counterpulsation therapy, should we continue to use it ... · anterior stemi complicated by...

IICE 2015, Thessaloniki Sep 10th

Counterpulsation therapy, should we

continue to use it? Other circulatory

support devices for high- risk PCI.

Ioannis Iakovou, MD, PhD

Onassis Cardiac Surgery Center

Athens, Greece


Cardiogenic shock

• 5-10% of pts after a heart attack

• 60000-70000 pts in Europe/year

• In the last years the mortality rate was reduced mainly by earlyreopening of the infarct-related artery

• Still extremely high, approx. 50% @ 30 days


PREDICTION OF CARDIOGENIC SHOCK IN THECARDIAC CATHETERISATION LABORATORY

Poor coronary reperfusion (TIMI Grade <3)

Left main coronary occlusion

Left ventricular ejection fraction <25%

Age >75 years

All with 2 of the 4 risk factors died.

Garcia-Alverez A et al. Am j Cardiol 2009; 103:1073-77


OUTLOOK FOR SURVIVORS OF CARDIOGENICSHOCK

• GUSTO: 88% of those discharged from hospital are alive at oneyear

• SHOCK: 3 and 6 year survival 79% and 62%

• Around 50% of patients remain free from heart failure symptoms.


The Damaging Effects of High Dose Inotropes

Elevated stroke work and wall tension.

Increased myocardial oxygen consumption.

Depletion of energy reserves.

Endocardial necrosis & impaired diastolic function.

Overall negative effect on myocardial recovery.


CPS/ECMO

• Percutaneous heart lung-machine

• Centrifugal pump

• Hemodynamic support>4.5l/min

• Can increase preload and afterload

• No randomized control trials or

large cohorts.


ECMO circuits

For VA/ECMO, due to arterial cannula size (in iliacs), may need toinclude distal perfusion cannula based upon limb exam, andtypically needs surgical explant


Routine vs prophylactic use of CPSfor high-risk PCI

Teirstein et al JACC 1993


IABP history

History:

• 1962 Animal studies

Moulopoulos et al, Am Heart J 1962;63:669-675

• 1968 clinical description in shock

Kantrowitz et al, JAMA 1968;203:135-140

• 1973 Hemodynamic effects in shock, Mortality unchanged

Scheidt et al, NEJM 1973;288:979-984

• > 40 years > 1 Million patients treated, low complication rate,

Benchmark registry

Ferguson et al, JACC 2001;38:1456-1462


IABP - why use it?

Increase coronary perfusion pressure

Increase myocardial oxygen supply without increasing demand

Decrease afterload

But increase in cardiac output is only 0.5-0.8 L/min


IABP in Myocardial Infarction andCardiogenic Shock

• Improves diastolic flow velocities after angioplasty

• Allows for additional intervention to be done more safely


• Cardiogenic shock

• Refractory angina despite maximal medical management

• Cardiac failure after a cardiac surgical procedure

• Perioperative treatment of complications due to myocardial

infarction

• Failed PCI

• Mitral regurgitation

• As a bridge to cardiac transplantation

Indications for IABP


• Severe aortic insufficiency

• Aortic aneurysm

• Aortic dissection

• Limb ischemia

• Thromboembolism

Contraindications to IABP


• Limb ischemia

• Thrombosis

• Emboli

• Bleeding and insertion site

• Groin hematomas

• Aortic perforation and/or dissection

• Renal failure and bowel ischemia

• Neurologic complications including paraplegia

• Heparin induced thrombocytopenia

• Infection

Complications


Hemodynamics before, during and afterIACP

Mueller H et al J Clin Invest 1971

The effect of IACP (22-94 hr) on hemodynamics and cardiac energeticswas evaluated in 10 patients in shock after acute MI decrease in afterload/preload, PCWP, SVR modest increase in CO, slight increase in coronary flow


PAMI-II trial

Stone et al JACC 1997

a prophylactic IABP strategy after primary PTCA in hemodynamically stable high risk patientswith AMI does not decrease the rates of infarct-related artery reocclusion or reinfarction (p=NS for

both), promote myocardial recovery or improve overall clinical outcome

High risk patients were randomized to 36 to 48 h of IABP (n = 211) or traditional care (n = 226)


Balloon Pump-Assisted Coronary Intervention Study (BCIS-1)



Perera D, et al. AHJ 2009



Main trial found no differencein primary endpoint of MACCEat hospital discharge ormortality at 6 months

Perera D, et al. JAMA 2010



301 high-risk PCI patients randomized to receive elective IABP support

(n = 151) or no planned IABP (n = 150). Mortality data derived from

nationwide databases up to median of 51 months.

