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MCC 260405

REVIEW

CURRENT
OPINION The place of extracorporeal life support in
cardiogenic shock
Marc Pineton de Chambrun a,b, Nicolas Bréchot a,b, and Alain Combes a,b

Purpose of review
Temporary circulatory support (TCS) devices are increasingly used as a salvage therapy for patients with
refractory cardiogenic shock. The exact place of the different TCS devices in the management of
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cardiogenic shock patients remains unclear and intensely debated. This article provides an overview on
new cardiogenic shock classification, currently available devices, place of TCS in the management of
cardiogenic shock patients, and discusses the results of recent case series and trials in this setting.
Recent finding
A new classification system for cardiogenic shock has recently been proposed to homogenize definitions of
cardiogenic shock and appropriately differentiate patient subsets in clinical trials and registries. Although
the routine use of intraaortic balloon pump is no more recommended a other TCS are increasingly used
and investigated but many advantages favor the use of venoarterial extracorporeal membrane oxygenation
(VA-ECMO) as the first-line TCS.
Summary
TCS devices have become the cornerstone of the management of patients with refractory cardiogenic
shock. VA-ECMO has emerged as the first-line support system in this setting, with a growing number of
accepted indications. Large adequately powered randomized controlled trials are now underway and
should help to determine the respective place of different TCS devices in strategies to treat cardiogenic
shock patients.
Keywords
cardiogenic shock, intraaortic balloon pump, temporary circulatory support, venoarterial extracorporeal
membrane oxygenation

INTRODUCTION
Temporary circulatory support (TCS) devices
have become the cornerstone of the management
of patients with refractory cardiogenic shock,
although their use only received a Class IIb rec-
ommendation from the European Society of Car-
diology (ESC) [1,2]. The intraaortic balloon pump
(IABP) is now not recommended for routine use in
acute myocardial infarction (AMI) cardiogenic
shock by ESC guidelines, since the large IABP-
SHOCK II trial, which randomized 600 patients
with cardiogenic shock complicating AMI, found
no difference in mortality and any of the second-
ary study endpoints between IABP or conventional
treatment [3–6]. More recently, two large propen-
sity-matched case-controlled series showed that
routine treatment with an intravascular micro
axial left ventricle assisting device (LVAD) was also
not associated with lower 30-day all-cause mortal-
ity compared with matched patients with IABP
&
[7,8 ]. Four adequately powered randomized con-
trolled trials are now underway to evaluate Impella
device (NCT01633502) and venoarterial extracor-
poreal membrane oxygenation (VA-ECMO,
NCT03813134, NCT03637205, NCT04184635) in
cardiogenic shock complicating AMI.
a
Service de Médecine Intensive-Réanimation, Institut de Cardiologie,
APHP Hôpital Pitié-Salpêtrière and bSorbonne Université, INSERM,
UMRS_1166-ICAN, Institute of Cardiometabolism and Nutrition, Paris,
France
Correspondence to Alain Combes, Service de Médecine Intensive-
Réanimation, Institut de Cardiologie, APHP Hôpital Pitié-Salpêtrière,
F-75013 Paris, France. Tel: +33 1 42 16 38 16;
fax: +33 1 42 16 38 17; e-mail: alain.combes@aphp.fr
Curr Opin Crit Care 2020, 26:000–000
DOI:10.1097/MCC.0000000000000747

