anticipate
B… Be prepared
C… Communicate
D… Deep Breaths

62. Disasters

64. “SKS” Stenting of Unprotected Left Main Bifurcation Lesion
70% distal LMCA &
70-80% ostial LAD &
80-90% prox LCX
0-10% residual LMCA/LAD
& 0-10% LMCA/LCX post
3.25/9 mm NC Monorail
3.0/13 mm Zeta in LMCA/LAD & 3.0/12 mm Express in LMCA/LCX

65. I II III Future Directions First Conclusion Future Recommendations ?
Radial: I A
Femoral: I C
Future Recommendations ?
AHA/ACC/ESC
Future Directions I II
III
Evidence &/or Agreement
(Beneficial, Useful, Effective)
Conflicting Evidence
Divergence of opinion
(Usefulness, Efficacy)
II a weight in favor
II b less well established
Not Useful/Effective
Potentially Harmful
First
Conclusion
Multiple randomized trials or meta-analyses
Single randomized trial or non-randomized studies
C. Only consensus opinion of experts, case studies or standard of care

66. Causes of Cardiogenic Shock
Tamponade/rupture
1.7%
Other
7.5%
Isolated RV Shock
3.4%
VSD
4.6%
Acute Severe MR
8.3%
Predominant LV Failure
74.5%
Shock Registry
JACC :1063 66

67. Management of Patients in Cardiogenic Shock: Recommendations
Early shock, Diagnosed on Hospital Presentation
Delayed onset shock Echocardiogram to rule out mechanical defects
IABP
Fibrinolytic therapy if all of the following are present:
>90 minutes to PCI
2. <3 hours post MI onset
No contraindications
Arrange rapid trnsfer to PCI/CABG Center
Arrange rapid transfer to PCI/CABG Center
Cardiac Catheterization and Coronary Angiography
Hochman, Circulation 107: 2998, 2003

68. SHOCK Trial Acute Myocardial Infarction Randomization
Emergency Revascularization
Initial Medical Stabilization
IABP/Pharmacoligic Support
Possible Prior Thrombolysis
Emergency Early PTCA/CABG ≤6 hrs
IABP/Pharmacoligic Support
Thrombolysis Unless Absolute Contraindication
Possible Delayed Revascularization > 54 hrs
Hochman, AHJ 137: 313, 1999

69. Training center: Simulation Set-up

70. Algorithm for Coronary Spasm

71. Definition That which is referred That which makes you stronger….
That which requires additional underwear
That which requires a team approach
In the end, knowing when to stop