Role of Percutaneous Assist Devices
in the Catheterization Laboratory
Khaled M. Ziada, MD
Gill Foundation Professor of Interventional Cardiology
Director, Cardiovascular Catheterization Laboratories
Gill Heart Institute, University of Kentucky
Presenter Disclosure Information
KHALED M. ZIADA, MD
Gill Foundation Professor of Interventional Cardiology
FINANCIAL DISCLOSURE
No relevant financial relationships to disclose.
Outline
o High Risk Patients
o Cardiogenic shock
o High risk PCI
o Mechanical Assist Devices
o Ideal features
o Intra-aortic balloon counter-pulsation (IABP)
o Impella
o Tandam Heart
o ECMO
o
Case Studies
o Overview of device features and selection
Objectives
o High Risk Patients
Cardiogenic shock
o Describe theoclassifications
of cardiogenic shock, the
o High risk PCI
causes and patho-physiology of cardiogenic shock, and its
clinical manifestations
o Mechanical Assist Devices
o Determine the
diagnostics,
o Ideal
features monitoring and resource
Intra-aortic balloon
countermobilization of opercutaneous
revascularization,
mechanical
pulsation (IABP)
support and revascularization
strategies.
o Impella
o Tandam Heart
theopercutaneous
ECMO
o Describe
LV assist devices available in
treating heart failure patients
o Case Studies
o Overview of device features and
selection
High Risk Patient Subgroups
NO STANDARDIZED DEFINTIONS
o Cardiogenic Shock
o High-risk coronary revascularization
o Severe LV dysfunction
o PCI unprotected LMT
o Multi-vessel PCI with LV dysfx.
o PCI on last remaining conduit
o End-stage refractory heart failure
o Bridge to destination VAD or Tx
o Post-operative low cardiac output syndrome
Definitions – Cardiogenic Shock
o Shock
A syndrome of significantly impaired tissue perfusion leading to
cell hypoxia/injury and subsequent vital organ dysfunction.
o Classification of Shock
Severe impairment of any component of the circulatory system.
● Hypo-volemic
● Cardiogenic
●
●
Distributive
Extra-cardiac Obstructive
o Cardiogenic Shock
Shock resulting from acute reduction in cardiac function caused
by direct damage to myocardium and/or intra-cardiac
mechanical abnormality.
Causes of Cardiogenic Shock
Acute Myocardial Infarction (MI)
- STEMI or NSTEMI
- LV or RV infarction
Mechanical Complications of MI
- VSD
- Acute MR
- Free wall rupture
Primary Valve Disorders
- Critical AS
- Acute MR
- Acute AI
Primary Myocardial Disorders
- Acute Myocarditis
- Stress-induced LV dysfunction (Takotsubo)
- End-stage cardiomyopathy
Pathophysiology of Cardiogenic Shock
.
Hochman, J.S. Circulation 2003;107:2998-3002
Pathophysiology of Cardiogenic Shock
.
Hochman, J.S. Circulation 2003;107:2998-3002
Hemodynamics of Cardiogenic Shock
Typical
Reduced cardiac index <2.0 L/min/m2
Reduced systolic BP <90mm Hg and/or
mean BP <60mm Hg
Elevated PCWP >18mm Hg
Elevated SVR
Atypical or pre-shock
Normal or mildly reduced systolic BP
Normal or low PCWP <18mm Hg
Normal or low SVR
Indications of SG catheterization
Class I recommendation:
- Progressive ↓BP unresponsive to
fluids or when fluids are contraindicated
-Suspected mechanical complications
-Class IIa recommendation:
- ↓BP without pulmonary congestion not
responsive to fluid Rx
- Cardiogenic shock
- Severe/progressive HF or pulmonary
edema not responding to Rx
- Persistent hypoperfusion without ↓BP or
pulmonary congestion
- During administration of vasopressor and/
or inotropic agents
Mechanisms of Shock in Acute MI
Rupture Other
7%
RV MI
1%
3%
VSD
4%
Acute
MR
7%
o Most commonly a large
anterior MI (prox-mid
LAD occlusion)  40%
myocardium
o Smaller MI in already
impaired LV
o Smaller MI  mechanical
complication
o Three vessel disease &/or
LMT involvement in >80%
cases
Jacobs, A. et al. JACC 2003;41:1273-9
Acute MI – Incidence of Cardiogenic Shock
o The #1 cause of death in patients presenting with AMI
o Incidence of shock
NRMI
10
GRACE
6-9%
5
5-10%
0
1995
1998
2001
>290,000
US STEMI pts
2004
’00
‘01
‘02
‘03
‘04
> 44,000 global
STEMI & NSTEMI pts
‘05
Percutaneous Assist Devices
Intra-Aortic Balloon Counter-pulsation
o Mainstay of hemodynamic
support for cardiogenic shock pts
o Percutaneous femoral access
o Size down to 7F, volume ranges
from 34-50 mL.
o Main mechanisms of action:
●
●
●
●
Improve cardiac index
Reduce afterload
Reduce LVEDP & PCWP
Improve coronary perfusion
o IABP is a temporary support
Intra-Aortic Balloon Counter-pulsation
Does IABP support improve survival or other outcomes?