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Cardiogenic shock
KEY POINTS
 A new classification system for cardiogenic shock has
been recently proposed by the Society for
Cardiovascular Angiography and Intervention.
 VA-ECMO is the first-line temporary circulatory support
in patients with refractory cardiogenic shock, with a
growing number of accepted indications.
 Impella and intraaortic balloon pump may be
associated with VA-ECMO to decrease left ventricle
pressures and improve outcomes.
 Sepsis-associated cardiomyopathy, massive pulmonary
embolism, and refractory cardiac arrest are among
emerging indications for VA-ECMO.
 Large, adequately powered, randomized clinical trials
are now underway to determine the respective place of
different temporary circulatory support devices in
strategies to treat cardiogenic shock patients.
CARDIOGENIC SHOCK: DEFINITION AND
CLASSIFICATION
Definition
Cardiogenic shock is defined as a state of critical
end-organ hypoperfusion and hypoxia because of
primary cardiac dysfunction [9]. The diagnosis
of cardiogenic shock can be made on the basis of
clinical criteria (hypotension, pulmonary conges-
tion, cold extremities, oliguria, altered mental
status, etc.), biochemical findings of inadequate
tissue perfusion (acute kidney insufficiency,
hypoxic hepatitis, elevated arterial lactate, etc.)
and hemodynamic parameters (reduced cardiac
index and elevated pulmonary capillary wedge pres-
sure). However, the ESC guidelines definition of
cardiogenic shock [1] and these applied in the major
randomized trials [3,10–12] focusing on cardiogenic
shock are heterogenous (Table 1).
New Society for Cardiovascular Angiography
and Intervention classification
Patients with cardiogenic shock represent a hetero-
geneous population with varying prognosis based
on severity of illness, cause, and comorbidities. The
Society for Cardiovascular Angiography and Inter-
vention (SCAI) recently proposed a new cardiogenic
shock classification featuring five stages (A–E) of
increasing severity based on clinical, biological,
and hemodynamic signs of cardiogenic shock
&&
(Table 2) [13 ]. The purpose of this initiative was
to provide a simple tool for bedside evaluation,
prognostication, and treatment optimization of
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patients with cardiogenic shock. It also intended
to homogenize definitions of cardiogenic shock to
appropriately differentiate patient subsets in clinical
trials and registries. In a cohort of 10 000 patients
admitted to a cardiac intensive care unit, the SCAI
cardiogenic shock scores stages A–E frequencies at
admission were 46.0, 30.0, 15.7, 7.3, and 1.0% with
an associated hospital mortality of 3.0, 7.1, 12.4,
&&
40.4, and 67% (P < 0.001), respectively [14 ]. Thus,
SCAI classification provides a robust risk prognosis
stratification in cardiogenic shock patients.
THE PLACE OF TEMPORARY
CIRCULATORY SUPPORT IN
CARDIOGENIC SHOCK
Intraaortic balloon pump
The IABP-SHOCK II trial, which randomized 600
patients with cardiogenic shock complicating
AMI, found no difference in mortality and any of
the secondary study endpoints between IABP or
conventional treatment [3,5,6]. These results led
to a downgrading of the IABP in the ESC guidelines
with a current class IIIB recommendation against
the routine use of the IABP in cardiogenic shock,
although the IABP may still be considered in
patients with AMI mechanical complications (class
IIa, level C) [1].
Percutaneous active temporary circulatory
support devices
Since the publication of the negative results of the
IABP-Shock II trial, percutaneous active TCS are
increasingly used [15]. Current devices include the
TandemHeart (TandemLife, Pittsburgh, PA, USA)
which is a percutaneous LVAD consisting of an
extracorporeal centrifugal continuous flow pump
that drains blood from the left atrium via a cannula
introduced transseptally through the femoral vein.
Blood is then pumped back to the femoral artery at a
&
flow rate of up to 3.5 l/min [8 ,23]. The Impella 2.5,
CP, or 5.0 (ABIOMED Inc., Danvers, MA, USA) are
catheter-based axial flow pumps with a propeller at
the tip of the catheter which is positioned retro-
gradely across the aortic valve into the left ventricle.
Impella devices directly vent the left ventricle and
provide more physiologic support than VA-ECMO,
which increases left ventricle afterload [16–20].
However, the evidence supporting the use of these
devices in cardiogenic shock is limited. Indeed, a
meta-analysis including four trials randomizing 148
patients to either TandemHeartTM or Impella
(n ¼ 77) versus IABP (n ¼ 71) showed no difference
in 30-day mortality [15]. More recently, a study of
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The place of extracorporeal life support in cardiogenic shock Pineton de Chambrun et al.

