European Heart Journal (2015) 36, 1223–1230 REVIEW


Clinical update

Management of cardiogenic shock
Holger Thiele1*, E. Magnus Ohman2, Steffen Desch1, Ingo Eitel1, and Suzanne de Waha1
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; online publish-ahead-of-print 2 March 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.
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:
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2015. For permissions please email:

27 associated risk is anticipated to be high such as in the elderly or fol. all registries except one comparing multivessel pressure.17 Even though ap.16 Theoretically.7. low-molecular weight heparin. Currently. 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. is enrolling patients in Europe to fill the apparent gap of evidence. graphic findings. A diminished per.8.18 These patients have a higher mortality compared with in the CS setting. or direct thrombin inhibitors rates .21 – 26 serum lactate mainly measuring the degree of inflammation have Since non-randomized observational studies and registries are shown an association with mortality.14. impairment of microcirculation.16. multi- angiopoietin-1 and angiopoietin-2 which has been shown to impact centre CULPRIT-SHOCK trial (Clinicaltrials. these recommendations mortality were older age. IABP-SHOCK II). lower cardiac power index. anoxic brain damage. drugs. the prospective. Besides impaired enteral perfusion. CABG is rarely performed in CS with heparin.11 The impairment of microcir. culprit lesion only PCI showed a numerically or signifi- higher serum lactate. there is only one small randomized trial in 80 patients with single-vessel disease. However. Current guidelines encourage multivessel PCI of all critical and vasodilation contribute to the vicious circle of CS.20 During PCI. there is an urgent need for ran- culation and vascular leakage is influenced by an imbalance between domized data. it could be shown in non-CS infarction patients that registries. inflammation with capillary leakage. administration of oral P2Y12-inhibitors may be cularization in comparison to initial medical stabilization is .16. crushed ticagrelor can improve platelet inhibition in comparison to icians to recognize the benefit of revascularization even if the non-crushed tablets. it is well known that in CS. prone to treatment-selection bias.14.14 trials in CS for oral antiplatelets. It is well known that restoration of normal epicardial flow by PCI in lowing resuscitation. CABG and the flow after PCI in particular for the CS patient.29 However.7. PCI of the culprit lesion is accepted standard practice.3 – 5 Therefore. there is much uncertainty left at the discretion of the interventionalists (Figure 1).21 TRIUMPH.17 With a lack of spe- Therefore.16. as CABG may immediately be necessary based on angio- In current guidelines.18. the same recommendations apply as for whereas optimal management of additional non-culprit lesions is other types of acute coronary syndrome. the type of revascular. 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. plication of early revascularization has markedly increased in clinical crushed tablets need to be administered through a nasogastric practice. and PCI vs.17 In intubated patients. . deferred.1224 H. however.8 – 10 Multiple other biomarkers in addition to cant increased mortality for the multivessel approach. cific randomized trials in CS. Currently. Thiele et al. or clopidogrel plays a major role for the bioavailability of these 1. mendations.13 patients will be randomized to either immediate multivessel PCI However.12 In CS. adjunctive anticoagulation including unfractionated Despite these considerations. 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. lower left-ventricular are mainly based on pathophysiological considerations. rates are still unsatisfactory ranging from 50 to 70% in tube.5% in registries and randomized trials. need for vasopressor support. lower systolic blood as shown in Table 1. aspirin in all patients undergoing PCI. In general.7 should be co-administered with antiplatelets. microcirculatory impairment can easily be mea. ior in comparison to standard treatment with optional abciximab use ization might influence outcome. 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. unclear. more efforts are needed to convince clin. 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.19 Current guidelines. 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. typical factors associated with higher Due to the lack of prospective data. 706 from serial measurements was associated with dismal prognosis. Although the trial failed to meet the primary endpoint (superiority enteral resorption is impaired. there are IIb/IIIa-inhibitors in patients with high thrombus burden and slow only four observational reports evaluating PCI vs.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. sured sublingually by sidestream darkfield imaging. Notably ejection fraction.16. limited data suggest similar mortality rates with CABG and PCI.5. worse renal function.15 The number needed to save one life by early revas.16 Despite these guideline recom- shock spiral. early revascularization by either per. 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. randomized. 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. 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.17 There are no specific is the most important treatment strategy in CS complicating AMI. multivessel PCI is currently performed in only one-third By multivariable modelling from the major CS trials (SHOCK. a cornerstone during PCI and since publication of the SHOCK trial cularize Occluded Coronaries for cardiogenic shocK (SHOCK) trial novel antiplatelet therapies have emerged. staged PCI. Recently. to one-fourth of CS patients with multivessel disease. vessel. and 6 NCT01927549) mortality.