IABP – Cardiogenic Shock
The SHOCK Trial
Should We Emergently Revascularize Occluded
Coronaries for Cardiogenic Shock?*
* IABP was used in 86% of patients in each group
Hochman, J.S. et al. N Engl J Med 1999;341:625-34
IABP – Acute MI without Shock
The CRISP AMI Trial
Counter-pulsation to Reduce Infarct Size Pre-PCI in Anterior MI
Stable Ant MI 1ry PCI
Routine IABP (n=161)
No routine IABP (n=176)
p value
30 day events
Death
1.9%
4.0%
0.26
Stroke
1.9%
0.6%
0.35
Major Bleeding
3.1%
1.7%
0.49
6 months events
Death
1.9%
5.2%
0.12
Death/re-MI/new HF
6.3%
10.9%
0.15
Death/shock/new HF
5.0%
12.0%
0.03
Patel, M et al. JAMA 2011, 306: 1329-37
IABP – High-Risk PCI subsets
BCIS-1 Trial
Balloon-Pump Assisted Coronary Intervention Trial
p=0.32
Perera D et al. JAMA 2010, 304: 867-874
IABP – High-Risk PCI subsets
BCIS-1 Trial
Balloon-Pump Assisted Coronary Intervention Trial
High Risk PCI
Elective IABP
(n=151)
No routine IABP
(n=150)
HR
(95% CI)
5 year all cause mortality
(total 100 deaths)
42 (27.8%)
58 (38.7%)
0.66
(0.44-0.98)
Perera D et al. I2 ACC March 2012
Intra-Aortic Balloon Counter-pulsation
IMPACT on SURVIVAL is CONTROVERSIAL
o SHOCK trial (borderline favorable effect) vs. SHOCK
registry (no effect) at one year
o Single center studies (favorable) vs. meta-analyses
(generally neutral)
o Randomized trials did not meet the primary endpoints
to prove conclusively the value of IABP support
ACC/AHA Guideline recommendation for use of IABP
in infarct related cardiogenic shock – class 1B
Percutaneous LVADs – Impella ®
o A miniaturized pump motor that is delivered to the LV, with
inlet and outlet holes straddling the aortic valve
o Femoral access (13F)
o Arterial access only — faster and easier to deliver
o Next generation will be able to provide 3.5L support
o Impella 5.0 requires a cut-down and Impella LD is used
intra-operatively
Percutaneous LVADs – Impella ®
Case #1
o 69 year old male with known 3 vessel CAD, severely
impaired LV (<25%) and decompansated CHF
o Angiography reveals severe lesions in LAD, LCX and
RCA is totally occluded.
o In addition, he has severe left external iliac disease
o Plan multi-vessel PCI with Impella support.
Percutaneous LVADs – Impella ®
Does Impella support improve survival or other outcomes?
Percutaneous LVADs – Impella ®
The PROTECT II Trial
Prospective Multicenter Randomized Trial
Comparing IMPELLA to IABP in High Risk PCI
o Multicenter randomized controlled trial
o High-risk PCI: an attempt to standardize the definition
o 30 day composite endpoint of major adverse events (MAEs):
Death, stroke/TIA, MI , TVR, cardiac or vascular operation for limb
ischemia, AKI, worsening of AI, severe hypotension, CPR/VT, PCI failure
o Plan to enroll 654 patients, but study was terminated by
DSMB after enrolling 426 patients due to futility
Percutaneous LVADs – Impella ®
The PROTECT II Trial
Non-Emergent high-risk PCI patients requiring prophylactic hemodynamic support:
LVEF ≤35% with unprotected LM, last patent conduit, or 3 vessel disease
R
1:1
IABP + PCI
IMPELLA 2.5 + PCI
Primary Endpoint = 30-day Composite MAE rate
Follow-up of the Composite MAE rate at 90 days
*Major Adverse Events (MAE) : Death, stroke/TIA, MI , TVR, cardiac or vascular operation for
limb ischemia, AKI, worsening of AI, severe Hypotension, CPR/VT, angiographic failure
Percutaneous LVADs – Impella ®
The PROTECT II Trial
IABP
(N=223)
Impella
(N=224)
p-value
9.5%
14.9%
0.088
Median # of RA passes/pt (IQ range)
2.0 (2.0-4.0)
5.0 (3.5-8.5)
0.004
Median RA time/lesion (IQ range sec)
40 (20-47)
60 (40-97)
0.005
3.1%
8.0%
0.024
17.5%
25.4%
0.041
8.2±21.1
1.9±2.7
<0.001
37.7%
5.7%
<0.001
Procedural Characteristics
Rotational Atherectomy (RA)
RA of Left Main Artery
% of SVG Treatment or RA use
Total Support Time (hour)
Discharge from Lab on device