Table 1. Definition of cardiogenic shock in ESC guidelines and major randomized clinical trialsa
Title Diagnosis/inclusion criteria Ref

ESC guidelines SBP < 90 mmHg with adequate volume and II or III [1]
Clinical hypoperfusion: Cold extremities, oliguria, mental confusion, dizziness, and narrow pulse pressure
Laboratory hypoperfusion: metabolic acidosis, elevated lactate, elevated creatinine
SHOCK trial SBP < 90 mmHg for 30 min or support to maintain SBP  90 mmHg [11]
Endorgan hypoperfusion (urine output < 30 ml/h or cool extremities and heart rate >60 bpm)
Hemodynamic criteria: cardiac index of 2.2 l/min/m2 and PCWP  15 mmHg
TRIUMPH trial Patency of IRA spontaneously or after PCI [10]
Refractory cardiogenic shock > 1 h after PCI with SBP < 100 mmHg despite vasopressors
(dopamine  7 mg/kg/min or norepinephrine or epinephrine  0.15 mg/kg/min)
Endorgan hypoperfusion
Clinical or hemodynamic criteria for elevated left ventricle filling pressure
LVEF < 40%
IABP-Shock II trial SBP < 90 mmHg for 30 min or catecholamines to maintain SBP > 90 mmHg [3]
Clinical pulmonary congestion
Impaired organ perfusion with at least one of the following:
Altered mental status
Cold/clammy skin and extremities
Urine output < 30 ml/h
Lactate >2.0 mmol/l
CULPRIT-Shock trial Planned early revascularization by PCI [12]
Multivessel CAD defined as >70% stenosis in at least two major vessels (2 mm diameter) with
identifiable culprit lesion
SBP < 90 mmHg for >30 min or catecholamines required to maintain SBP > 90 mmHg
Pulmonary congestion
Impaired organ perfusion with at least one of the following:
Altered mental status
Cold/clammy skin and extremities
Urine output <30 ml/h
Lactate > 2.0 mmol/l
DAN-Shock trial STEMI of less than 36 h duration NCT01633502
Cardiogenic shock of less than 24 h duration
SBP < 100 mmHg and/or need for vasopressor therapy
Peripheral signs of tissue hypoperfusion:
Lactate  2.5 mmol/l
SvO2 < 55% with a normal PaO2
LVEF<45% visually estimated or by wall motion score index > 1.6
ECLS-Shock trial Cardiogenic shock complicating STEMI or NSTEMI NCT03637205
Planned revascularization (PCI or alternatively CABG)
SBP <90 mmHg for >30 min or catecholamines required to maintain pressure SBP > 90 mmHg
Signs of impaired organ perfusion with at least one of the following:
Altered mental status
Cold/clammy skin and extremities
Urine output < 30 ml/h
Arterial lactate >3 mmol/l
EURO-Shock trial Cardiogenic shock within 24 h of onset of ACS symptoms NCT03813134
CGS can only be secondary to ACS (Type 1 MI STEMI or N-STEMI) or secondary to ACS following
previous recent PCI
PCI has been attempted
Persistence of cardiogenic shock >30 min after successful or unsuccessful revascularization of culprit
coronary artery
SBP < 90 mmHg for >30 min, or vasopressor/inotropic therapy to maintain SBP > 90 mmHg
Clinical signs of pulmonary congestion
Signs of impaired organ perfusion with at least one of the following:
Altered mental status
Cold/clammy skin and extremities
Urine output < 30 ml/h
Serum lactate > 2.0 mmol/l
ANCHOR trial Cardiogenic shock complicating acute myocardial infarction NCT04184635
Revascularization by PCI for acute myocardial infarction has been performed or is planned in the following
60 min
SBP < 90 mmHg for >30 min or catecholamine support required to maintain SBP > 90 mmHg
Signs of pulmonary congestion
Signs of impaired organ perfusion with at least one of the following:
Altered mental status
Cold/clammy skin and extremities
Urine output < 30 ml/h
Serum lactate > 2.0 mmol/l

ACS, acute coronary syndrome; CABG, coronary artery bypass graft; CAD, coronary artery disease; ESC, European Society of Cardiology; IABP, intraaortic
balloon conterpulsation; IRA, infarction related artery; LVEF, left ventricle ejection fraction; NSTEMI, non-ST-elevation myocardial infarction; PCI, percutaneous
coronary intervention; PCWP, pulmonary capillary wedge pressure; SBP, systolic blood pressure; STEMI, ST-elevation myocardial infarction.
a &&
Adapted from [33 ].