.. % hazard ratio (95% CI) . SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK.. IABP-SHOCK.....84) PCI.. Intraaortic balloon pump in shock......57 (0. Webb et al.25 735 46.. PCI.Management of cardiogenic shock 1225 Table 1 Mortality for multivessel vs....72–2.....15–1.84) Yang et al... TRIUMPH...........38–0.8 35.............. Figure 1 Current evidence from randomized clinical trials in CS in the PCI era.4 43. IABP... Sepsis Occurrence in Acutely Ill Patients II...8 1...28) Zeymer et al.....0 30............. confidence interval. percutaneous coronary intervention.. The SOAP II trial was neutral with respect to mortality for the overall trial....25) Van der Schaaf et al... SHOCK. SOAP II....75 (1......... percutaneous coronary intervention.22–1.. CABG.....5 27. coronary artery bypass grafting.. CI. culprit lesion only PCI in cardiogenic shock in registries Trial N Mortality Mortality culprit Adjusted odds ratio or multivessel PCI.....23 3087 36. The relative risk and 95% confidence intervals (CI) are depicted for the various randomized interventions....21 336 48...24 266 20..8 1.26 338 35.22 161 60 53 Not reported (P ¼ 0. thus the predefined cardiogenic shock subgroup results should be interpreted with caution......95) Bauer et al..61–1.. CS.......4 1............05–7.18 74 55 20 2.... % lesion only PCI..... Tilarginine Acetate Injection in a Randomized International Study in Unstable MI Patients With Cardiogenic Shock......86) Mylotte et al..5 (1. ... left-ventricular assist device.5 (1........ SMASH....06 (0............... Swiss Multicenter trial of Angioplasty for SHock.05) Cavender et al.. LVAD. intraaortic balloon pump.28 (0.6 1.. cardiogenic shock.9 0..8 37........

