Cardiogenic shock: staging, MCS selection and outcomes

This page covers how cardiogenic shock is defined and staged, the drugs used to hold perfusion, revascularisation when the cause is an infarct, the choice of mechanical support, and how shock teams fit in. ESC 2026 names cardiogenic shock as one of four clinical presentations of decompensated heart failure, alongside decompensated left-sided HF, decompensated right-sided HF and acute pulmonary oedema.^[1] Reperfusion in STEMI and decongestion in acute heart failure have their own pages.

• Related topic: STEMI: reperfusion strategy.
• Related topic: Acute heart failure.
• Related topic: NSTEMI: management.

What cardiogenic shock is

Picture a patient whose heart can no longer push enough blood to the organs: the hands are cold, the urine dries up and the lactate climbs.^[1] ESC 2026 defines cardiogenic shock as a state of critical end-organ hypoperfusion caused by primary cardiac dysfunction.^[1] The 2022 AHA/ACC/HFSA guideline describes a critical reduction in cardiac output manifest by end-organ dysfunction, and calls shock a commonly encountered clinical challenge with a high mortality.^[4]

Blood pressure is not the definition.^[1][4] ESC 2026 says shock is generally characterised by hypoperfusion and hypotension, but no specific blood pressure cut-off is defined, and any arbitrary threshold has inherent limitations.^[1] The 2022 AHA/ACC/HFSA guideline calls hypotension (for example, systolic blood pressure below 90 mmHg) the primary clinical manifestation of shock, but not sufficient for the diagnosis.^[4] It adds that end-organ hypoperfusion should be present as a consequence of cardiac dysfunction.^[4]

ESC 2026 also quotes the Shock Academic Research Consortium (SHARC) definition: a cardiac disorder that results in both clinical and biochemical evidence of sustained tissue hypoperfusion.^[1] Shock may also present as hypoperfusion with normotension, which ESC 2026 says has a better prognosis than hypotensive cardiogenic shock.^[1] The SCAI 2022 update makes a different comparison: patients with hypoperfusion and no hypotension are at higher risk of dying than patients with hypotension and preserved perfusion.^[6]

Definitions side by side

^{[1] [4]}

The same guideline also prints haemodynamic criteria.^[4] Table 23 of the 2022 AHA/ACC/HFSA guideline (Suggested Shock Hemodynamic Criteria) lists systolic blood pressure below 90 mmHg or mean blood pressure below 60 mmHg, cardiac index below 2.2 L/min/m2 and pulmonary capillary wedge pressure above 15 mmHg.^[4] Its fourth item, other haemodynamic considerations, lists cardiac power output ([CO x MAP]/451) below 0.6 W, shock index (HR/systolic BP) above 1.0, and for RV shock a pulmonary artery pulse index below 1.0, CVP above 15 mmHg and CVP-PCW above 0.6.^[4] Its footnote says the diagnosis requires at least one criterion together with a cardiac index below 2.0 L/min/m2 and systolic blood pressure below 90 mmHg; the footnote figure of 2.0 differs from the 2.2 printed in item 2.^[4]

^{[1] [4] [6]}

Staging severity: the SCAI shock stages

Shock is not a yes-or-no state.^[1][6] ESC 2026 says the Society for Cardiovascular Angiography and Interventions introduced the SCAI classification to address the severity of shock, with five categories: (A) at risk, (B) pre-shock, (C) classic, (D) deteriorating and (E) extremis.^[1] The SCAI 2022 update says its shock stage classification for adult patients was developed and released in 2019, and that progression across the stages is a dynamic process.^[6]

The five stages as ESC 2026 prints them

^[1]

The SCAI 2022 update gives fuller descriptors in its Table 3, split into what each stage typically includes and what it may include.^[6] Read both columns: each stage typically includes the first set of findings and may include the second.^[6]

SCAI 2022 update, Table 3: descriptors of shock stages

^[6]

Moving between stages

• B versus C: the line is hypoperfusion; the SCAI 2022 authors suggest that a lactate above 2 mmol/L is consistent with at least stage C, although some patients show other end-organ hypoperfusion with a normal lactate, and lactate can rise for other reasons such as mesenteric ischaemia or compartment syndrome.^[6]
• C versus D (SCAI 2022 suggestion): a patient who needs vasoactive drugs or MCS to reverse hypoperfusion or haemodynamic compromise is stage C; if that initial therapy fails, shown by the need to add one or more vasoactive drugs or MCS devices, stage D is present; if perfusion cannot be restored with multiple drugs and/or devices, or extremely high doses are needed, stage E is present.^[6]
• Time matters for D: in general, the need for more than one vasoactive agent or support device because initial therapy failed to maintain perfusion defines stage D, but a patient who needs more than one agent shortly after presentation can still be stage C, because time must pass after starting therapy to define stage D (SCAI 2022).^[6]
• D needs time in C; E does not: decompensation into stage D requires some time in stage C, whereas a catastrophic event may produce stage E from any lower stage (SCAI 2022).^[6]
• Recovery counts too: patients who respond and stabilise move to a progressively lower stage; those who fail to respond, deteriorate or suffer an acute catastrophic event such as cardiac arrest or myocardial rupture move higher (SCAI 2022).^[6]
• Cardiac arrest modifier: the SCAI 2022 update refined it to include only patients after cardiac arrest who fail to respond to verbal commands and/or have a Glasgow Coma Scale below 9; brief arrest with normal neurological status no longer qualifies.^[6]
• Acute only: the classification applies only to acute presentations and is not used to stage chronic cardiovascular disease (SCAI 2022).^[6]

Stage is not the same as prognosis.^[6] The SCAI 2022 update stresses the distinction between grading shock severity and predicting mortality risk.^[6] It calls the stage one component of mortality risk prediction, alongside aetiology or phenotype and other risk modifiers, and proposes a 3-axis model of shock severity, clinical phenotype and risk modifiers.^[6]

^{[1] [6]}

Epidemiology and causes

^{[2] [3]}

The landmark trials all enrolled infarct-related shock, but the causes are wider.^{[7][8][9][12][2][4]} ESC 2023 says shock occurs more frequently in the presence of complete coronary occlusion, and names ischaemia-related HF, acute severe mitral regurgitation and mechanical complications as the major precipitating causes in ACS.^[2] The 2022 AHA/ACC/HFSA guideline groups causes broadly into acute decompensation of chronic HF, acute myocardial dysfunction without preceding HF, and survivors of cardiac arrest.^[4]