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Cardiogenic shock

Table 2. The Society for Cardiovascular Angiography and Intervention (SCAI) cardiogenic shock classificationa

Stage Description Physical exam Biochemical markers Hemodynamics

A Patients at risk for Normal JVP Normal lactic acid Normal blood pressure
At risk cardiogenic shock Normal physical exam Normal renal function If hemodynamics done:
(i.e., large Cardiac index  2.5
myocardial CVP < 10
infarction, etc.) Pulmonary artery
saturation  65%
B Relative hypotension or Elevated JVP Normal lactic acid SBP < 90 OR MAP < 60
Beginning tachycardia without Rales in lung fields Minimal renal OR drop > 30 mmHg
hypoperfusion No sign of peripheral function impairment from baseline
hypoperfusion Elevated BNP Pulse > 100 bpm
If hemodynamics done:
Cardiac index  2.2
Pulmonary artery
saturation  65%
C Hypoperfusion May include any of: May include any of: May include any of:
Classic requirering Look unwell, panicked Lactate  2 SBP < 90 OR MAP < 60
intervention beyond Ashen, mottled, dusky Creatinine doubling OR drop > 30 mmHg
volume resuscitation Cold, clammy >50% drop in GFR from baseline
to restore perfusion Volume overload Elevated LFTs AND
(inotrope, pressors or Extensive rales Elevated BNP Need for drugs/device
TCS) Killip class 3 or 4 used to maintain blood
NIV or mechanical pressure above
ventilation These targets
Altered mental status Hemodynamics:
Urine output < 30 ml/h Cardiac index < 2.2
PCWP > 15
RAP/PCWP  0.8
PAPI < 1.85
Cardiac power
output  0.6
D Deteriorating/ Similar to category C Any of stage C Any of stage C Any of Stage C
Doom but getting worse AND AND
Failure to respond to Deteriorating Need for multiple pressors
initial interventions or TCS devices to
maintain perfusion
E Cardiac arrest with Near pulselessness CPR No SBP without
Extremis ongoing CPR and/or Cardiac collapse pH  7.2 resuscitation
ECMO Mechanical ventilation Lactate  5 PEA or refractory
Multiple ongoing Defibrillator used ventricular tachycardia/
intervention ventricular fibrillation
Hypotension despite
maximal support

BNP, Brain natriuretic peptide; CPR, cardiopulmonary resuscitation; CVP, central venous pressure; ECMO, extracorporeal membrane oxygenation; GFR,
glomerular filtration rate; JVP, jugular venous pressure; LFTs, liver function tests; MAP, mean arterial pressure; NIV, noninvasive ventilation; PAPI, pulmonary artery
pulsatility index; PCWP, pulmonary capillary wedge pressure; PEA, pulseless electric activity; RAP, right arterial pressure; SBP, systolic blood pressure; SCAI,
Society for Cardiovascular Angiography and Intervention; TCS, temporary circulatory support.
a &&
Adapted from [13 ].

237 AMI patients who received the Impella propen-
sity-matched with 237 patients from the IABP-
SHOCK II trial, there was no significant difference
in 30-day all-cause mortality (49 versus 46%,
P ¼ 0.64) [7]. In a large-scale registry study including
48 306 patients of whom 50% had cardiogenic
shock, undergoing percutaneous coronary interven-
tion (PCI) with TCS support at 432 hospitals in the
USA, the use of Impella was even associated with
increased mortality (adjusted OR [95% confidence
interval (CI)] ¼ 1.17 [1.10–1.24], P < 0.001) [21]. The
rates of serious adverse events, including infections,
stroke, and bleeding were more frequent in patients
receiving the Impella [7,21]. Another propensity-
matched registry-based retrospective cohort study
including patients with AMI complicated by cardio-
genic shock undergoing PCI between October 1,
2015 and December 31, 2017 compared intravascu-
lar microaxial LVAD (mostly Impella) to IABP.
Patients were matched on demographics, clinical