Long-term all-cause mortality rate was 33%, amounting to 28% for

elective IABP vs. 39% for no IABP

At 5 years, Kaplan-Meier curves show that IABP use reduced the risk

of mortality (HR 0.64; 95% CI 0.42-0.96)

Implications: Contrary to lackluster short-term results, elective IABP

use during high-risk PCI reduces all-cause mortality at 5 years.

Perera D, et al. Circulation. 2012


CRISP-AMI340 pts with ST elevation MI within 6 hours of the onset of pain

Patel et al JAMA 2011

Among patients with acute anterior STEMI without shock, IABC plus primary PCIcompared with PCI alone did not result in reduced infarct size.


Intraaortic Balloon Counterpulsation Reduces Mortality in LargeAnterior MI Complicated by Persistent Ischemia

CRISP-AMI substudy: 36 patients with large STEMI and poor ST-segment

resolution (n = 15 IABP and 21 control), representing 11% of overall trial.

At 6 months, none of the patients in the IABP group had died, compared

with 5 in the control group (0 vs 24%; P = .046)

Trend favoring IABP therapy also seen for the composite endpoint of death,

cardiogenic shock, or new/worsening heart failure (7% vs 33%; log-rank P =

.06).

Implications: IABP therapy seems most beneficial in patients with large

anterior STEMI complicated by persistent ischemia.

van Nunen LX, et al. EuroIntervention. 2014


IABP prior to PCI vs. IABP after PCI


Rapid Reperfusion. Would you go thesame speed on these two Cases?


7 RCT, 1000 patients No difference in Death, LVEF


25 25 3139

51

86

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ALKK

GUSTO I

GUSTO II

I

Euro H

eart

Survey

Wor

cester

-Reg

istry

NRMI-2

NRMI 2

-4

SHOCK-Reg

istry

SHOCK-Tria

l

Anderson et al. JACC 1997;30:708-715Hasdai et al. Eur Heart J 1999;20:128-135Goldberg et al. NEJM 1999;340:1162-1168Zeymer et al. ESC 2009, Abstract

Barron et al. Am Heart J 2001;141:933-939Sanborn et al. JACC 2000; 36:1123-1129Hochman et al. NEJM 1999;341:625-634Zeymer et al. Eur Heart J 2004;25:322-328

IABP

Use

(%)

IABP-Use in Cardiogenic Shock


80 57 45

600

55

302398

0

100

200

300

400

500

600

700

SHOCK TRIUMPH SMASH PRAGUE -7

TACTICS IABP-SHOCK I

IABP-SHOCK II

N P

atie

nts

Patient Inclusion in Cardiogenic Shock-Studies

Stop

ped

due

tom

issi

ng e

ffect

Stop

ped

slow

recr

uitm

ent

Stop

ped

Slow

recr

uitm

ent

Und

erpo

wer

ed

Surro

gate

end

poin

t


IABP-shock II study600 pts randomized to conventional optimal Rx vs. IABP

Theile et al ESC 2012


30 Day Mortality: Good to be YOUNG


12 mo data…good if <50 yo!


Antman et al. Circulation. 2004;110:82-292O’Gara et al. Circulation. 2013;127:e362-e425Van de Werf et al. Eur Heart J. 2008;29:2909-2945Steg et al. Eur Heart J. 2012;33:2569-2619

GuidelinesIABP in STEMI complicated by cardiogenic shock


What do we think we know?

•IABP in pts with anterior MI but no shock did not reduce infarct size

(CRISP-AMI)

•Guidelines in both US and Europe: recently Class I to Class IIA and IIB

•Some: “IABP in shock patients may help doctors more than patients”

•After looking at data….”should anyone get an IABP?”