• Mechanical complications of MI (ACC/AHA 2025): ventricular septal rupture, mitral valve insufficiency due to papillary muscle infarction or rupture, and free wall rupture; timely reperfusion therapy has reduced their incidence.^[3]
• Right ventricle (ESC 2026): pulmonary embolism and acute MI involving the right ventricle are possible causes of decompensated right HF that need to be excluded during initial evaluation and treated; in the most severe cases it can manifest as refractory shock.^[1]
• Inflammatory heart disease (2022 AHA/ACC/HFSA): in the absence of ischaemic disease, recent onset with accelerating haemodynamic decompensation may represent inflammatory heart disease, particularly with conduction block or ventricular arrhythmias.^[4]

Pathophysiology and device physiology

The failing pump starves the organs, and perfusion, more than pressure, is what you are tracking.^[1] ESC 2026 says hypoperfusion is not a synonym for hypotension, although patients with decompensated HF and hypotension also experience inadequate perfusion.^[1] It adds that serum lactate, an objective marker, may help identify peripheral hypoperfusion and monitor therapy.^[1]

Chronic heart failure changes the picture.^[6] The SCAI 2022 update says that, because of compensatory mechanisms and adaptations, patients with chronic HF may display a lower stage, or a falsely reassuring clinical picture despite high-risk haemodynamics.^[6] It adds that these differences are most evident in stages A and B and converge in later stages, with stages C, D and E tending to appear similar regardless of chronicity.^[6] It also notes that lactate may be dissociated from haemodynamics in chronic HF.^[6]

The right ventricle can drive shock on its own.^[1] ESC 2026 describes decompensated isolated right-sided HF as elevated RV and right atrial pressures leading to systemic congestion and, in more advanced stages, hypoperfusion.^[1] It can also impair LV filling and reduce systemic cardiac output through ventricular interdependence.^[1]

How each device supports the circulation

Temporary MCS devices

^{[3] [1]}

ESC 2026 says active unloading with a microaxial flow pump or an IABP aims to mitigate the adverse effects of ECLS on the heart.^[1] It adds that a recent RCT of routine LV unloading by a transseptal left atrial cannula versus ECLS alone showed no effect on death.^[1] Devices can be combined to meet specific needs for LV unloading or combined left and right ventricular support (ESC 2026).^[1]

^{[3] [9] [1] [7] [8]}

Clinical presentation and bedside assessment

ESC 2026 says hypoperfusion is not a synonym for hypotension, although patients with decompensated HF and hypotension also experience inadequate perfusion.^[1] ESC 2026 Table 12 (signs, symptoms and altered laboratory tests in congestion and hypoperfusion profiles) lists the hypoperfusion profile.^[1]

What hypoperfusion looks like

^[1]

• Normal blood pressure does not exclude shock: shock may also present as hypoperfusion with normotension (ESC 2026), and SCAI stage C typically presents with relative hypotension, but hypotension is not required (SCAI 2022).^[1][6]
• Chronic HF may look better than it is: compensatory mechanisms and adaptations may give a falsely reassuring clinical picture despite high-risk haemodynamics, a difference most evident in stages A and B that converges in later stages (SCAI 2022).^[6]
• Mechanical complications (ACC/AHA 2025): commonly present with recurrent or refractory chest pain or a new murmur with disproportionate HF, cardiogenic shock or sudden cardiac death, within the first week after an acute MI.^[3]

Differential diagnosis

Hypotension with poor perfusion is not always the heart.^[1] ESC 2026 says septic and hypovolaemic shock also manifest with hypotension and end-organ hypoperfusion, and that mixed forms of shock often exist simultaneously.^[1]

What else to consider

^{[1] [6] [3] [4]}

Investigations

Measure perfusion, find the cause, and decide early who needs invasive numbers.^[1][4] ESC 2026 says the diagnostic work-up and rescue treatment should start promptly and simultaneously, and that identifying and possibly treating acute causes is crucial.^[1] The 2022 AHA/ACC/HFSA guideline adds invasive haemodynamic assessment when there is insufficient clinical improvement to initial measures.^[4]

• Lactate: ESC 2026 says the biochemical manifestation of inadequate tissue perfusion is best measured by arterial lactate, with a value above 2 mmol/L required; SCAI 2022 stage E typically includes a lactate of 8 mmol/L or more.^[1][6]
• Kidney and liver: ESC 2026 names acute kidney injury and/or acute hepatic injury as additional markers; SCAI 2022 stage C may include a creatinine increase to 1.5 x baseline (or 0.3 mg/dL) or more than 50% drop in GFR, and increased LFTs.^[1][6]
• Invasive haemodynamics: for stage C, SCAI 2022 marks invasive assessment as strongly recommended, with cardiac index below 2.2 L/min/m2 and PCWP above 15 mmHg; it says other parameters, such as the right atrial to wedge pressure ratio and the pulmonary artery pulsatility index, are now advised to identify RV failure that may potentially need dedicated RV or biventricular support.^[6]
• Pulmonary artery catheter (2022 AHA/ACC/HFSA): placement of a PA line may be considered to define haemodynamic subsets and appropriate management strategies (COR 2b, LOE B-NR).^[4]
• Why the catheter (2022 AHA/ACC/HFSA supportive text): if time allows, escalation to MCS should be guided by invasive haemodynamics; several observational experiences associate PA catheter use with improved outcomes, particularly with short-term MCS; and it may be useful when the cause of hypotension or end-organ dysfunction is uncertain, particularly when shock is not responding to empiric initial measures.^[4]
• Echocardiography (ACC/AHA 2025 text; no class or level given for this sentence): urgent echocardiography, which may include an initial point-of-care ultrasound by trained clinicians, is indicated for patients with cardiogenic shock, haemodynamic instability or suspected mechanical complications.^[3]
• Coronary angiography: in shock complicating ACS, ESC 2023 recommends immediate coronary angiography with PCI of the infarct-related artery if indicated (Class I, Level B).^[2]

Immediate management

When temporary MCS may be needed, involve the Shock Team early, and treat and investigate at the same time.^[1] ESC 2026 recommends consulting the Shock Team in patients with suspected cardiogenic shock and a potential indication for temporary MCS.^[1] It says in-hospital management of decompensated HF can be divided into three general phases (its Figure 12), and that patients with cardiogenic shock usually remain in phase 1 for several days and may never reach phase 2.^[1]