Percutaneous LVADs – Impella ®
The PROTECT II Trial
p=0.029
51.4%
p=0.10
Results for
All Patients
(N=426)
42.7%
↓ 21% MAE
40.8%
34.9%
IABP
IMPELLA
N=211
N=215
N=210 N=213
30 day MAE
90 day MAE
27
Percutaneous LVADs – Impella ®
The PROTECT II Trial
p=0.003
51.1%
p=0.009
Results without
Atherectomy
(N=374)
42.4%
↓ 30% MAE
↓ 30% MAE
35.9%
IABP
IMPELLA
29.5%
N=191 N=183
N=190 N=181
30 day MAE
90 day MAE
28
Percutaneous LVADs – Impella ®
The PROTECT II Trial
Death, Stroke, large MI, TVR
Post-hoc
Analysis for
All Patients
(N=426)
IABP
IMPELLA
Log rank test, p=0.04
29
Percutaneous LVADs – Impella ®
Case #2
o 56 year old male with known 3 vessel CAD, s/p 4
vessel CABG, severely impaired LV (<20%) and acuteon-chronic CHF, severe CKD on HD
o Angiography reveals severe lesions in LAD and RCA,
distal LCX/OM lesion and failure of all grafts including 3
SVGs and LIMA to LAD.
o Plan multi-vessel PCI with Impella support.
Percutaneous LVADs – TandemHeart ®
o A miniaturized percutaneous
cardiac bypass pump
o Femoral access
o Requires arterial and venous
access
o Requires trans-septal puncture,
venous catheter placed in LA
o More time consuming and
technically challenging
Percutaneous LVADs – ECMO
o A miniaturized percutaneous
cardiac bypass pump
o Femoral and/or neck access
o Requires arterial and venous
access
o Non-pulsatile, does NOT improve
coronary blood flow
o Not time consuming to insert, but
requires a perfusionist
Percutaneous LVADs – Complications
o Primarily related to vascular access
o device size
o limb ischemia
o trans-septal puncture
o Bleeding
o access-related
o anticoagulation
o Thrombo-embolism and stroke
o Infection
o Others e.g. hemolysis
Percutaneous LVADs – Comparison Table
Device
Maximal Active
Flow (L/min)
IABP
Effect on
Cardiac
Output
+
No Active Flow
TandemHeart
>5.0 L/min
+
Infection, Limb ischemia,
Stroke, Dissection, Bleeding
+++
Markedly increase
coronary blood flow
and significantly
reduces O2 Demand.
+++
Arterial and Venous
Access and trans-septal
puncture required
+++
Infection, Limb ischemia,
Stroke, Bleeding,
Thromboembolism, Small
residual ASD may be
present
++
++++
Markedly increases
coronary blood flow
and markedly reduces
O2 Demand
++
Single Arterial Access
Required
++
Infection, Limb ischemia,
Stroke, Dissection,
Bleeding, Hemolysis
++++
+/Limited Increase CBF
but also O2 Demand
++++
Arterial and venous
access required with
large cannulae;
perfusionist required
++++
Infection, Limb ischemia,
Stroke, Dissection,
Bleeding, Hemolysis,
Thrombocytopenia
2.5 L/min
ECMO
Risk for
Complications
(1-4+)
+++
3.5-4.0 L/min
Impella 2.5*
Effect on Coronary
Complexity of Insertion
Blood Flow
(1-4+)
and O2 Demand
(1-4+)
++
+
Limited Increase in
One arterial access
coronary blood flow required. Relatively safe
and limited reduction in with smallest cannulas
O2 demand
of all the devices
Percutaneous LVADs – Selection in Cath Lab
Which is ideal for cardiogenic shock?
o Impella 2.5 provides support for high risk PCI and
impending shock, but is probably not adequate for
established shock
o In those patients, Impella 5.0, TandemHeart or ECMO
are more appropriate due to the full support that they
provide (~5L/min)
o ECMO may be reasonable as a bridge to further
therapy in shocked patients, particularly those after
cardiac arrest or in ATN.
Percutaneous LVADs – Selection in Cath Lab
Which is ideal for high-risk PCI?
o The evidence that high risk PCI requires hemodynamic
support remains controversial
o Operator and laboratory expertise are paramount in
identifying such patients and adjusting procedural technique
accordingly
o IABP and Impella 2.5 provide options for such support
when it is needed
o PROTECT II did not meet its primary endpoint, but
subgroup and post-hoc analyses hint towards superiority of
Impella in certain clinical scenarios