Percutaneous left ventricular assist devicesrational for usage

Even with revascularisation and IABP support mortality fromcardiogenic shock post STEMI remains ≥50%

Recovery of myocardial performance following successfulrevascularisation may take several days. During this timemany patients succumb to low cardiac output

If effective, active cardiac support could be provided whileawaiting the beneficial effects of revascularisation, survivalrates may be enhanced


LVAD THEORETICAL ADVANTAGES

Superior LV pressure and volume unloading with enhancedremodeling capability

Decreased wall tension with improved endocardial bloodflow

Beating, non-working heart has low metabolic requirement

Presumed enhanced ability for cellular repair and survival

New Devices and Strategies toManage CGS



LVAD THEORETICAL ADVANTAGES

Prevention of lethal reperfusion injury in animals

Release of cytokines by the heart have been documentedin patients post PCI in AMI and implicated in thepathophysiology of CGS

LVAD support may allow for resolution of theseinflammatory and neurohormonal abnormalities withrecovery of LV function and hemodynamics – patients whorecover are frequently NYHA Class I




Percutaneous Assist Devices -Overview

Thiele et al, Eur Heart J 2007; 28:2057-2063

Tandem Heart™ Impella Recover®LP 5.0

Impella Recover®LP 2.5

Catheter size (French) - 9 9

Cannula size (French) 21 venous12-19 arterial

21 12

Flow (l/min) Max. 4.0 Max. 5.0 Max. 2.5

Pump speed (rpm) Max. 7,500 Max. 33,000 Max. 33,000

Insertion/Placement

Peripheral(Femoral artery + LA)

Peripheral surgical(Femoral artery)

Percutaneous(Femoral artery)

Anticoagulation + + +

Recommended duration ofuse

- 14 days 7 days 5 days

CE-Certification + + +

FDA PMN IDE Trial IDE Trial

Relative costs incomparison to IABP

+++++ +++ +++


Tandem Heart pLVAD

Left atrial-to-femoral arterial LVAD Low speed centrifugal continuous

flow pump 21F venous transseptal cannula 17F arterial cannula Maximum flow 4L/minute


Tandem Heart Outcome Data

42%

47%45%

36%

0%

5%

10%

15%

20%

25%

30%

35%

40%

45%

50%

Thiele (n=41) Burkhoff (n=33)

30 d

ay m

orta

lity

(%)

Tandem HeartIABP

Improved haemodynamic parameters

Increase in bleeding, limb ischaemia, and sepsisThiele EHJ 2005;26:1276. Burkhoff AHJ 2006;152:e1

p=NS


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

Pressure Lumen

Motor

Blood outlet

Blood Inlet


ISAR-SHOCK trial

JACC 2008;52:1584-8


Impella outcome data

1 RCT of Impella 2.5 in AMI Cardiogenic Shock

ISAR-SHOCK

26 patient RCT Impella vs IABP Cardiac Index, MAP (by 10mmHg) vs IABP Complications ≤ IABP Overall 30-day mortality was 46% in both groups

JACC 2008;52:1584-8


Thiele et al. Burkhoff et al. Seyfarth et al.

LVAD TandemHeart TandemHeart Impella LP2.5Control IABP IABP IABP

N of patients 41 33 26Setting Single-center Multi-center Two-centerInclusion period 2000-2003 2002-2004 2004-2007

Randomization Yes Yes Yes

PLVAD vs. IABP for treatment of cardiogenicshock: a meta-analysis of controlled trials

Cheng et al. Eur Heart J 2009;30:2102-2108


-2 -1 1 20

0.55 (0.23 ; 0.87)

0.16 (-0.14 ; 0.46)

0.36 (-0.16 ; 0.88)

0.35 (0.09 ; 0.61)Pooled

2.30.6 1.80.4

LVADmeansd

IABPmeansd

2.20.6 2.10.2

2.20.6 1.80.7

Favors IABP Favors LVAD

P(heterogeneity) = 0.22I2 = 34.0%

Cardiac IndexMean Difference

Burkhoff et al.

Seyfarth et al.

Thiele et al.