Oxygen and ventilation

• ESC 2026, Recommendation Table 9: oxygen is recommended with SpO2 below 90% or PaO2 below 60 mmHg to correct hypoxaemia (Class I, Level C).^[1]
• ESC 2026 text (no class or level given for this sentence): non-invasive ventilation is recommended in acute pulmonary oedema or cardiogenic shock with respiratory failure, to improve oxygenation and reduce the need for intubation.^[1]
• Caution (ESC 2026): positive pressure decreases venous return and right and left ventricular preload, may decrease cardiac output and blood pressure, and should be used with caution with reduced preload reserve and hypotension (for example, decompensated right-sided HF).^[1]
• ESC 2026 row: non-invasive positive pressure ventilation should be considered with respiratory distress (respiratory rate above 25 breaths/min, SpO2 below 90%), started as soon as possible to decrease distress and reduce the risk of intubation (Class IIa, Level B2).^[1]
• ESC 2026 row: intubation is recommended in decompensated HF with persistent and progressive respiratory failure despite oxygen or non-invasive ventilation, to correct hypoxaemia (Class I, Level C).^[1]
• Intubation criteria (ESC 2026 footnote): cardiac or respiratory arrest; progressive worsening of altered mental status; progressive worsening of respiratory failure with hypoxaemia (PaO2 below 60 mmHg, PaCO2 above 50 mmHg and pH below 7.35) despite or intolerant of NIV; persistent haemodynamic instability; need for airway protection.^[1]

Vasopressors

ESC 2026 favours norepinephrine.^[1] ESC 2026 says some studies, although with limitations, support norepinephrine as first choice compared with dopamine or epinephrine.^[1] Its row reads: vasopressors, preferably norepinephrine, may be considered in cardiogenic shock to increase blood pressure and vital organ perfusion (Class IIb, Level C).^[1]

• Dopamine: ESC 2026 reports an RCT including patients with unspecified shock in which dopamine versus norepinephrine was associated with a significantly higher rate of arrhythmic events; in the cardiogenic shock subgroup, a mortality benefit was seen with norepinephrine, although without a significant P value for interaction.^[1]
• Epinephrine: ESC 2026 reports a small trial of infarct-related shock in which epinephrine and norepinephrine had similar effects on cardiac index; the trial was stopped prematurely because of a higher incidence of refractory shock with epinephrine.^[1]
• Vasopressin and targets (ESC 2026): vasopressin has not been studied in cardiogenic shock so far, and the target mean blood pressure is not well defined.^[1]

Inotropes and inodilators

Inotropes buy perfusion at a cost, and ESC 2026 and the 2022 AHA/ACC/HFSA guideline word their use differently.^[1][4] ESC 2026, in its Recommendation Table 9 for decompensated heart failure, says inotropic agents may be considered with systolic blood pressure below 90 mmHg and evidence of hypoperfusion not responding to standard treatment, including a fluid challenge, to improve perfusion (Class IIb, Level C).^[1] Because of the risks of arrhythmia and myocardial ischaemia, it says they are not routinely recommended in decompensated HF and should be used cautiously.^[1]

The 2022 AHA/ACC/HFSA guideline says intravenous inotropic support should be used in cardiogenic shock to maintain systemic perfusion and preserve end-organ performance (COR 1, LOE B-NR).^[4] Its supportive text notes few prospective data and a paucity of randomised trials, and favours these agents as the first therapeutic consideration when organ hypoperfusion persists despite empiric volume replacement and vasopressors.^[4]

• No agent is proven best: ESC 2026 reports a Cochrane analysis that found insufficient evidence of a mortality benefit for any inotrope in cardiogenic shock or low cardiac output, and an RCT that found no difference between milrinone and dobutamine; the 2022 AHA/ACC/HFSA text finds no robust evidence of a clear benefit of one agent over another.^[1][4]
• Patients on beta-blockers (ESC 2026): no relevant RCTs of levosimendan in cardiogenic shock are available, but on the basis of mode of action, levosimendan or phosphodiesterase-III inhibitors may be preferred over dobutamine.^[1]

Vasoactive drugs: ESC 2026 supplementary Tables S15 and S16

^[1]

Other drugs

• Foundational HF therapy (ESC 2026): in patients already receiving it, continuation and/or rapid reintroduction as soon as possible is recommended, and discontinuation is not recommended unless there are clear signs of hypoperfusion or specific clinical indications.^[1]
• Advanced HFrEF, ESC 2026 Recommendation Table 12: down-titration or discontinuation of beta-blockers or ivabradine should be considered in selected patients with advanced HFrEF and evidence of organ hypoperfusion despite initial treatment, to increase cardiac output and improve symptoms (Class IIa, Level C).^[1]
• Opiates (ESC 2026 row): routine use is not recommended in decompensated HF unless pain or anxiety is severe or intractable, because of the risk of harm (Class III, Level C).^[1]

Revascularisation in infarct-related shock

When the cause is an infarct, opening the artery comes first.^[2][4] ESC 2023 says early revascularisation with PCI or CABG is recommended for acute MI complicated by shock, on the basis of the SHOCK trial.^[2] The 2022 AHA/ACC/HFSA guideline says urgent revascularisation is paramount in acute MI.^[4]

Revascularisation rows

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• Timing (ACC/AHA 2025 supportive text and synopsis; no class or level given for these sentences): the supportive text recommends that primary PCI should be performed in STEMI with cardiogenic shock as soon as possible, ideally within 90 minutes, to reduce mortality; the synopsis adds that treatment delays to primary PCI are associated with worse survival in STEMI with haemodynamic instability.^[3]
• NSTEMI (ACC/AHA 2025 synopsis): immediate revascularisation with PCI or CABG is also recommended in high-risk patients with NSTEMI who are in cardiogenic shock.^[3]
• Where to send them (ESC 2023): with or without ST-segment elevation or equivalent ECG patterns, these patients should be transferred as soon as possible to a tertiary care centre (for example, a shock centre) where invasive angiography can be performed, supported by specialists with relevant experience (the Shock Team).^[2]
• Surgery: ESC 2023 calls surgical revascularisation a valuable option when attempted PCI of the infarct-related artery has failed or the anatomy is not amenable to PCI; ACC/AHA 2025 says observational studies suggest emergency CABG remains an option when shock is not amenable to PCI or PCI is unsuccessful.^[2][3]
• Peri-operative support (ESC 2023): for emergency CABG, prophylactic or on-demand mechanical circulatory support may be considered on the basis of pre-operative status, such as age, comorbidities, electrical instability, extent of jeopardised myocardium, ischaemia duration, right ventricular involvement and surgical feasibility.^[2]

