1. Cath Lab Essentials : LV Assist Devices for Hemodynamic Support (IABP, Impella, Tandem Heart)
Michael A. Gibson, MD
Assistant Professor of Medicine
University of California, Irvine
Division of Cardiology
Talk briefly describes the functioning and assets of the most common devices used today. It gives an overview of the current evidence and indications for left ventricular assist device use in cardiogenic shock and high-risk percutaneous coronary intervention.

2. Goals
To compare and contrast mechanical LV assistance and percutaneous support devices in terms of their designs and ideal applications
Review current indications for commonly used devices
Describe the factors that should be considered when choosing the most appropriate devices

3. Causes of Cardiogenic Shock
Devices are predominantly used in the management of HF and CS. Most common cause of CS is LV failure. CS complicates 5-10% of acute MI cases ~40,000-50,000 patients per year in the US. Mechanical complications of MI (VSD, free wall rupture, acute MR) are less frequent causes of CS.
Cardiology Clinics, 2013; 31(4): ,

4. Physiology of Cardiogenic Shock: A Downward Spiral
Myocardial Infarction
Damaged heart muscle
Blood pressure [ BP] 1
Vasodilation [SVR ]
Inflammatory activation
(TNF-α, IL-6) 6 2 5
NO synthesis
Cardiac output [ CO] 4
Myocardial perfusion 3 7
Hemodynamic support 11 12
Myocardial ischemia
Venous return 8 BP
SVR 10
Hypoperfusion causes release of catecholamines, which increase contractility and peripheral blood flow, but catecholamines also increase myocardial oxygen demand and have proarrhythmic and myocardiotoxic effects.
The decrease in CO caused by MI and sustained by ongoing ischemia triggers release of catecholamines, which constrict peripheral arterioles to maintain perfusion of vital organs.
Vasopressin and angiotensin II levels increase in the setting of MI and shock, which leads to improvement in coronary and peripheral perfusion at the cost of increased afterload, which may further impair myocardial function.
Activation of the neurohormonal cascade promotes salt and water retention; this may improve perfusion but exacerbates pulmonary edema. The reflex mechanism of increased systemic vascular resistance (SVR) is not fully effective, as demonstrated by variable SVR, with median SVR during CS in the normal range.
In some patients, SVR may be low, similar to septic shock. In fact, sepsis was suspected in 18% of the SHOCK trial cohort, 74% of whom developed positive bacterial cultures. SVR was lower in these patients, and low SVR preceded the clinical diagnosis of infection and culture positivity by days.
Cardiogenic shock can cause the systemic inflammatory response syndrome (SIRS) and suggest that inappropriate vasodilation as part of SIRS results in impaired perfusion of the intestinal tract, which enables transmigration of bacteria and sepsis. SIRS is more common with increasing duration of shock even though levels of interleukin-6 and tumor necrosis factor have been found to be elevated on admission among MI patients who were initially in Killip class I and later developed CS. Cytokine levels rise more dramatically over the 24 to 72 hours after MI. Tumor necrosis factor and interleukin-6 have myocardial depressant action. TNF also induces coronary endothelial dysfunction, which may further diminish coronary flow.
Excess NO may also contribute to SIRS. MI is associated with increased expression of inducible NO synthase, which leads to excess NO, which causes vasodilation, myocardial depression, and interference with catecholamine action. Although isoform-nonselective NO synthase inhibitors appeared to improve hemodynamics and outcome in small studies of CS patients, NG-monomethyl-L-arginine at the same dose and duration did not reduce mortality in a large multicenter trial. NG-monomethyl-L-arginine did, however, result in an early blood pressure rise in patients with persistent shock despite vasopressors and opening of the infarct artery, which suggests that excess NO contributes to hypotension. 13 9
Coronary artery perfusion
Reperfusion :
PCI or CABG CO 14
Reducing inflammatory response: ?
Myocardial ischemia
Death 15
CO & BP

5. Mortality
CS remains the leading cause of death in MI with mortality rates still 40–60%.
GUSTO-I trial 11-year survival in patients with cardiogenic shock complicating MI who survived 30 days. Survival was 67% in non-shock and 28% in shock patients.

6. Mortality rates decreased in overall cardiogenic shock (from 62
Mortality rates decreased in overall cardiogenic shock (from 62.8% to 47.7%), cardiogenic shock on admission (from 73.8% to 46.6%)
and cardiogenic shock developing during hospitalization (from 60.9% to 48.9%)

7. Rates of PCI and intraaortic balloon counterpulsation increased, whereas rates of fibrinolytic therapy decreased.
Rates of PCI increased to greater than 60% and balloon pump use increased to greater than 30%.
In contrast, rates of coronary artery bypass graft surgery remained stable.

