European Heart Journal Advance Access published March 1, 2015

European Heart Journal REVIEW

doi:10.1093/eurheartj/ehv051

Clinical update

Management of cardiogenic shock

Holger Thiele1*, E. Magnus Ohman2, Steffen Desch1, Ingo Eitel1, and Suzanne de Waha1
1
Medical Clinic II (Cardiology/Angiology/Intensive Care Medicine), University Heart Centre Luebeck, University Hospital Schleswig-Holstein, Ratzeburger Allee 160, Luebeck 23538,
Germany; and 2Duke University Medical Centre, Durham, NC, USA

Received 30 December 2014; revised 4 February 2015; accepted 11 February 2015

Cardiogenic shock (CS) remains the most common cause of death in patients with acute myocardial infarction although mortality could be
reduced from formerly 80% to 40 – 50%. In addition to percutaneous coronary intervention or coronary artery bypass grafting, catecholamines,
fluids, intraaortic balloon pumping (IABP), and also active assist devices are widely used for CS management. However, there is only limited
evidence for any of the above treatments except for early revascularization and the relative ineffectiveness of IABP. This updated review will there-
fore outline the management of CS complicating acute myocardial infarction with major focus on evidence-based revascularization techniques,
intensive care unit treatment including ventilation, transfusion regimens, adjunctive medication, and mechanical support devices.
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Keywords Shock † Heart failure † Treatment † Percutaneous coronary intervention † Myocardial infarction † Assist device

reduction, CS remains the leading cause of death in AMI with mortal-

Introduction ity rates still approaching 40 – 50% according to recent registries and
Cardiogenic shock (CS) is defined as a state of critical endorgan hypo- randomized trials.3 – 5,7
perfusion due to reduced cardiac output. Notably, CS forms a spec- The underlying causes, the pathophysiology, and treatment of
trum that ranges from mild hypoperfusion to profound shock. CS complicating AMI have been reviewed previously.1,6 This
Established criteria for the diagnosis of CS are: (i) systolic blood pres- update will outline evidence-based therapeutic management of CS
sure ,90 mmHg for .30 min or vasopressors required to achieve a complicating AMI with major focus on revascularization techniques,
blood pressure ≥90 mmHg; (ii) pulmonary congestion or elevated intensive care unit treatment including ventilation, transfusion regi-
left-ventricular filling pressures; (iii) signs of impaired organ perfusion mens, adjunctive medication, and mechanical support devices.
with at least one of the following criteria: (a) altered mental status; (b)
cold, clammy skin; (c) oliguria; (d) increased serum-lactate. The diag-
nosis of CS can usually be made on the basis of easy-to-assess clinical Pathophysiology and prognosis
criteria without advanced haemodynamic monitoring although it has assessment
previously been recommended to assess cardiac index and pulmon- The pathophysiology of CS is complex and has been summarized
ary capillary wedge pressure.1 previously.1,6 In brief, ischaemia induces profound depression of
Acute myocardial infarction (AMI) with subsequent ventricular dys- myocardial contractility, which initiates a vicious spiral of reduced
function is the most frequent cause of CS accounting for 80% of cardiac index and low blood pressure which in combination impair
cases. Mechanical complications such as ventricular septal (4%) or cardiac power index and further promote coronary ischaemia. The
free wall rupture (2%), and acute severe mitral regurgitation (7%) reduction in cardiac index causes severe tissue hypoperfusion
are less frequent causes of CS after AMI.2 Non-AMI-related CS may which is most sensitively measured by serum lactate and may finally
be caused by decompensated valvular heart disease, acute myocarditis, lead to death if the circle is not successfully interrupted by adequate
arrhythmias, etc. with heterogeneous treatment options. treatment measures. It has been recognized that CS cannot only
Cardiogenic shock complicating AMI occurs in the range from 5 to be attributed to the loss of left-ventricular function but is rather
15%.3 – 5 This translates in 40 000 to 50 000 patients per year in the the result of derangements in the entire circulatory system. Initial
USA and 60 000 to 70 000 in Europe.6 Despite advances in treat- compensatory vasoconstriction is subsequently counteracted by
ment mainly by early revascularization with subsequent mortality pathological vasodilation. Among others, development of systemic