The SHOCK trial reached its result late.^[2][3] ESC 2023 reports that the SHOCK trial compared emergency revascularisation with initial medical stabilisation in 302 patients with acute MI complicated by shock, of whom about 60% had anterior MI and 85% had multivessel disease.^[2] It reports no difference in mortality at 30 days (the primary end point), but lower mortality at 6 months with revascularisation; 64% of that arm had PCI and 36% CABG.^[2] ACC/AHA 2025 reports that the patients were randomised to medical therapy or emergency revascularisation, and that the mortality benefit was maintained through 1 and 6 years.^[3]

Culprit-only PCI

Most of these patients have more than one diseased artery, and the temptation is to fix them all.^[2][3] ESC 2023 says PCI during the index procedure should be restricted to the infarct-related artery, on the basis of CULPRIT-SHOCK, which included ACS with and without ST-segment elevation or equivalent.^[2] ACC/AHA 2025 says that in STEMI complicated by shock and multivessel disease, a multivessel PCI strategy is associated with worse outcomes.^[3]

Culprit-only rows

^{[2] [3] [5]}

• CULPRIT-SHOCK design (abstract): a multicentre RCT of 706 patients with multivessel disease, acute MI and cardiogenic shock, assigned to PCI of the culprit lesion only (with the option of staged revascularisation of non-culprit lesions) or immediate multivessel PCI; the primary end point was death or severe renal failure leading to renal-replacement therapy within 30 days.^[12]
• 30 days (abstract): the primary end point occurred in 45.9% with culprit-lesion-only PCI and 55.4% with multivessel PCI (relative risk 0.83; 95% CI 0.71 to 0.96; P = 0.01); relative risk of death 0.84 (0.72 to 0.98) and of renal-replacement therapy 0.71 (0.49 to 1.03).^[12]
• 1 year (abstract of the same randomised trial): death occurred in 50.0% with culprit-lesion-only PCI and 56.9% with multivessel PCI (relative risk 0.88; 95% CI 0.76 to 1.01), and mortality did not differ significantly; repeat revascularisation (32.3% versus 9.4%) and rehospitalisation for HF (5.2% versus 1.2%) were more frequent with culprit-lesion-only PCI.^[13]
• How the guidelines read it: ESC 2023 reports that mortality did not differ significantly at 1 year; ACC/AHA 2025 reports that the rates of death or renal replacement therapy were significantly higher with multivessel PCI at 30 days and 1 year.^[2][3]
• The caveat (ACC/AHA 2025): CULPRIT-SHOCK enrolled patients only if there was an identifiable culprit lesion; with an unstable-appearing non-culprit lesion or an uncertain culprit, the decision on multivessel PCI may be more nuanced.^[3]

^{[12] [13] [2] [3] [5]}

Mechanical circulatory support: which device, for whom

Mechanical support is for selected patients.^[1][3] ESC 2026 says temporary MCS should be considered as an option for stabilising haemodynamics and enhancing end-organ perfusion in highly selected patients.^[1] It reports a recent meta-analysis suggesting benefit in highly selected patients with ST-elevation MI complicated by shock and no hypoxic brain injury, although rates of severe complications remain high.^[1]

ACC/AHA 2025 notes that randomised trials of MCS devices remain hard to conduct because of a relative lack of equipoise among treating physicians, which leads to selective enrolment and limits generalisability.^[3] The 2022 AHA/ACC/HFSA guideline says vascular, bleeding and neurological complications are common to MCS devices, and that the patient's wishes, prognosis and trajectory, and the therapeutic risk, should as far as possible be understood before invasive temporary MCS.^[4]

Microaxial flow pump

• ESC 2026, Recommendation Table 10: temporary MCS with a microaxial flow pump should be considered in selected patients with cardiogenic shock caused by ST-elevation MI with LV systolic dysfunction and no risk of hypoxic brain injury, to reduce the risk of death (Class IIa, Level B1).^[1]
• No risk of hypoxic brain injury (ESC 2026 footnote): no out-of-hospital cardiac arrest with persistent Glasgow coma scale below 8 after return of spontaneous circulation, and no resuscitation or resuscitation lasting less than 10 min.^[1]
• ACC/AHA 2025: in selected patients with STEMI and severe or refractory cardiogenic shock, insertion of a microaxial intravascular flow pump is reasonable to reduce death (COR 2a, LOE B-R); the word selected points to its supportive text.^[3]
• Who is selected (ACC/AHA 2025 supportive text): patients with clinical features consistent with the DanGer Shock inclusion criteria, in particular STEMI with SCAI shock stage C, D or E, not comatose, with adequate peripheral vasculature for large-bore access.^[3]
• NHFA/CSANZ 2025 (MJA 2026 summary): in select people with STEMI or acute coronary occlusion MI (ACOMI) and cardiogenic shock, consider left ventricular assist devices (weak; moderate certainty); the MJA text behind this row cites, as its reference 45, the DanGer Shock trial report (Microaxial Flow Pump or Standard Care in Infarct-Related Cardiogenic Shock).^[5][7]
• Routine use (ESC 2026 text): routine use of microaxial flow pumps in cardiogenic shock is not recommended, and RCTs in non-infarct-related shock have yet to be conducted.^[1]

DanGer Shock is the trial behind these rows.^[3][1] In this international, multicentre RCT, patients with STEMI and cardiogenic shock were assigned to a microaxial flow pump (Impella CP) plus standard care or standard care alone, with death from any cause at 180 days as the primary end point.^[7] ACC/AHA 2025 reports that it enrolled 360 patients at 14 specialised European centres, with shock of less than 24 hours' duration and LVEF below 45%.^[3]

DanGer Shock in numbers

^{[3] [7] [1]}

ACC/AHA 2025 says its class reflects the balance between the reduction in death and the increased risks of bleeding, limb ischaemia and renal replacement therapy.^[3] It adds that the trial protocol did not dictate when the pump was placed, so the preferred timing is unclear.^[3] ESC 2026 says multiple open questions remain despite the mortality benefit.^[1]

Venoarterial ECMO (ECLS)