8. Emergency revascularisation - SHOCK Trial
p=0.03
p=0.11
85% of survivors NYHA Class I/II at 12 months after early revascularization or initial medical stabilization
Hochman JAMA 2000;285:190

9. Heart muscle can recover with support9
High Potential
of heart muscle recovery, Gain in Ejection Fraction
Low Potential
of heart muscle recovery, Loss in Ejection Fraction
The medical community recognizes that, in the immediate hours after an acute MI or heart attack, the heart muscle, if supported properly, has a high potential to recover and regain a healthy ejection fraction. Ejection fraction is essentially a measurement of the heart‘s pumping efficiency and power. The heart muscle is the only muscle in the body that needs constant supply of blood with oxygen or it will switch into a hibernation mode to protect itself. (explain darkened area)
In this stage, it will either recover with help or die within hours to days—the dead muscle is called an infarct. If this muscle support is applied too late in the process, more muscle will likely die. Then, the heart will dilate and the muscle wall will thin out (-point to figure-))—resulting in loss of heart muscle which will affect the patient‘s life. In its most basic sense, heart muscle recovery allows a patient to leave the hospital with their own heart. Some causes of heart attacks include clots in the heart from plaque, adverse events from stents or viruses that attack the muscle.
The community recognizes this problem- but does not directly treat it. Today, the cardiologists focus on opening up the blockage with PCI—or angioplasty and stents. However, this only addresses the plumbing for the heart and not the pumping Remember, the heart only has one function—and that is to pump blood. The dilemma for the last 40 years has been – How do you support or pump blood with the heart muscle quickly, percutaneously and safely–without causing more harm to the critical patient? THIS is where IMPELLA makes the difference.
New England Journal of Medicine: 2003; 348:

10. Intra-Aortic Balloon Pump
Introduced in 1968 (Kantrowitz)
First “true percutaneous” support device
Cheapest, commonest (20% of all cardiogenic shock cases), CO 0.5L/min
Stabilize pt, but not full support
No outcome benefit
Hemodynamic Effects:
Diastolic pressure 
CO/cardiac workload 
MAP
LV Wall Tension 
PCWP
Oxygen Demand 
LV Volume
Coronary Blood Flow 

11. Onset systole Adjust timing deflate
In early inflation or late deflation- increased afterload and increased myocardial O2 consumption
In late inflation or early deflation- Decreased physiologic benefit
Onset systole
deflate
Adjust timing

12. Nair et al Journal of Invasive Cardiology 2011

13. Nair et al Journal of Invasive Cardiology 2011

14. Early Trials and Registry Data for IABP

15. IABP in Cardiogenic Shock Primary PCI
Retrospective analysis of 23,180 patients from NRMI database
7268 treated by IABP (trend towards improved mortality)

17. Time After Randomization (Days)
IABP-Shock II Trial: Results Primary Study Endpoint:
30-day Mortality
(IABP in Cardiogenic Shock and Primary PCI)
Mortality (%)
P=0.92 by log-rank test
Relative risk 0.96; 95% CI ; P=0.69 by Chi2-Test
The use of intraaortic balloon counterpulsation did not significantly reduce 30-day mortality in patients with cardiogenic shock complicating acute myocardial infarction for whom an early revascularization strategy was planned.
METHODS
In this randomized, prospective, open-label, multicenter trial, we randomly assigned 600 patients with cardiogenic shock complicating acute myocardial infarction to intraaortic balloon counterpulsation (IABP group, 301 patients) or no intraaortic balloon counterpulsation (control group, 299 patients). All patients were expected to undergo early revascularization (by means of percutaneous coronary intervention or bypass surgery) and to receive the best available medical therapy. The primary efficacy end point was 30-day all-cause mortality. Safety assessments included major bleeding, peripheral ischemic complications, sepsis, and stroke.
Thiele H et al. NEJM 2012;367:1287.
Time After Randomization (Days)

18. Indications for IABP High Risk PCI Cardiogenic Shock
Refractory Ischemia
Left Main
3 Vessel CAD
VT/VFib
MR or VSD after MI
Severe CHF--? Bridge to Transplant
Pre-operative stablization
Weaning therapy after CABG

19. Contraindication to IABP
Severe Peripheral vascular disease
Aortic regurgitation
Aortic Dissection
PDA
HOCM
Heparin intolerance
Bleeding Diathesis
Sepsis

20. Complications of IABP Vascular Access bleeding/complications
Limb Ischemia
Infection
Thrombocytopenia
Migration and aortic arch trauma
Other non-vascular (CVA, embolization of cholesterol, balloon rupture)
Air embolism risk (reduced by using helium gas)

22. Impella Continuous axial flow pump Simple insertion
Increases cardiac output & unloads LV
LP 2.5 – CO 2.5 L/min
CP 4.0 L/min
14 F percutaneous approach
LP 5.0
21 F surgical cutdown; Maximum 5L flow

23. Impella insertion
The Impella CP is built on the same foundation as the Impella 2.5, but provides more than a 50% increase in pumped blood volume (approx. 4L/min)

24. Principles of Impella Design
Mimic Heart’s Natural Function
Inflow
(ventricle)
Outflow
(aortic root)
aortic
valve
EDV, EDP
AOP
Flow
O2 Demand
O2 Supply
Cardiac Power Output
Myocardial Protection
Systemic Hemodynamic Support
Naidu S S Circulation 2011;123: 24

25. Systemic Hemodynamic Support
CO Increase … Valgimigli et al.,Cath Cardiov Interv (2005)
7.4 L/min
Impella 2.5
High risk PCI patient
Demonstrated net CO increase with simultaneous ventricular unloading
CO Increase
6.0 L/min
Impella
(2.4)
LV unloading
Native CO
5.0 25

26. 26 patients with CS secondary to MI randomized to IABP vs Impella 2. 5
26 patients with CS secondary to MI randomized to IABP vs Impella 2.5. The assigned device was implanted following revascularization and measurement of
baseline hemodynamic parameters.