* Corresponding author. Tel: +49 451 500 2501, Fax: +49 451 500 6437, Email: [email protected]
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2015. For permissions please email: [email protected].
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inflammation with capillary leakage, impairment of microcirculation, unclear. Current guidelines encourage multivessel PCI of all critical
and vasodilation contribute to the vicious circle of CS. Bleeding and stenoses or highly unstable lesions in addition to the culprit lesion
transfusion further contribute to inflammatory derangements in the (class IIa B recommendation) in CS.16 Despite these guideline recom-
shock spiral. mendations, multivessel PCI is currently performed in only one-third
By multivariable modelling from the major CS trials (SHOCK, to one-fourth of CS patients with multivessel disease.7,21
TRIUMPH, IABP-SHOCK II), typical factors associated with higher Due to the lack of prospective data, these recommendations
mortality were older age, anoxic brain damage, lower left-ventricular are mainly based on pathophysiological considerations. Notably
ejection fraction, lower cardiac power index, lower systolic blood as shown in Table 1, all registries except one comparing multivessel
pressure, need for vasopressor support, worse renal function, and PCI vs. culprit lesion only PCI showed a numerically or signifi-
higher serum lactate.8 – 10 Multiple other biomarkers in addition to cant increased mortality for the multivessel approach.18,21 – 26
serum lactate mainly measuring the degree of inflammation have Since non-randomized observational studies and registries are
shown an association with mortality.11 The impairment of microcir- prone to treatment-selection bias, there is an urgent need for ran-
culation and vascular leakage is influenced by an imbalance between domized data. Currently, the prospective, randomized, multi-
angiopoietin-1 and angiopoietin-2 which has been shown to impact centre CULPRIT-SHOCK trial (Clinicaltrials.gov: NCT01927549)
mortality.12 In CS, microcirculatory impairment can easily be mea- is enrolling patients in Europe to fill the apparent gap of evidence.
sured sublingually by sidestream darkfield imaging. A diminished per- With the primary endpoint defined as mortality and/or renal
fused capillary density at baseline and a lack of improvement derived failure requiring renal replacement therapy within 30 days, 706
from serial measurements was associated with dismal prognosis.13 patients will be randomized to either immediate multivessel PCI
However, the clinical value of these new biomarkers and imaging in comparison to culprit lesion only PCI with potentially subsequent
methods has not yet been finally defined. staged PCI.