• ECLS-SHOCK design (abstract): a multicentre RCT in acute MI complicated by cardiogenic shock with early revascularisation planned, comparing early ECLS plus usual medical treatment with usual medical treatment alone; the primary outcome was death from any cause at 30 days.^[8]
• Result (abstract): of 417 patients analysed, death at 30 days was 47.8% with ECLS and 49.0% with control (relative risk 0.98; 95% CI 0.80 to 1.19; P = 0.81).^[8]
• Harms (abstract): moderate or severe bleeding 23.4% versus 9.6% (relative risk 2.44), and peripheral vascular complications warranting intervention 11.0% versus 3.8% (relative risk 2.86).^[8]
• Pooled data: an individual patient data meta-analysis of four RCTs (567 patients) comparing early routine VA-ECMO with optimal medical therapy alone in infarct-related shock found no significant reduction in 30-day death (OR 0.93; 95% CI 0.66 to 1.29), with more major bleeding (OR 2.44) and peripheral ischaemic vascular complications (OR 3.53).^[14]
• ECMO-CS: ESC 2023 reports that this trial randomised 122 patients (51% with STEMI) with rapidly deteriorating or severe shock to immediate VA-ECMO or an initially conservative strategy that allowed downstream VA-ECMO, and that immediate VA-ECMO did not improve clinical outcomes; ACC/AHA 2025 reports no difference at 30 days in the primary composite of all-cause death, resuscitated cardiac arrest and implementation of another MCS device; ESC 2023 says the roughly 40% crossover, heterogeneous phenotypes and inclusion of crossover in the primary end point mean the trial cannot answer whether MCS reduces mortality.^[2][3]
• Non-ischaemic shock (ESC 2026): RCTs of ECLS in non-ischaemic cardiogenic shock have yet to be performed.^[1]

Intra-aortic balloon pump

• IABP-SHOCK II at 30 days (abstract): in a randomised, prospective, open-label, multicentre trial of 600 patients with shock complicating acute MI, all expected to undergo early revascularisation, death at 30 days was 39.7% with IABP and 41.3% with control (relative risk 0.96; 95% CI 0.79 to 1.17; P = 0.69).^[9]
• No other signal (abstract): no significant differences in secondary end points or process-of-care measures, including time to haemodynamic stabilisation, ICU stay, lactate, catecholamine dose and duration, and renal function; major bleeding, peripheral ischaemic complications, sepsis and stroke did not differ significantly.^[9]
• 12 months and 6 years (later reports of the same trial): death at 12 months was 52% versus 51% (relative risk 1.01); at long-term follow-up 6.2 years (interquartile range 5.6 to 6.7) after randomisation, mortality was 66.3% versus 67.0% (relative risk 0.99).^[10][11]
• ESC 2026 text: routine IABP is not recommended in unselected shock; ESC 2026 reports a trial that randomised 40 patients with post-MI shock to IABP or standard care, in which IABP did not significantly augment cardiac output or any other haemodynamic variable, and reports that in advanced HF shock IABP had no survival benefit compared with standard care; the decision to use an IABP should be highly individualised, based on patient-specific factors and the availability of alternative therapies.^[1]

The MCS rows side by side

Temporary MCS rows by region

^{[1] [3] [5] [2]}

Two older rows still apply, but only in part, among the guidelines checked for this topic.^[2][4] ESC 2023 says that in patients with ACS and severe or refractory shock, short-term MCS may be considered (Class IIb, Level C).^[2] The newer ESC 2026 rows above apply instead for a microaxial flow pump in selected STEMI-related shock with LV systolic dysfunction and no risk of hypoxic brain injury.^[1] They also apply for temporary MCS in unselected shock caused by acute MI, and for temporary MCS as a bridge to definitive treatment with mechanical complications related to MI.^[1] The 2022 AHA/ACC/HFSA guideline says that in cardiogenic shock, temporary MCS is reasonable when end-organ function cannot be maintained by pharmacological means to support cardiac function (COR 2a, LOE B-NR).^[4] In shock caused by acute MI, the newer ACC/AHA 2025 rows above apply where they speak: a microaxial flow pump in selected STEMI with severe or refractory shock, short-term MCS with a mechanical complication as a bridge to surgery, and no routine IABP or VA-ECMO.^[3]

Shock teams and systems of care

Device choice is a team decision made in a centre that can deliver it.^[1] ESC 2026 recommends a multidisciplinary Shock Team for potential candidates for temporary MCS, to guide device selection (modality and type) on the basis of patient and HF characteristics (Class I, Level C).^[1] Its text says the Shock Team includes a cardiologist specialised in HF, a cardiothoracic surgeon, an interventional cardiologist and an intensive care specialist, working at an experienced advanced HF centre that is high-volume for temporary MCS.^[1]

• 2022 AHA/ACC/HFSA: in cardiogenic shock, management by a multidisciplinary team experienced in shock is reasonable (COR 2a, LOE B-NR); for patients not rapidly responding to initial shock measures, triage to centres that can provide temporary MCS may be considered to optimise management (COR 2b, LOE C-LD).^[4]
• Team make-up and evidence (2022 AHA/ACC/HFSA text): HF and critical care specialists, interventional cardiologists and cardiac surgeons, capable of providing palliative care; most documented experience suggests outcomes improve after shock teams are instituted.^[4]
• Transfer early (2022 AHA/ACC/HFSA text): transfer to centres capable of such support should be considered early when shock has a trajectory of worsening end-organ malperfusion.^[4]
• Shock centre (ESC 2023): with or without ST-segment elevation, patients with shock complicating ACS should be transferred as soon as possible to a tertiary care centre, such as a shock centre, where invasive coronary angiography can be performed, supported by specialists with relevant experience (the Shock Team).^[2]
• Hub and spoke (SCAI 2022 proposal): spoke centres with MCS capability would manage stage C and consider referral when progression to stage D occurs, before stage E; transfers for futile care in unrecoverable high-risk patients do not change outcomes and deny capacity to others.^[6]
• Mechanical complications (ACC/AHA 2025 supportive text): transfer to a Level 1 cardiac intensive care unit with temporary MCS devices and multidisciplinary surgical, interventional, HF and palliative care teams is recommended, and emerging data after the creation of shock teams support the transfer of haemodynamically unstable patients from community hospitals to centres with multidisciplinary expertise.^[3]