only major advances acidosis. Although not specifically investigated in CS. as well as transfusion contribute to inflammation. vasopressors. Only small differences in ventricular assist devices (LVAD) are used in patients not responding haemodynamics.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. prevent or or dobutamine) or placebo. Hypothermia come. 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.1226 H. However. their use should be restricted to the shortest pos. no specific rando- Fluid administration in CS is mainly based on pathophysiological con.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). depends on optimal filling pressures pulmonary artery catheters.7 there is only limited evidence by concomitant use of mechanical support devices.7. for different devices. data derived from randomized nosis. In analogy to septic shock. mia. lung. hypothermia is also ferred over dopamine when the blood pressure is low.34 However. Further.38.43. However. leading to initial vasoconstriction. inotropes caemia. Thiele et al.17 generally applied for patients with CS after resuscitation. . standard treatment on cardiac power index (clinicaltrials. showing the relevance of this condition in CS.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. In a randomized transfusions in acute coronary syndromes itself increase mortality.14. hydropic decompensation. 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. as well as thromboembolism and stress ulcer prophylaxis Irrespective of early revascularization.44 Therefore. Despite this protective ventilation should be performed to prevent pulmonary lack of evidence.97. vs. metabolic been reviewed previously. reverse MODS mechanical circulatory support to improve haemo- vival benefit in comparison with enoximone (Hazard ratio 0. length of hospital stay. and optimal timing are limited. devices for mechanical support in CS. multiple measures clinical trials on the effectiveness and safety. thermia trials patients in CS were excluded. tory anomalies unless there is a clinical bleeding problem. and/or refractory hyperkalaemia. blood randomized data showing a prognostic benefit.41 Application of hypothermia in non-resuscitated CS patients which is often performed in clinical practice. differential indications are generally recommended. Active percutaneous left- confidence interval 0. Intensive care unit treatment nutrition. Pulse Contour Cardiac Output (PiCCOw) or other systems should vention or treatment of multiorgan system dysfunction (MODS). 95% dynamics and outcome became appealing.36 Formerly it from randomized trials comparing catecholamines in CS.31 Therefore. Moreover.35.11–0. In addition. optimal and new considerations are covered here. IABP-SHOCK II trial.7 Animal trials and sible duration and the lowest possible dose.34 Because much of haemodynamic management include initial stabilization with volume expansion to obtain euvolae. Urinary production should be measured and continuous devices is increasingly being performed. first non-randomized human trials showed improved haemo- As inotropic agent. as shown in a recent Cochrane review. there are no will increase oxygen delivery and thus is beneficial. Levosimendan showed a borderline sur.33. and ineffective oxygen delivery. be used in all complicated courses. improve survival. evidence for inotropes and vasodilators in CS is very limited. fluids.11. from 20 to 90% depending on the definition used and also influenced tered in 90% of patients in CS. vasopressors. glycaemic control to .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. more than 40% of patients were resuscitated tion and vasoconstrictors may impair microcirculation as well as before randomization with subsequent induced hypothermia tissue perfusion.0 mmol/L by avoiding hypogly- Fluids. Despite an increasing number of different percutaneous for the treatment of CS patients since it has a major impact on prog. was generally believed that raising haemoglobin levels via transfusion more.40 Although in the relevant randomized hypo- whereas on the other hand it is stated that norepinephrine is pre. mized trial in CS has been performed with these monitoring systems. norepinephrine accepted intensive care strategies are to avoid the correction of labora- should be the first choice as vasopressor.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. Moderate/severe bleeding is common in patients with CS ranging Despite the frequent use of catecholamines which are adminis. intraaortic adverse cardiac events were tion.39 the target mean blood pressure should be titrated to 65– 70 mmHg as a higher blood pressure is not associated with beneficial out.6. and inotropes plus additional therapy for the pre.34 If invasive ventilation is required.41 Currently. In the Because catecholamines increase myocardial oxygen consump. percutaneous mechanical support with active injury.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). platelet associated with significantly more arrhythmic events for the overall aggregation. bleeding itself study cohort but with a lack of significant reduction in mortality. despite beneficial effects on haemodynamics. Figure 1).7 Other inotropes may also be beneficial from pathophysiological considerations with such as levosimendan or phosphodiesterase-inhibitors are of interest multiple beneficial targets. the basic treatment measures should be provided. the current NCT01890317). when blood pressure is low. siderations. and frequency of major to standard treatment including catecholamines.

. CE............ Food and Drug Administration.... (D) iVAC 2Lw.. (C) extracorporeal life support......... no significant difference could be observed supported IABP use in CS with a Class I recommendation..0 Pump speed (rpm) Pulsatile.. Based between the two treatment groups..........69)... IABP does not improve relevant haemo. FDA.... conformite´ europe´enne.. ECLS.0 Max....0 Impellaw 2...0 Max...7 There were also no differences on a systematic meta-analysis. Max...45 Before 2012 and 2013.... Impellaw (B)..... extracorporeal life support system. 7............8 Max.......7– 4. 41.0 Max... 4. intraaortic balloon pumping.. randomized. 7500 Max. TandemHeartTM ....46 Due to a lack of randomized mechanical support at stable implantation rates from 2007 to 2011 trials....... ..... 5... American and European guidelines (39..3%. 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. renal Figure 2 Schematic drawings of current percutaneous mechanical support devices for CS: intraaortic balloon pump (A)... 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....... these recommendations have been in any of the secondary endpoints such as serum lactate.47 In the largest... 51 000 Max... 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.... 33 000 Max......42 meta-analysis and a higher mortality following IABP was observed Intraaortic balloon pumping improves the diastolic and lowers in the PCI era....7 vs................ multicentre trial in CS the endsystolic pressure without affecting the mean blood pressure.17....5 Impellaw CP ECLS (multiple systems) ...... Table 2 Technical features of currently available percutaneous support devices iVAC 2Lw TandemHeartTM Impellaw 5.. 2. left ventricular....... 600 patients with CS complicating AMI In comparison to control...5 3... only registries with conflicting results were included in this of 50 000 per year based on a national survey in the USA. P ¼ 0.. LV.................. 51 000 Max.Management of cardiogenic shock 1227 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.. (IABP-SHOCK II trial)......