Management Peri-interventional antiplatelet and antithrombotic medication

Revascularization Antithrombotic therapy including antiplatelets and anticoagulation is
Early revascularization as shown in the SHould we emergently revas- a cornerstone during PCI and since publication of the SHOCK trial
cularize Occluded Coronaries for cardiogenic shocK (SHOCK) trial novel antiplatelet therapies have emerged.16,17 There are no specific
is the most important treatment strategy in CS complicating AMI.14 trials in CS for oral antiplatelets, however, it is well known that in CS,
Although the trial failed to meet the primary endpoint (superiority enteral resorption is impaired. Besides impaired enteral perfusion,
of early revascularization over medical therapy on 30-day mortality) mechanical ventilation with inability to swallow prasugrel/ticagrelor
there was a significant mortality reduction at longer follow-up of 1/2, or clopidogrel plays a major role for the bioavailability of these
1, and 6 years.14,15 The number needed to save one life by early revas- drugs. In general, administration of oral P2Y12-inhibitors may be
cularization in comparison to initial medical stabilization is ,8. deferred, as CABG may immediately be necessary based on angio-
In current guidelines, early revascularization by either per- graphic findings. Prasugrel/ticagrelor or clopidogrel in case of contra-
cutaneous coronary intervention (PCI) or coronary artery bypass indications for the newer oral antiplatelets is indicated in addition to
grafting (CABG) is a class 1B recommendation.16,17 Even though ap- aspirin in all patients undergoing PCI.16,17 In intubated patients,
plication of early revascularization has markedly increased in clinical crushed tablets need to be administered through a nasogastric
practice, rates are still unsatisfactory ranging from 50 to 70% in tube. Recently, it could be shown in non-CS infarction patients that
registries.3 – 5 Therefore, more efforts are needed to convince clin- crushed ticagrelor can improve platelet inhibition in comparison to
icians to recognize the benefit of revascularization even if the non-crushed tablets.27
associated risk is anticipated to be high such as in the elderly or fol- It is well known that restoration of normal epicardial flow by PCI in
lowing resuscitation. CS is lower in comparison to non-CS patients and failure to achieve a
normal flow impacts mortality.28 Because of the late and impaired
Revascularization in multivessel coronary artery disease onset of oral antiplatelets glycoprotein IIb/IIIa-inhibitors may be
Approximately 70 – 80% of patients with CS present with multivessel beneficial in CS. Observational data support a potential mortality
disease defined as coronary stenoses/occlusions in more than one benefit by use of intravenous platelet inhibitors in CS.29 However,
vessel.7,14,18 These patients have a higher mortality compared with in the CS setting, there is only one small randomized trial in 80
patients with single-vessel disease.19 Current guidelines, recommend patients (with 35% cross-over in the standard treatment group)
early revascularization by PCI or CABG depending on coronary which failed to confirm that routine upstream abciximab use is super-
anatomy and amenability to PCI.16 Theoretically, the type of revascular- ior in comparison to standard treatment with optional abciximab use
ization might influence outcome. However, there is much uncertainty left at the discretion of the interventionalists (Figure 1).30 Current
because all previous trials assessing the effect of revascularization on considerations and experience suggest a liberal use of glycoprotein
outcome did not specify the type of reperfusion. Currently, there are IIb/IIIa-inhibitors in patients with high thrombus burden and slow
only four observational reports evaluating PCI vs. CABG and the flow after PCI in particular for the CS patient.
limited data suggest similar mortality rates with CABG and PCI.20 During PCI, adjunctive anticoagulation including unfractionated
Despite these considerations, CABG is rarely performed in CS with heparin, low-molecular weight heparin, or direct thrombin inhibitors
rates ,5% in registries and randomized trials.5,7 should be co-administered with antiplatelets.16,17 With a lack of spe-
Therefore, PCI of the culprit lesion is accepted standard practice, cific randomized trials in CS, the same recommendations apply as for
whereas optimal management of additional non-culprit lesions is other types of acute coronary syndrome.
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Table 1 Mortality for multivessel vs. culprit lesion only PCI in cardiogenic shock in registries

Trial N Mortality Mortality culprit Adjusted odds ratio or

multivessel PCI, % lesion only PCI, % hazard ratio (95% CI)
..................................... ..........................................................................................................................................
Webb et al.18 74 55 20 2.75 (1.05 – 7.25)
Van der Schaaf et al.22 161 60 53 Not reported (P ¼ 0.05)
Cavender et al.23 3087 36.5 27.8 1.5 (1.22 – 1.95)
Bauer et al.21 336 48.8 37.4 1.28 (0.72 – 2.28)
Zeymer et al.25 735 46.8 35.8 1.5 (1.15 – 1.84)
Yang et al.26 338 35.0 30.6 1.06 (0.61 – 1.86)
Mylotte et al.24 266 20.4 43.9 0.57 (0.38 – 0.84)

PCI, percutaneous coronary intervention; CI, confidence interval.