31. Significant rise in serum free hemoglobin due to hemolysis which improved with weaning of the device.

35. Tandem Heart Left atrial-to-femoral arterial LVAD
21F venous transseptal cannula
17F arterial cannula
Maximum flow 4-5L/min
Hemodynamic Effects
Percutaneously inserted circulatory assist device that pumps blood from the left atrium through a extracorporeally through a centrifugal pump to the femoral arterial system via a transseptally placed left atrial cannula, thereby bypassing the LV. CO 
MAP 
PCWP  35

36. Transseptal puncture
21 F cannula in LA
21-Fr transseptal cannula

37. Tandem Heart and cannulae
15-19 Fr femoral arterial cannula
Venous cannula arterial return cannula

38. Days after Randomization
TandemHeart Shock study: Randomized Comparison of IABP with PTVA (VAD) Device in Patients with Cardiogenic Shock
Kaplan–Meier Survival Estimates for 30 Day Survival
100 90 80 70 60 50 40 30 20 10
PTVA-VAD:
Cardiac Power Index (CO x MBP)
Hemodynamic parameters
Metabolic parameters
Vascular complications
PTVA-VAD
57% %
IABP
55%
P = 0.86
Thiele et al, Eur Heart J 2005;26:1276
Days after Randomization

40. 57 yo F w/ PMH of dilated cardiomyopathy diagnosed 4 years ago, DMII, HTN presenting in cardiogenic shock from ECRMC. At this time she had acute kidney injury requiring CRRT, acute liver injury, on Bipap, high dose milrinone.
CXR from morning at 9:55

41. CXR from afternoon at 19:14

42. CXR from just over a week later.

43. Compared with the MI-alone group, the percent of total LV myocardium infarcted was reduced by 42% in the MI+unload group (49±14% of all myocardium versus 28±7% of all myocardium, MI versus MI+unload; P=0.03)
To account for regional perfusion of the LAD, no differences in LAD length (80±3 versus 78±3 mm, MI versus MI+unload; P=0.4) or LV mass (32±6
versus 31±6 g, MI versus MI+unload; P=0.72) distal to the stent were observed between the MI and MI+unload groups.
Circulation. 2013;128:

44. In both the MI and MI+unload groups, LAD occlusion led to a similar increase in both creatine kinase-MB (4+2% versus 4+1%, MI versus MI+unload; P=0.53) and troponin-I ( versus , MI versus MI+unload; P=0.6) values after 120 minutes of ischemia.
In contrast, after 120 minutes of reperfusion, creatine kinase-MB (8.7±1% versus 5.1±0.5%, MI versus MI+unload; P=0.03) and troponin-I (9.7±2 versus
4.5±1.4, MI versus MI+unload; P=0.001) values were significantly lower in the mechanically supported group
Mechanically unloading the LV despite delaying coronary reperfusion reduces LV wall stress and may promote myocardial salvage, leading to significantly reduced myocardial injury.
This leads into the upcoming TRIS (TandemHeart to Reduce Infarct Size) Trial which will be similar to CRISP AMI. THis will be a prospective, randomized, controlled trial designed to evaluate the use of TandemHeart prior to revascularization as compared to PCI alone in acute STEMI patients. Cardiac MRI will be used to determine MI size and 1 year mortality will be looked at as a secondary endpoint.

45. Approach to cardiogenic shock
Systolic BP > mm Hg and good mentation: consider IABP to help prevent shock.
Consider IABP in:
Bridge to surgery
Severe HF
Cardiogenic shock (mild to moderate)
BP < 70, or on inotropes and vasopressors: consider Impella (2.5, CP, 5L) or TandemHeart (4-5L)
Biventricular Cardiogenic Shock: Extracorporeal membrane oxygenation

46. Optimal Support Device
Optimal Timing (early, late, futility)
Optimal Support Device
Optimal
Therapy
Optimal management of device (avoiding complications)
Euro Heart J(2015) 36, 1223–1230

47. Questions What are the complications of IABP? vascular complications
CVA
embolization of cholesterol
balloon rupture
All of the above

48. Questions An IABP achieve its action through a counter pulsation
A. Deflates during systole
B. Inflates during diastole
What is used to inflate and deflate the balloon?
helium used (reduced chance of air embolism if the balloon were to rupture)