Specific scenarios

Mechanical complications of MI

• ESC 2023, Recommendation Table 9: with haemodynamic instability, emergency surgical or catheter-based repair of mechanical complications of ACS is recommended, based on Heart Team discussion (Class I, Level C).^[2]
• ACC/AHA 2025: patients with a mechanical complication of ACS should be managed in a facility with cardiac surgical expertise (COR 1, LOE C-EO), and short-term MCS devices are reasonable for haemodynamic stabilisation as a bridge to surgery (COR 2a, LOE B-NR).^[3]
• ESC 2026: temporary MCS should be considered with mechanical complications related to MI as a bridge to definitive treatment (Class IIa, Level C); the choice of passive IABP or active percutaneous MCS should be based on shock severity as assessed by the Shock Team.^[1]
• Large ventricular septal defect (ESC 2026 footnote): use temporary MCS with caution, because of a possible increase in left-to-right shunt (VA-ECLS) or shunt inversion (microaxial flow pump); ACC/AHA 2025 says an IABP has been shown to reduce left-to-right shunting and improve haemodynamics in ventricular septal rupture, with and without shock.^[1][3]
• Free-wall rupture (ESC 2026 footnote): temporary MCS should be avoided, but VA-ECLS can be considered to allow emergent surgery in profound shock and/or cardiac arrest if there is no sign of irreversible brain injury.^[1]
• ESC 2023, Recommendation Table 14 (ACS complications): an IABP should be considered in patients with haemodynamic instability or cardiogenic shock due to ACS-related mechanical complications (Class IIa, Level C).^[2]
• Surgical risk (ACC/AHA 2025): mortality with surgery is highest in patients with cardiogenic shock and in those needing early emergency or urgent intervention after acute MI.^[3]

Advanced heart failure and acute-on-chronic shock

• ESC 2026, Recommendation Table 10: temporary MCS should be considered in selected patients with HF-related haemodynamic instability as a bridge to recovery, decision, bridge, candidacy or transplantation (BTR, BTD, BTB, BTC or BTT) (Class IIa, Level C).^[1]
• ESC 2026, Recommendation Table 12: continuous inotropes should be considered in advanced HFrEF with low cardiac output and evidence of hypoperfusion or end-organ dysfunction, as BTD, BTT or bridge to durable MCS, to increase cardiac output and improve symptoms (Class IIa, Level C).^[1]
• ESC 2026 text: the SCAI classification may be useful in identifying patients for temporary MCS as a possible bridge to advanced therapies; ESC 2026 reports that IABP had no survival benefit in advanced HF shock compared with standard care.^[1]
• 2022 AHA/ACC/HFSA text: shock treatment is a temporising strategy until the cause has been treated (for example, revascularisation in ST-elevation MI), the heart recovers (for example, myocarditis), or a definitive solution such as a durable LVAD or transplant can be accomplished.^[4]

Myocarditis presenting in shock

• ESC 2025 myocarditis guideline (text): fulminant myocarditis is a rare and severe presentation and a cause of cardiogenic shock, and should be treated accordingly with inotropic or vasopressor support or, if needed, MCS.^[16]
• ESC 2025, Recommendation Table 11: a timely and dedicated Shock Team discussion is recommended in myocarditis with haemodynamic compromise, to decide on the need for escalation to MCS and to determine a long-term management plan (Class I, Level C).^[16]
• ESC 2025, Recommendation Table 11: temporary MCS (its footnote lists IABP, percutaneous LV assist device and VA-ECMO) should be considered in myocarditis with cardiogenic shock or acute decompensation in chronic myocarditis, to stabilise the patient (Class IIa, Level C).^[16]
• 2022 AHA/ACC/HFSA text: in the absence of ischaemic disease, recent onset with accelerating haemodynamic decompensation may represent inflammatory heart disease, and myocarditis is its example of a cause that may recover.^[4]

Right ventricular shock

• Causes to exclude (ESC 2026): pulmonary embolism and acute MI involving the right ventricle.^[1]
• Ventilation (ESC 2026): non-invasive positive pressure ventilation decreases venous return and preload, and should be used with caution in patients with reduced preload reserve and hypotension, that is, decompensated right-sided HF.^[1]
• Devices: microaxial flow pumps depend on adequate right ventricular function to fill the LV (ACC/AHA 2025); DanGer Shock excluded overt right ventricular failure (ACC/AHA 2025); devices can be combined for left and right ventricular support (ESC 2026).^[3][1]

Complications and pitfalls

• Device harms are real: in DanGer Shock the composite safety end point occurred in 24.0% versus 6.2% and renal-replacement therapy in 41.9% versus 26.7%; in ECLS-SHOCK moderate or severe bleeding occurred in 23.4% versus 9.6% (abstracts).^[7][8]
• Waiting for hypotension: ESC 2026 sets no blood pressure cut-off, and SCAI 2022 says hypoperfusion without hypotension carries a higher risk of death than hypotension with preserved perfusion.^[1][6]
• Trusting lactate alone: the SCAI 2022 update says lactate may be dissociated from haemodynamics in chronic HF, other end-organ hypoperfusion can occur with a normal lactate, and lactate can rise from causes other than shock.^[6]
• Stenting every lesion: ACC/AHA 2025 says routine PCI of a non-infarct-related artery at the time of primary PCI should not be performed in ACS complicated by shock, because of the higher risk of death or renal failure (COR 3: Harm, LOE B-R).^[3]
• Reaching for a balloon pump by habit: ESC 2026 does not recommend IABP in unselected cardiogenic shock because of the lack of effect (Class III, Level B1).^[1]
• Forgetting the afterload of VA-ECMO: ESC 2026 says ECLS may harm the heart through the afterload increase from retrograde flow.^[1]
• Inotropes and dopamine: ESC 2026 cites risks of arrhythmia and myocardial ischaemia with inotropes, and reports an RCT in unspecified shock in which dopamine was associated with a significantly higher rate of arrhythmic events than norepinephrine.^[1]
• Femoral access: ACC/AHA 2025 says best practices for insertion of all MCS devices, including multimodality use of fluoroscopy and ultrasound, should be used when feasible for femoral access.^[3]

Prognosis and disposition

Mortality stays high even in trials.^[11][3] The 6-year report of IABP-SHOCK II concludes that mortality is still very high, with two thirds of patients with shock complicating acute MI dying despite contemporary treatment with revascularisation.^[11] ACC/AHA 2025 gives an early mortality rate of 40% to 50% for cardiogenic shock in STEMI.^[3]