Figure 1 Current evidence from randomized clinical trials in CS in the PCI era. The relative risk and 95% confidence intervals (CI) are depicted for
the various randomized interventions. The SOAP II trial was neutral with respect to mortality for the overall trial, thus the predefined cardiogenic
shock subgroup results should be interpreted with caution. SHOCK, SHould we emergently revascularize Occluded Coronaries for cardiogenic
shocK; SMASH, Swiss Multicenter trial of Angioplasty for SHock; SOAP II, Sepsis Occurrence in Acutely Ill Patients II; TRIUMPH, Tilarginine
Acetate Injection in a Randomized International Study in Unstable MI Patients With Cardiogenic Shock; IABP-SHOCK, Intraaortic balloon pump
in shock; IABP, intraaortic balloon pump; LVAD, left-ventricular assist device; PCI, percutaneous coronary intervention; CABG, coronary artery
bypass grafting; CS, cardiogenic shock.
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Intensive care unit treatment nutrition, glycaemic control to ,11.0 mmol/L by avoiding hypogly-
Fluids, vasopressors, inotropes caemia, as well as thromboembolism and stress ulcer prophylaxis
Irrespective of early revascularization, the basic treatment measures should be provided.34 Because much of haemodynamic management
include initial stabilization with volume expansion to obtain euvolae- depends on optimal filling pressures pulmonary artery catheters,
mia, vasopressors, and inotropes plus additional therapy for the pre- Pulse Contour Cardiac Output (PiCCOw) or other systems should
vention or treatment of multiorgan system dysfunction (MODS). be used in all complicated courses.34 However, no specific rando-
Fluid administration in CS is mainly based on pathophysiological con- mized trial in CS has been performed with these monitoring systems.
siderations. Moderate/severe bleeding is common in patients with CS ranging
Despite the frequent use of catecholamines which are adminis- from 20 to 90% depending on the definition used and also influenced
tered in 90% of patients in CS,7 there is only limited evidence by concomitant use of mechanical support devices.7,14,35,36 Formerly it
from randomized trials comparing catecholamines in CS. Further- was generally believed that raising haemoglobin levels via transfusion
more, despite beneficial effects on haemodynamics, there are no will increase oxygen delivery and thus is beneficial. However, blood
randomized data showing a prognostic benefit. In a randomized transfusions in acute coronary syndromes itself increase mortality.37
comparison of 1679 patients with shock including 280 CS patients Alterations in erythrocyte nitric oxide biology in stored blood may
treatment with dopamine in comparison to norepinephrine was provide a partial explanation, leading to initial vasoconstriction, platelet
associated with significantly more arrhythmic events for the overall aggregation, and ineffective oxygen delivery. In addition, bleeding itself
study cohort but with a lack of significant reduction in mortality. as well as transfusion contribute to inflammation.37 Recent trials in
The predefined CS subgroup—the percentage of CS due to AMI non-CS patients with bleeding could clearly demonstrate that a re-
is not reported—had lower mortality with norepinephrine strictive transfusion regimen can improve outcome and general
(Figure 1).31 Therefore, when blood pressure is low, norepinephrine accepted intensive care strategies are to avoid the correction of labora-
should be the first choice as vasopressor. In analogy to septic shock, tory anomalies unless there is a clinical bleeding problem.38,39
the target mean blood pressure should be titrated to 65 – 70 mmHg
as a higher blood pressure is not associated with beneficial out- Hypothermia
come.32 The current European STEMI guidelines are partly confusing Therapeutic hypothermia is established for out-of-hospital cardiac
and recommend in contrast to current evidence dopamine (IIa/C arrest patients with shockable rhythm to prevent brain injury and
recommendation) over norepinephrine (IIb/B recommendation), improve survival.40 Although in the relevant randomized hypo-
whereas on the other hand it is stated that norepinephrine is pre- thermia trials patients in CS were excluded, hypothermia is also
ferred over dopamine when the blood pressure is low.17 generally applied for patients with CS after resuscitation. In the
Because catecholamines increase myocardial oxygen consump- IABP-SHOCK II trial, more than 40% of patients were resuscitated
tion and vasoconstrictors may impair microcirculation as well as before randomization with subsequent induced hypothermia