blood is aspirated from the left ventricle through the catheter lumen into the mem- brane pump. the heat exchanger. in-hospital mortality of ECLS patients was as high as Assist.7%). In a cross-over vs. the pump ejects the blood back through the catheter. data on timing of IABP insertion derived requirement of perfusionists. amputation (4.3%). com- PCI. a type II error cannot be definitely excluded. the mortality was lower discharge compared with those treated after PCI. trials are available.62 years and those with cardio- and CP systems (Abiomed Europe. 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. patients who were Since IABP support has been in place for nearly five decades. PCI in high-risk anterior infarction patients without CS resulted in major bleeding (40. 63.35 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. and significant infection (30. However. as in all negative trials. Germany).16 percutaneous use for venoarterial ECLS with one single-centre. In addition.50 Furthermore.55 In a more recent pro- Currently available devices include the TandemHeartTM (Cardiac spective report.14. ing for potential confounding variables.5. or previously called extracorporeal membrane oxygenators are lysis argue against any clinically meaningful IABP effect.4%. The discharge. The mode of action of different devices has been described pre- viously. 51% in the control group (P ¼ 0. Inc. When the heart is in the systolic phase. non- randomized retrospective analysis showing improved survival rates Percutaneous left-ventricular assist devices with ECLS in comparison to historical control. lack of direct left-ventricular unloading. 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.54 Main more. complica- data even showing harm than benefit by IABP insertion before tions are substantial with lower extremity ischaemia (16. no subgroups could be identified with a potential quent with LVAD therapy with no difference in 30-day mortality advantage of IABP support.51 in a recent meta-analysis of 1866 CS patients. 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. stroke (5. (Figure 1). even when adjust- than anticipated and marginally lower in comparison to other previ. 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.16 There is currently only the indication for IABP use in mechanical and the high flow (Table 2).48 Further. The elderly patient group of . IABP.10 Further.4%) as shown no effect on infarct size.0. or length of intensive care unit treat. subsequently opening the catheter valve and delivering the blood to the ascending aorta through the side outflow port.8%). other hand. the lack of benefit for any of the investigated sec.7 The 12-month follow-up analysis con.43. no additional rando- mized trials have been performed.10 evaluation among patients with refractory CS. There is limited experience in CS for complications with a IIaC recommendation.9%). catecholamine doses.56 (PulseCath BV.5) vs. Integral features of extracorporeal life support (ECLS) systems the lack of benefit at 12-month follow-up and in the as-treated ana.44 Figure 2 shows the different devices and Table 2 provides an updated overview of technical features and left-ventricular unloading properties. USA) and the microaxial Impellaw 2. and lower pulmonary capillary wedge pressure. The Netherlands). Furthermore. the upgraded to Impella 5. pressure. one Impellaw 2. Thiele et al.52 In the USpella registry. the blood pump. thereby creating an ‘extra heart beat’.0 from 2.53 For the iVAC system. function.6. With respect to evidence. Aachen.1228 H. no ous trials in CS despite similar baseline characteristics.49.2%.35 Patients treated with active Figure 3 Considerations on use of mechanical support for LVADs demonstrated higher cardiac index. a randomized trial of IABP insertion prior to partment syndrome (10. bleeding complications and inflammation were more fre- ment. A certain cross-over rate might also have influenced the results. since the publishing of a meta-analysis in 2009 reporting the results of the only three randomized trials comparing percutaneous LVADs (two trials TandemHeartTM . and an oxygenator. On the . Pittsburgh. the neutral results in all subgroup analyses. During the diastolic phase.5 had a trend to better survival at negative results of IABP-SHOCK II triggered some discussions. However. frequent only 13. Furthermore. more. from small registries in CS are limited and conflicting with more rise in afterload. 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.7 However. 5.36 Complication rates Consequently. 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. and a limited support time. Extracorporeal life-support systems ondary study endpoints.9%). The device dir- ectly unloads the ventricle by active aspiration and simultaneously creates a counter pulsating flow in the ascending aorta. higher mean arterial multiorgan system dysfunction prevention and therapy.91).