Cardiac index

Percutaneous LVAD patients had higher CI


Mean Arterial Pressure

Percutaneous LVAD patients had higher MAP

-50 -25 0 25 50

5.5 (-2.9 ; 13.9)

18.6 (9.4 ; 27.9)

16.0 (0.5 ; 31.5)

12.8 (3.6 ; 22.0)Pooled

7610 7016

LVADmeansd

IABPmeansd

9116 7212

8718 7122

Favors IABP Favors LVAD


Mean Arterial PressureMean Difference

Burkhoff et al.

Seyfarth et al.

Thiele et al.


-20 -10 0 10 20

-5.6 (-9.2 ; -2.1)

-8.4 (-11.0 ; -5.8)

-1.0 (-5.2 ; 3.2)

-5.3 (-9.4 ; -1.2)

Burkhoff et al.

Seyfarth et al.

Pooled

Thiele et al. 165 227

LVADmeansd

IABPmeansd

164 253

195 206

Favors LVAD Favors IABP


Pulmonary Wedge PressureMean Difference

Pulmonary Capillary Wedge Pressure

Percutaneous LVAD patients had lower PCWP


30-day mortality

Percutaneous LVAD patients had similar mortality

0.1 1 10

0.95 (0.48 ; 1.90)

1.33 (0.57 ; 3.10)

1.00 (0.44 ; 2.29)

1.06 (0.68 ; 1.66)Pooled

Favors LVAD Favors IABP

30-day mortalityRelative Risk

9/21 9/20

LVADn/N

IABPn/N

9/19 5/14

6/13 6/13

24/53 20/47

P(heterogeneity) = 0.83I2 = 0%

Burkhoff et al.

Seyfarth et al.

Thiele et al.


LVAD or IABP?Complications

Cheng et al. Eur Heart J 2009;30:2102-2108

LVADn/N

IABPn/N

Limb ischemiaRelative Risk

P (heterogeneity)=0.38R2=0%

Thiele et al

Burkhoff et al

Seyfarth et al

Pooled

0.0001 0.01 1 100 10000IABP betterLVAD better

14.32 (0.87 – 235.4)

1.47 (0.31 – 6.95)

3.00 (0.13 – 67.51)

2.59 (0.75 – 8.97)

7/21 0/20

4/19 2/14

1/13 0/13

12/53 2/47

LVADn/N

IABPn/N

BleedingRelative Risk

P (heterogeneity)=0.73R2=0%

Thiele et al

Burkhoff et al

Pooled

0.01 0.1 1 10 100IABP bstterLVAD better

2.26 (1.30 – 3.94)

2.95 (0.74 – 11.80)

2.35 (1.40 – 3.93)

19/21 8/20

8/19 2/14

27/40 10/34

LVADn/N

IABPn/N

Fever or sepsisRelative Risk

P (heterogeneity)=0.10R2=62.1%

Thiele et al

Burkhoff et al

Pooled

0.01 0.1 1 10 100IABP betterLVAD better

1.62 (1.00 – 2.63)

0.59 (0.19 – 1.80)

1.11 (0.43 – 2.90)

17/21 10/20

4/19 5/14

21/40 15/34


LVAD or IABP?

Bleeding

Invasiveness

+ -

Implantation procedure

LVAD

Hemodynamic support Better LV-unloading

Costs


Potential treatment algorithm for patients with CS complicatingAMI (asterisks denote supported by randomized controlled

trials).

Thiele H et al. Eur Heart J 2010;31:1828-1835


Recommendations on how toapproach shock

• If a pt has a SBP of 75-80 mm Hg the aim is to increase BP over the

next couple of days while keeping them out of shock; use IABP

• Do not use IABP in all high risk pts; but consider in the following

situations:

• Severe HF

• Bridge to surgery

• Impeding CS

• Mild CS


Conclusions

• For more severe cases of CS (SBP approx 40,50,60, 70 mmHg) or ptsrequiring high doses of inotropes or vasopressors we (may) have theoption of percutaneous LVAD (Tandemheart or Impella) which providesuperior hemodynamic support compared to IABP

• Until now, we cannot recommend to replace IABP by percutaneousLVAD as first-choice approach in the mechanical management ofcardiogenic shock

• Routine use of IABP in AMI is not evidence based

• Studies with pre-PCI deployment of IABP are needed


Thank You!

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