tissue perfusion, their use should be restricted to the shortest pos- showing the relevance of this condition in CS.7 Animal trials and
sible duration and the lowest possible dose. first non-randomized human trials showed improved haemo-
As inotropic agent, dobutamine may be given simultaneously to dynamics and a reduction in catecholamine use with hypothermia
norepinephrine in an attempt to improve cardiac contractility in CS.41 Application of hypothermia in non-resuscitated CS patients
which is often performed in clinical practice.7 Other inotropes may also be beneficial from pathophysiological considerations with
such as levosimendan or phosphodiesterase-inhibitors are of interest multiple beneficial targets.41 Currently, a randomized trial in non-
in CS based on their improvement of myocardial contractility resuscitated CS patients is investigating the impact of hypothermia
without increasing oxygen requirements and potential for vasodila- vs. standard treatment on cardiac power index (clinicaltrials.gov:
tion. However, as shown in a recent Cochrane review, the current NCT01890317).
evidence for inotropes and vasodilators in CS is very limited.33
Only four very small studies were eligible for this meta-analysis and Mechanical support
three trials with a total of 63 participants with high overall risk of To overcome the limitations of inotropes and vasopressors with
bias compared levosimendan to standard treatment (enoximone limited effects to maintain adequate perfusion pressure, prevent or
or dobutamine) or placebo. Levosimendan showed a borderline sur- reverse MODS mechanical circulatory support to improve haemo-
vival benefit in comparison with enoximone (Hazard ratio 0.33; 95% dynamics and outcome became appealing. Active percutaneous left-
confidence interval 0.11 – 0.97; Figure 1). Only small differences in ventricular assist devices (LVAD) are used in patients not responding
haemodynamics, length of hospital stay, and frequency of major to standard treatment including catecholamines, fluids, intraaortic
adverse cardiac events were observed.33 balloon pumping (IABP) and may also play a role as first line treat-
Optimal treatment of MODS in the intensive care unit is essential ment. Despite an increasing number of different percutaneous
for the treatment of CS patients since it has a major impact on prog- devices for mechanical support in CS, data derived from randomized
nosis. Although not specifically investigated in CS, multiple measures clinical trials on the effectiveness and safety, differential indications
are generally recommended.34 If invasive ventilation is required, lung- for different devices, and optimal timing are limited. Despite this
protective ventilation should be performed to prevent pulmonary lack of evidence, percutaneous mechanical support with active
injury. Urinary production should be measured and continuous devices is increasingly being performed.42
renal replacement therapy be initiated in case of acute renal failure The evidence of mechanical circulatory support in CS shock has
with clinical signs of uraemia, hydropic decompensation, metabolic been reviewed previously.6,43,44 Therefore, only major advances
acidosis, and/or refractory hyperkalaemia. Moreover, optimal and new considerations are covered here.
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Intraaortic balloon pumping downgraded to IIb B in the 2012 ESC guidelines and to IIa B in
Intraaortic balloon pumping is the most widely used device for the 2013 American guidelines.17,46 Due to a lack of randomized
mechanical support at stable implantation rates from 2007 to 2011 trials, only registries with conflicting results were included in this
of 50 000 per year based on a national survey in the USA.42 meta-analysis and a higher mortality following IABP was observed
Intraaortic balloon pumping improves the diastolic and lowers in the PCI era.47 In the largest, randomized, multicentre trial in CS
the endsystolic pressure without affecting the mean blood pressure. (IABP-SHOCK II trial), 600 patients with CS complicating AMI
In comparison to control, IABP does not improve relevant haemo- undergoing early revascularization were randomized to either IABP
dynamic parameters such as cardiac index or cardiac power or conventional treatment. In the primary endpoint 30-day mortality
index.45 Before 2012 and 2013, American and European guidelines (39.7 vs. 41.3%; P ¼ 0.69), no significant difference could be observed
supported IABP use in CS with a Class I recommendation. Based between the two treatment groups.7 There were also no differences
on a systematic meta-analysis, these recommendations have been in any of the secondary endpoints such as serum lactate, renal