The class of recommendation and level of evidence according to ESC guidelines is provided if NCT01633502) compares the Impellaw CP with who still had non-invasive therapeutic options. A potential benefit of an early has also not been determined. Open questions of mechanical support stage of CS. intraaortic balloon pump.17 IABP. The optimal support optimal timing of device insertion. However.16. Several other subjective criteria. use might lead to complications associated with invasive mechanical An ongoing Danish randomized multicentre trial (DanShock. also be futile situations where even the best device available will Thoratec. The relation of these considerations use at onset of CS could be prevention of MODS. USA). 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. 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. CA. not be able to change clinical outcome.46 . early is depicted in Figure 3. leading to adverse clinical outcome in patients Clinicaltrials. Furthermore. Timing and appropriate Despite all these uncertainties. support devices.17. 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.Management of cardiogenic shock 1229 Figure 4 Treatment algorithm for patients with cardiogenic shock complicating acute myocardial infarction. 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). Pleasanton.16. appro.7 There may Europe such as the HeartMate PHPTM (Percutaneous Heart Pump. 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.

and FAST-MI French Nationwide Registries. Empen K.33: 2535 –2543. Dzavik V. 6. Cardiovascular research 1287 –1296. Eitel I. Richardt G. Conflict of interest: none declared. Buerke M. Fuernau G. Stauffer JC. several decades. Feth L. Ruzyllo W. N Engl J Med 2012. Thiele H.57 Blanchard D. Schneider S. Boland J. Lemm H. Am Heart J 2010. Pfisterer ME. Schuler G. Intraaortic balloon support for myocardial infarction with cardiogenic shock. of mechanical complications would be beyond the scope of 3. Olbrich H-G. Danchin N. Ebelt H. Jewbali LS.119:1211 –1219. Hausleiter J. Prondzinsky R. Urban P. it may even more be the seminal trial for the generation Bo¨hm M. Thiele et al. Hennersdorf M. Spronk PE. Buller CE. Reynolds HR. Several guidance documents make recommenda. Werdan K.34:1651 – 1662. intervention.14 The SHOCK trial was a milestone and the subsequent 618 –626. Kellner P. Aissaoui N.160:443–450. Circulation 2009. Unverzagt S. 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Gore JM.46 This should be the motivation for future research in CS. be applied more rigorously for CS. Eur Heart J 2010. reduction in mortality in clinical practice. Desch S. Sleeper LA. Fiedler MG. management of. Zeymer U. Schiele F. 13. Schneider S. Future studies assessing Geppert A. Lagrand WK. Fuhrmann J.101:375 –384. Cardiogenic shock complicating acute myocardial in- dations for CS management. management and outcome: a report from the SHOCK Trial clinical practice is shown in Figure 4. Predictors of 30-day mortality in patients with refractory cardiogenic shock following acute myocardial infarction any drug. Eur Heart J 2013. Lessard D. Heinroth KM. Po¨ss J. Lefevre T. Empen K. Dzavı´k V.1230 H. Neumann F-J. to be judged according to their clinical efficacy. Improved outcome of cardiogenic shock at the acute stage of myocardial infarction: a report from the USIK 1995. Schuler G. Cheng JM.31:1828 –1835. 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