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The place of extracorporeal life support in cardiogenic shock Pineton de Chambrun et al.
history, presentation, infarct location, coronary anat-
omy, and clinical laboratory data. Among 1680 pro-
pensity-matched pairs, there was a significantly
higher risk of in-hospital death associated with use
of an intravascular microaxial LVAD compared with
IABP (45.0 versus 34.1%, absolute risk difference,
10.9% [95% CI, 7.6–14.2], P < 0.001, respectively)
and also higher risk of in-hospital major bleeding
(31.3 versus 16.0%, absolute risk difference, 15.4%
&
[95% CI, 12.5–18.2], P < 0.001) [8 ]. A large random-
ized trial comparing the Impella CP against conven-
tional treatment in 360 AMI cardiogenic shock
patients is now ongoing (NCT01633502).
Venoarterial extracorporeal membrane
oxygenation
VA-ECMO has become the first-line therapy in the
setting of cardiogenic shock, as it provides both
respiratory and cardiac support, is easy to insert, even
at the bedside, provides stable flow rates, and is
associated with less organ failure after implantation
compared with large biventricular assist-devices
that require open-heart surgery [22–25]. With the
improvement of biomaterials and technologies, VA-
ECMO can now stay in place several days or even
weeks, as a bridge to ‘decision’ that includes recovery,
transplantation, long-term mechanical circulatory
support or withdrawal in case of futility [15,26].
Compared with percutaneous active TCS devices,
VA-ECMO is less expensive, allows rapid improve-
ment in oxygenation and is the only short-term
device suitable for patients with severe biventricular
failure. However, guidelines from the ESC (Class IIb,
Level of Evidence C) recommended that TCS implan-
tation should only be considered in selected cardio-
genic shock patients [27]. High-grade scientific
evidence supporting the use of VA-ECMO in cardio-
genic shock is urgently awaited [28]. Three large,
adequately powered randomized controlled trials
(NCT03813134, NCT03637205, NCT04184635) cur-
rently underway should clarify the role of VA-ECMO
in AMI patients with cardiogenic shock.
Left ventricle unloading: combining
intraaortic balloon pump or Impella to
venoarterial extracorporeal membrane
oxygenation?
As VA-ECMO provides retrograde blood flow in the
aorta, it increases left ventricle afterload, may decrease
or abolish heart ejection and may induce pulmonary
edema by increasing left ventricle end-diastolic pres-
sure [29,30]. Combining IABP and VA-ECMO support
may decrease left ventricle pressures and the
occurrence of pulmonary edema under VA-ECMO,
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particularly in patients with marked left ventricle
dilation and very low spontaneous residual
ejection under VA-ECMO (aortic velocity–time inte-
gral < 5 cm) [29,30]. In a Meta-analysis including 17
studies and 3997 patients, mortality was lower (54
versus 65%, RR 0.79, 95% CI [0.72–0.87]; P < 0.00001)
in patients with concomitant left ventricle unloading
which most frequently combined VA-ECMO and
&
IABP [31 ]. Another meta-analysis included 62 obser-
vational studies and 7995 patients wherein 3458
received left ventricle venting during VA-ECMO
(mainly IABP and Impella device). Left ventricle vent-
ing significantly improved weaning from VA-ECMO
(68.4 versus 46.7%, OR 0.62 [95% CI, 0.47–0.83];
P ¼ 0.001) and reduced 30-day mortality (50.9 versus
60.2%; RR 0.86 [95% CI, 0.77–0.96]; P ¼ 0.008). Inter-
estingly only early venting was significantly reduced
&&
30-day mortality [32 ]. Future randomized studies
are warranted to determine if these combination
strategies are superior to stand-alone devices.
RECENT EVIDENCE IN SELECTED
INDICATIONS
Acute myocardial infarction
AMI is the most frequent cause of cardiogenic shock,
representing up to 70% of cases and occurring in 5–
10% of patients with AMI. Despite major therapeutic
advances, mortality of cardiogenic shock in the set-
ting of AMI remained unacceptably high (40–50%)
&&
in recent years [33 ]. In a large US national database