Figure 2 Schematic drawings of current percutaneous mechanical support devices for CS: intraaortic balloon pump (A), Impellaw (B),
TandemHeartTM , (C) extracorporeal life support, (D) iVAC 2Lw.

Table 2 Technical features of currently available percutaneous support devices

iVAC 2Lw TandemHeartTM Impellaw 5.0 Impellaw 2.5 Impellaw CP ECLS

(multiple systems)
..................................... ..........................................................................................................................................
Catheter size (F) 11 (expandable) — 9 9 9
Cannula size (F) 17 21 venous 21 12 17 – 21 venous
12 – 19 arterial 16 – 19 arterial
Flow (L/min) Max 2.8 Max. 4.0 Max. 5.0 Max. 2.5 3.7 – 4.0 Max. 7.0
Pump speed (rpm) Pulsatile, Max. 7500 Max. 33 000 Max. 51 000 Max. 51 000 Max. 5000
40 mL/beat
Insertion/ Percutaneous Percutaneous (femoral Peripheral Percutaneous Percutaneous Percutaneous (femoral
Placement (femoral artery + vein for left surgical (femoral (femoral artery + vein)
artery) atrium) (femoral artery) artery)
artery)
LV unloading + ++ ++ + + 2
Anticoagulation + + + + + +
Recommended 221 days 214 days 10 days 10 days 10 days 27 days
duration of use
CE-certification + + + + + +
FDA 2 + + + + +
Relative costs ++ +++++ ++++ +++ ++++ +(+)