Death rates in the comparator arms of the landmark trials

^{[9] [11] [12] [13] [7] [8]}

• Stage and risk: observational validation studies of 166 to 10004 patients uniformly show an association between SCAI stage and mortality across populations (SCAI 2022).^[6]
• Age: the SCAI 2022 update calls age a well-known continuous risk factor for adverse outcomes in cardiogenic shock.^[6]
• Where they go (ESC 2023): after reperfusion, it is recommended to admit high-risk ACS patients (including all STEMI patients) to a CCU or intensive cardiac care unit, and cardiogenic shock is listed among the conditions that act as acute risk modifiers.^[2]
• Where they go (ACC/AHA 2025): patients with ACS and ongoing angina, haemodynamic instability, uncontrolled arrhythmias, suboptimal reperfusion or cardiogenic shock should be admitted to a cardiac intensive care unit to reduce cardiovascular events (COR 1, LOE C-EO).^[3]
• Course (ESC 2026): in-hospital management of decompensated HF can be divided into three general phases, and patients with cardiogenic shock usually remain in phase 1 for several days and may never reach phase 2.^[1]

Special populations

• Older patients: age is a continuous risk factor in shock (SCAI 2022), and age is one of the pre-operative factors ESC 2023 lists for peri-operative MCS planning around emergency CABG.^[6][2]
• Comatose survivors of cardiac arrest: the ESC 2026 microaxial pump row applies only with no risk of hypoxic brain injury, and DanGer Shock excluded comatose patients after out-of-hospital arrest; the SCAI cardiac arrest modifier marks patients who fail to respond to verbal commands and/or have a Glasgow Coma Scale below 9.^[1][3][6]
• Patients taking beta-blockers: ESC 2026 says no relevant RCTs of levosimendan in cardiogenic shock are available, but on the basis of mode of action, levosimendan or phosphodiesterase-III inhibitors may be preferred over dobutamine; the Table S16 entry says dobutamine effects may be blunted by beta-blockers.^[1]
• Chronic HF with acute decompensation: patients may display a lower SCAI stage or a falsely reassuring picture despite high-risk haemodynamics, differences most evident in stages A and B that converge in later stages; lactate may also be dissociated from haemodynamics in chronic HF (SCAI 2022).^[6]
• Pregnancy (ESC 2025 pregnancy guideline, Recommendation Table 20): inotropes and/or vasopressors are recommended in pregnant women with cardiogenic shock, with levosimendan, dobutamine and milrinone as recommended agents (Class I, Level C), and urgent delivery by caesarean section is recommended as soon as the foetus is viable, taking gestational age, comorbidities and the available level of care into account (Class I, Level C).^[15]
• Pregnancy (ESC 2025 text): levosimendan is given as a continuous infusion without a loading dose, dobutamine is an option and adrenaline should be avoided; MCS, preferably VA-ECMO, should be considered in severe refractory cardiogenic shock; pregnant women with acute HF need urgent admission and referral to an expert centre with advanced HF care, on-site surgery and MCS.^[15]

Evidence, guidelines and regional differences

^{[1] [2] [3] [4] [5]}

The inotrope rows differ in wording, strength and setting between the two regions.^[1][4] ESC 2026, in its Recommendation Table 9 for decompensated heart failure, says inotropic agents may be considered with systolic blood pressure below 90 mmHg and hypoperfusion not responding to standard treatment, including fluid challenge, to improve perfusion (Class IIb, Level C).^[1] The 2022 AHA/ACC/HFSA guideline says intravenous inotropic support should be used in cardiogenic shock to maintain systemic perfusion and preserve end-organ performance (COR 1, LOE B-NR).^[4]

Rows that changed

• IABP (ESC 2026 Table 6, revised recommendations): the 2021 row (IABP is not routinely recommended in post-MI cardiogenic shock, Class III, Level B) became IABP is not recommended in unselected patients with cardiogenic shock, due to the lack of effect (Class III, Level B1).^[1]
• Bridging MCS (ESC 2026 Table 6): the 2021 row (short-term MCS should be considered in patients with cardiogenic shock as a BTR, BTD, BTB, with further indications including treatment of the cause of shock or long-term MCS or transplantation, Class IIa, Level C) became temporary MCS should be considered in selected patients with HF-related haemodynamic instability as a BTR, BTD, BTB, BTC or BTT (Class IIa, Level C).^[1]
• Continuous inotropes (ESC 2026 Table 6): the 2021 row (continuous inotropes and/or vasopressors may be considered in low cardiac output with evidence of organ hypoperfusion as bridge to MCS or heart transplantation, Class IIb, Level C) became continuous inotropes should be considered in advanced HFrEF with low cardiac output and evidence of hypoperfusion or end-organ dysfunction, as BTD, BTT or bridge to durable MCS, to increase cardiac output and improve symptoms (Class IIa, Level C).^[1]
• Short-term MCS in ACS (ESC 2023, Class IIb, Level C): among the guidelines checked for this topic, partly superseded by the ESC 2026 rows for a microaxial flow pump in selected patients with shock caused by ST-elevation MI with LV systolic dysfunction and no risk of hypoxic brain injury, for temporary MCS in unselected shock caused by acute MI, and for temporary MCS with mechanical complications related to MI (as a bridge to definitive treatment); otherwise (other patients, or other devices) it remains the ESC 2023 row.^[2][1]
• Temporary MCS when end-organ function cannot be maintained by pharmacological means (2022 AHA/ACC/HFSA, COR 2a, LOE B-NR): among the guidelines checked for this topic, partly superseded in shock caused by acute MI by the ACC/AHA 2025 rows on a microaxial flow pump in selected STEMI with severe or refractory shock, short-term MCS with a mechanical complication as a bridge to surgery, and routine IABP or VA-ECMO (not recommended); otherwise it remains the 2022 AHA/ACC/HFSA row.^[4][3]

ANZ practice

The 2025 NHFA/CSANZ ACS guideline is summarised in the MJA (2026), and its Table 3 (summary of recommendations for hospital care and reperfusion strategies) carries four rows under acute management of ACS with cardiogenic shock.^[5] The guideline was developed with GRADE methodology, and Table 3 gives each of these four rows a strength of recommendation and a certainty of evidence.^[5]

• Revascularisation: in people with ACS and cardiogenic shock, perform PCI of the infarct-related artery only (strong; moderate certainty).^[5]
• IABP: routine insertion is not recommended (strong; high certainty).^[5]
• VA-ECMO: routine use is not recommended (strong; moderate certainty).^[5]
• Left ventricular assist devices: consider in select people with STEMI/ACOMI and cardiogenic shock (weak; moderate certainty).^[5]
• Why (MJA text): routine IABP and VA-ECMO are not recommended because of increased risk of bleeding and vascular complications with no survival benefits, though they may be considered in select cases; left ventricular assist devices are supported in select people with STEMI/ACOMI and shock, given potential survival benefits despite increased bleeding and vascular complication risks.^[5]