spanning from 2000 to 2014, a steady increase was
identified in the utilization of VA-ECMO among
patients with AMI. In approximatively 9 million
AMI admissions, VA-ECMO was used in 2962
(<0.01%) and in 0.5 and 0.3% AMI admissions com-
plicated by cardiogenic shock and cardiac arrest,
respectively. VA-ECMO use was 11 times higher in
2014 as compared with 2000 (odds ratio, 11.37 [95%
CI, 7.20–17.97]) whereas in-hospital mortality with
VA-ECMO was 59.2% overall but decreased from
&
100% (in 2000) to 45.1% (in 2014) [34 ]. A study
comparing patients with refractory cardiogenic shock
complicating ST-segment elevation AMI implanted
with VA-ECMO before (n ¼ 12) or after (n ¼ 34) PCI
reported an improved 6-month survival (58.3% versus
14.7%, P ¼ 0.006) in patients with early VA-ECMO
implantation. However, the proportion of patients
achieving door-to-balloon time <90 min was lower
(9.1 versus 32%) [35]. In 106 consecutive patients
implanted with VA-ECMO around PCI for refractory
cardiogenic shock, the implantation of VA-ECMO
before or during PCI granted the most favorable
30-day survival compared with implantation after
PCI [36].
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Cardiogenic shock
Massive pulmonary embolism
Some patients with massive pulmonary embolism
(MPE) will develop right ventricular failure, hypox-
emia, and severe hemodynamic instability. In this
setting, VA-ECMO might lower their RV overload,
improve hemodynamic status, and restore tissue
oxygenation [37]. However, whether VA-ECMO
should be used as a stand-alone therapy or associated
with surgical or catheter-based embolectomy is still
debated. In a large series of 180 MPE, 52 patients
received VA-ECMO: as a standalone therapy (n ¼ 18),
after failed fibrinolysis (n ¼ 20) or before/after
embolectomy (n ¼ 7/n ¼ 10). Mortality was higher
in patients that required VA-ECMO implantation
(ECMO group: 62% versus no-ECMO group: 43%,
P ¼ 0.008); however, patients in the VA-ECMO and
embolectomy group (30-day mortality 29%) had the
&&
most favorable outcome [38 ]. In a series of 41 con-
secutive patients with MPE managed using a proto-
colized approach in which RV function was evaluated
3–5 days after VA-ECMO support a only patients with
unrecovering RV function underwent surgical embo-
lectomy. Using this approach, 73% responded to
anticoagulation alone and 27% required surgical
embolectomy with an overall 90-day survival of
&&
97 and 100%, respectively [39 ]. Another team estab-
lished an MPE protocol in which VA-ECMO was
favored to thrombolytic therapy in patients
who remained in cardiogenic shock or under cardio-
pulmonary resuscitation (CPR) despite supportive
measures. After VA-ECMO implantation, surgical
embolectomy was the preferred strategy for all
patients. Over 36 consecutive patients, 25% died
under VA-ECMO, 19% could be weaned from VA-
ECMO with a 71.4% survival and 56% underwent
surgical embolectomy with a 94.7% survival [40 ].
&
Future randomized studies are warranted to
determine the best strategy for MPE patients under
VA-ECMO.
Cardiac arrest
VA-ECMO support to restore circulation during car-
diac arrest is known as extracorporeal CPR (E-CPR).
Although there are no randomized controlled trials
reporting the efficacy of E-CPR, its use has been
steadily increasing [41], despite being the subject
of controversies [42]. In a population-based registry,
including 13 191 out-of-hospital cardiac arrest from
Paris region, between May 2011 and January 2018,
4% (n ¼ 525) were treated with E-CPR which was not
associated with increased hospital survival (E-CPR
8%, conventional-CPR 9%, P ¼ 0.91). E-CPR was not
associated with hospital survival after adjusted mul-
tivariate analysis, after conditional logistic regres-
sion with matching on a propensity score. In the E-
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CPR group, factors associated with hospital survival
were initial shockable rhythm (OR, 3.9; 95% CI,
1.5–10.3; P ¼ 0.005), transient return on spontane-
ous circulation before VA-ECMO (OR, 2.3; 95% CI,
1.1–4.7; P ¼ 0.03), and prehospital VA-ECMO