IABP, intraaortic balloon pumping; ECLS, extracorporeal life support system; LV, left ventricular; CE, conformité europé enne; FDA, Food and Drug Administration.
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function, catecholamine doses, or length of intensive care unit treat- other hand, bleeding complications and inflammation were more fre-
ment. In addition, no subgroups could be identified with a potential quent with LVAD therapy with no difference in 30-day mortality
advantage of IABP support.7 The 12-month follow-up analysis con- (Figure 1).35 Recent observational studies with the Impellaw device
firmed these negative findings with a mortality of 52% in the IABP have suggested some benefit with this device in CS. In a cross-over
vs. 51% in the control group (P ¼ 0.91).10 evaluation among patients with refractory CS, patients who were
Since IABP support has been in place for nearly five decades, the upgraded to Impella 5.0 from 2.5 had a trend to better survival at
negative results of IABP-SHOCK II triggered some discussions. The discharge.52 In the USpella registry, patients directly treated with
sample size calculation was based on the assumption of a higher Impella prior to PCI in CS had an overall better survival at hospital
mortality in the control group. However, the mortality was lower discharge compared with those treated after PCI, even when adjust-
than anticipated and marginally lower in comparison to other previ- ing for potential confounding variables.53 For the iVAC system, no
ous trials in CS despite similar baseline characteristics.14,48 Further- trials are available.
more, as in all negative trials, a type II error cannot be definitely
excluded. A certain cross-over rate might also have influenced the
results. However, the lack of benefit for any of the investigated sec- Extracorporeal life-support systems
ondary study endpoints, the neutral results in all subgroup analyses, Integral features of extracorporeal life support (ECLS) systems
the lack of benefit at 12-month follow-up and in the as-treated ana- or previously called extracorporeal membrane oxygenators are
lysis argue against any clinically meaningful IABP effect.10 Further- the blood pump, the heat exchanger, and an oxygenator.54 Main
more, it has been criticized that timing of IABP insertion was left to drawbacks of these devices are large cannula sizes potentially
the discretion of the operator resulting in IABP insertion pre-PCI in causing lower limb ischaemia and bleeding complications, frequent
only 13.4%.7 However, data on timing of IABP insertion derived requirement of perfusionists, lack of direct left-ventricular unloading,
from small registries in CS are limited and conflicting with more rise in afterload, and a limited support time. Furthermore, complica-
data even showing harm than benefit by IABP insertion before tions are substantial with lower extremity ischaemia (16.9%), com-
PCI.49,50 Furthermore, a randomized trial of IABP insertion prior to partment syndrome (10.3%), amputation (4.7%), stroke (5.9%),
PCI in high-risk anterior infarction patients without CS resulted in major bleeding (40.8%), and significant infection (30.4%) as shown
no effect on infarct size.51 in a recent meta-analysis of 1866 CS patients.36 Complication rates
Consequently, the results of IABP-SHOCK II influenced recent may be lowered by greater experience in percutaneous implantation
ESC revascularization guidelines with a further downgrading of the and by obligatory insertion of an antegrade perfusion cannula. Advan-
IABP with a new class IIIA recommendation for the routine use in tages are the low costs in comparison to other percutaneous LVADs
CS.16 There is currently only the indication for IABP use in mechanical and the high flow (Table 2). There is limited experience in CS for
complications with a IIaC recommendation.16 percutaneous use for venoarterial ECLS with one single-centre, non-
randomized retrospective analysis showing improved survival rates
Percutaneous left-ventricular assist devices with ECLS in comparison to historical control.55 In a more recent pro-
Currently available devices include the TandemHeartTM (Cardiac spective report, in-hospital mortality of ECLS patients was as high as
Assist, Inc, Pittsburgh, USA) and the microaxial Impellaw 2.5, 5.0, 63.2%. The elderly patient group of .62 years and those with cardio-
and CP systems (Abiomed Europe, Aachen, Germany). Furthermore, pulmonary resuscitation were even characterized by a mortality of
there is the newly available paracorporeal pulsatile device iVAC 2Lw 100% questioning the unselective use of ECLS.56
(PulseCath BV, The Netherlands). It is introduced percutaneously
through the femoral artery and can provide a pulsatile support of
2 L/min using an extracorporeal membrane pump via a 17 F
cannula. When the heart is in the systolic phase, blood is aspirated
from the left ventricle through the catheter lumen into the mem-
brane pump. During the diastolic phase, the pump ejects the blood
back through the catheter, subsequently opening the catheter valve
and delivering the blood to the ascending aorta through the side
outflow port, thereby creating an ‘extra heart beat’. The device dir-
ectly unloads the ventricle by active aspiration and simultaneously
creates a counter pulsating flow in the ascending aorta.
The mode of action of different devices has been described pre-
viously.6,43,44 Figure 2 shows the different devices and Table 2 provides
an updated overview of technical features and left-ventricular
unloading properties. With respect to evidence, since the publishing
of a meta-analysis in 2009 reporting the results of the only three
randomized trials comparing percutaneous LVADs (two trials
TandemHeartTM ; one Impellaw 2.5) vs. IABP, no additional rando-
mized trials have been performed.35 Patients treated with active Figure 3 Considerations on use of mechanical support for
LVADs demonstrated higher cardiac index, higher mean arterial multiorgan system dysfunction prevention and therapy.
pressure, and lower pulmonary capillary wedge pressure. On the
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Figure 4 Treatment algorithm for patients with cardiogenic shock complicating acute myocardial infarction. The class of recommendation
and level of evidence according to ESC guidelines is provided if available.16,17 IABP, intraaortic balloon pump.

Open questions of mechanical support stage of CS, whereas more aggressive devices with higher flow
Multiple open issues remain in mechanical device therapy such as rates may be reserved for more severe CS. The optimal support
optimal timing of device insertion. A potential benefit of an early has also not been determined. The relation of these considerations
use at onset of CS could be prevention of MODS. However, early is depicted in Figure 3.
use might lead to complications associated with invasive mechanical An ongoing Danish randomized multicentre trial (DanShock;
support devices, leading to adverse clinical outcome in patients Clinicaltrials.gov: NCT01633502) compares the Impellaw CP with
who still had non-invasive therapeutic options. Furthermore, appro- standard treatment and may further answer if an active device
priate patient selection is important and currently often based on implanted on a routine basis can reduce mortality. Several other
subjective criteria. Approximately 60% of CS patients will survive devices are currently under investigation to obtain CE-approval in
without any active device as shown in IABP-SHOCK II.7 There may Europe such as the HeartMate PHPTM (Percutaneous Heart Pump;
also be futile situations where even the best device available will Thoratec, Pleasanton, CA, USA).
not be able to change clinical outcome. Timing and appropriate Despite all these uncertainties, current European and American
patient selection is also influenced by the balance between efficacy guidelines recommend considering the use of a percutaneous assist
of any device and its device-related complications. Devices with device for circulatory support in refractory CS without any prefer-
low complication rates may be chosen more liberally in the early ence for device selection (IIa/C recommendation).16,17,46
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Figure 5 Number of patients included in major randomized cardiogenic shock trials.

Summarizing current evidence and ESC guideline recommen- 2. Hochman JS, Buller CE, Sleeper LA, Boland J, Dzavik V, Sanborn TA, Godfrey E,
White HD, Lim J, LeJemtel T. Cardiogenic shock complicating acute myocardial in-
dations for CS management,16,17 a treatment algorithm reflecting farction—etiologies, management and outcome: a report from the SHOCK Trial
clinical practice is shown in Figure 4. Further details on treatment Registry. J Am Coll Cardiol 2000;36:1063 – 1070.
of mechanical complications would be beyond the scope of 3. Aissaoui N, Puymirat E, Tabone X, Charbonnier B, Schiele F, Lefevre T, Durand E,
this review and have been summarized previously.57 Blanchard D, Simon T, Cambou J-P, Danchin N. Improved outcome of cardiogenic
shock at the acute stage of myocardial infarction: a report from the USIK 1995,
USIC 2000, and FAST-MI French Nationwide Registries. Eur Heart J 2012;33:
2535 – 2543.
Future perspectives 4. Goldberg RJ, Spencer FA, Gore JM, Lessard D, Yarzebski J. Thirty-year trends (1975
to 2005) in the magnitude of, management of, and hospital death rates associated
Randomized clinical trials in CS are difficult to perform and only few with cardiogenic shock in patients with acute myocardial infarction: a population-
based perspective. Circulation 2009;119:1211 – 1219.
randomized clinical trials powered to detect differences in
5. Jeger RV, Radovanovic D, Hunziker PR, Pfisterer ME, Stauffer JC, Erne P, Urban P.
clinical outcome achieved completion of the required patient Ten-year incidence and treatment of cardiogenic shock. Ann Intern Med 2008;149:
number (Figure 5).7,14 The SHOCK trial was a milestone and the 618 – 626.
6. Thiele H, Allam B, Chatellier G, Schuler G, Lafont A. Shock in acute myocardial
subsequent widespread application of early revascularization led to
infarction: the Cape Horn for trials? Eur Heart J 2010;31:1828 – 1835.
a significant reduction in mortality in clinical practice. The failure 7. Thiele H, Zeymer U, Neumann F-J, Ferenc M, Olbrich H-G, Hausleiter J, Richardt G,
of IABP in the IABP-SHOCK II trial should not be considered as the Hennersdorf M, Empen K, Fuernau G, Desch S, Eitel I, Hambrecht R, Fuhrmann J,
end of device therapy itself, it may even more be the seminal trial for Bö hm M, Ebelt H, Schneider S, Schuler G, Werdan K. Intraaortic balloon support
for myocardial infarction with cardiogenic shock. N Engl J Med 2012;367:
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shock II (IABP-SHOCK II) Trial. Lancet 2013;382:1638 – 1645.
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lines.16,17,46 This should be the motivation for future research in CS. Interleukin-6, -7, -8 and -10 predict outcome in acute myocardial infarction compli-
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