implantation (OR, 2.9; 95% CI, 1.5–5.9; P ¼ 0.002)
&
[43 ]. VA-ECMO might also be initiated in the case
of postcardiac arrest cardiogenic shock. In a series
reporting the outcomes of 94 patients implanted
with VA-ECMO in this setting, hospital and 12-
month survival rates were 28 and 27%, respectively,
and all one-year survivors were cerebral perfor-
mance category 1 [44].
Sepsis-associated cardiomyopathy
Profound myocardial depression may develop
because of severe septic shock. Recent data sug-
gested that VA-ECMO may rescue patients who
develop refractory cardiac failure in this setting
[45,46]. Larger studies are now needed to determine
whether the benefit of VA-ECMO outweighs the
risks, especially in cases where septic shock is com-
plicated by marked disturbances in coagulation.
Hypothermic cardiac arrest
Patients with accidental hypothermia without vital
signs increasingly receive VA-ECMO; however, there
is limited knowledge regarding the efficacy of this
rewarming method. In a large nationwide inpatient
database in Japan from July 2010 to March 2017,
patients with accidental hypothermia receiving CPR
were compared according to the use of VA-ECMO on
the day of admission. Over 1661 eligible patients,
318 (19%) received VA-ECMO on the day of admis-
sion resulting in 300 propensity-matched pair of
patients. In-hospital mortality was significantly
lower (risk difference: 13% [95% CI, 5.1–21%])
and the proportion of patients with ‘alert conscious-
ness’ at discharge was higher (risk difference: 8.3%
[95% CI, 1.9–15%]) in the VA-ECMO group com-
pared with the conventional CPR [47]. The HOPE
score is based on six independent covariates avail-
able at admission and allows to predict in-hospital
survival of accidental hypothermia receiving CPR. It
was recently validated in an external prospective
cohort of 122 patients. The empirical probability
of survival was 42% (95% CI, 33–51%) and the
Hosmer–Lemeshow test comparing empirical and
HOPE probabilities of survival was not significant
(P ¼ 0.08), suggesting good calibration. The area
under the receiver operating characteristic curve
was 0.825 (95% CI, 0.753–0.897), confirming the
excellent discrimination of the model. The negative
predictive value of a HOPE score cut-off of less than
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The place of extracorporeal life support in cardiogenic shock Pineton de Chambrun et al.
0.10 was excellent (97%) suggesting the HOPE score
may replace serum potassium in the future as the
triage tool when considering VA-ECMO rewarming
of a hypothermic cardiac arrest victim [48].
Drug-induced cardiogenic shock
VA-ECMO is increasingly used in drug-induced car-
diogenic shock but the evidence of VA-ECMO utility
in poisoning is limited. A study using the Extracor-
poreal Life Support Organization registry reported
the outcomes of 104 adult cases of severe poisoning
implanted with VA-ECMO between January 1, 2003
to July 30, 2018. Cardiovascular agents were
involved in 47.1% of the cases followed by opioids
(6.7%) and 34 cases experienced pre-ECMO cardiac
arrest. Median duration of VA-ECMO was 68 [IQR
25–75; 48–113] and 52.9% of the cases survived to
discharge [49].
CONCLUSION
TCS devices have become the cornerstone of the
management of patients with refractory cardiogenic
shock, although their use only received a Class IIb
recommendation from the European Society of
&&
Cardiology [13 ]. Because it is less expensive than
other devices, allows rapid improvement in oxygen-
ation and is the only short-term TCS suitable for
patients with severe biventricular failure, VA-ECMO
has emerged as the first-line support system in this
setting, with a growing number of indications. Ran-
domized clinical trials are now urgently needed to
determine the respective place of different TCS devi-
ces in strategies to treat cardiogenic shock patients.
Acknowledgements
None.
Financial support and sponsorship
None.
Conflicts of interest
There are no conflicts of interest.
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Volume 26  Number 00  Month 2020