Guidelines checked

A row called newer, or current, is so among the guidelines checked for this topic:

• Sources of the rows and statements used: ESC heart failure (2026, with supplementary data), acute coronary syndromes (2023), pregnancy (2025) and myocarditis and pericarditis (2025); ACC/AHA acute coronary syndromes (2025) and AHA/ACC/HFSA heart failure (2022, JACC version); the 2025 NHFA/CSANZ ACS guideline through its MJA (2026) summary; the SCAI SHOCK stage update (2022, JSCAI version); trial abstracts for DanGer Shock, ECLS-SHOCK, IABP-SHOCK II, CULPRIT-SHOCK and the VA-ECMO individual patient data meta-analysis.^{[1][2][15][16][3][4][5][6][7][8][9][12][14]}
• Also swept for newer rows on the same questions (the guidelines checked for this topic): ESC cardiac rehabilitation (2026), myocarditis and pericarditis, pregnancy, valvular heart disease and dyslipidaemias (2025), chronic coronary syndromes, hypertension, peripheral arterial and aortic diseases and atrial fibrillation (2024), endocarditis and cardiomyopathies (2023), and ventricular arrhythmias and non-cardiac surgery (2022); ACC/AHA aortic disease (2022), chronic coronary disease and atrial fibrillation (2023), hypertrophic cardiomyopathy (2024), blood pressure (2025), and pulmonary embolism and dyslipidaemia (2026).
• Not held as text, so not checked for this topic: the 2023 ISHLT/HFSA guideline on acute mechanical circulatory support, the 2026 EACTS/STS/AATS guidelines on temporary MCS in adult cardiac surgery, the 2025 ACC expert consensus statement on cardiogenic shock and the 2026 ESC association consensus statement on diagnostic criteria; ESC cardio-oncology and pulmonary hypertension (2022), diabetes (2023) and cardiovascular disease and chronic kidney disease (2026); ACC/AHA adult congenital heart disease (2025), cardiovascular-kidney-metabolic syndrome (2026) and perioperative management (2026).

Exam pearls

• Define it by perfusion: ESC 2026 says the biochemical manifestation of inadequate tissue perfusion is best measured by arterial lactate, with a value above 2 mmol/L required, and sets no blood pressure cut-off.^[1]
• SCAI B versus C is hypoperfusion; C versus D is failure of initial therapy, which needs time (SCAI 2022).^[1][6]
• Culprit only: ESC 2023 recommends infarct-related-artery-only PCI during the index procedure in ACS with multivessel disease presenting in shock (Class I, Level B); ACC/AHA 2025 says routine non-infarct-artery PCI at the time of primary PCI should not be performed in ACS complicated by shock (COR 3: Harm, LOE B-R).^[2][3]
• DanGer Shock: routine use of a microaxial flow pump with standard care in STEMI-related shock lowered 180-day death compared with standard care alone (45.8% versus 58.5%; hazard ratio 0.74), with more composite adverse events (abstract).^[7]
• IABP-SHOCK II and ECLS-SHOCK showed no mortality reduction at 30 days, and ACC/AHA 2025 does not recommend routine IABP or VA-ECMO in acute MI with shock, due to a lack of survival benefit (COR 3: No benefit, LOE B-R).^[9][8][3]
• No risk of hypoxic brain injury, in the ESC 2026 footnote, means no out-of-hospital arrest with persistent Glasgow coma scale below 8 after ROSC, and no resuscitation or resuscitation lasting less than 10 min.^[1]
• ESC 2026: vasopressors, preferably norepinephrine, may be considered in cardiogenic shock to increase blood pressure and vital organ perfusion (Class IIb, Level C); supplementary Table S16 lists norepinephrine at 0.2–1.0 μg/kg/min.^[1]

References16ShowHide

1. [1]Køber L, et al. 2026 ESC Guidelines for the management of heart failure. Eur Heart J, 2026.PMID 42661420
2. [2]Byrne RA, et al. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J, 2023.PMID 37622654
3. [3]Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2025.PMID 40013746
4. [4]Heidenreich PA, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2022.PMID 35379503
5. [5]Brieger DB, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian Clinical Guideline for Diagnosing and Managing Acute Coronary Syndromes 2025. Med J Aust, 2026.PMID 41693087
6. [6]Naidu SS, et al. SCAI SHOCK Stage Classification Expert Consensus Update: A Review and Incorporation of Validation Studies: This statement was endorsed by the American College of Cardiology (ACC), American College of Emergency Physicians (ACEP), American Heart Association (AHA), European Society of Cardiology (ESC) Association for Acute Cardiovascular Care (ACVC), International Society for Heart and Lung Transplantation (ISHLT), Society of Critical Care Medicine (SCCM), and Society of Thoracic Surgeons (STS) in December 2021. J Soc Cardiovasc Angiogr Interv, 2022.PMID 39130139
7. [7]Møller JE, et al. Microaxial Flow Pump or Standard Care in Infarct-Related Cardiogenic Shock. N Engl J Med, 2024.PMID 38587239
8. [8]Thiele H, et al. Extracorporeal Life Support in Infarct-Related Cardiogenic Shock. N Engl J Med, 2023.PMID 37634145
9. [9]Thiele H, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med, 2012.PMID 22920912
10. [10]Thiele H, et al. Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial. Lancet, 2013.PMID 24011548
11. [11]Thiele H, et al. Intraaortic Balloon Pump in Cardiogenic Shock Complicating Acute Myocardial Infarction: Long-Term 6-Year Outcome of the Randomized IABP-SHOCK II Trial. Circulation, 2019.PMID 30586721
12. [12]Thiele H, et al. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock. N Engl J Med, 2017.PMID 29083953
13. [13]Thiele H, et al. One-Year Outcomes after PCI Strategies in Cardiogenic Shock. N Engl J Med, 2018.PMID 30145971
14. [14]Zeymer U, et al. Venoarterial extracorporeal membrane oxygenation in patients with infarct-related cardiogenic shock: an individual patient data meta-analysis of randomised trials. Lancet, 2023.PMID 37643628
15. [15]De Backer J, et al. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy. Eur Heart J, 2025.PMID 40878294
16. [16]Schulz-Menger J, et al. 2025 ESC Guidelines for the management of myocarditis and pericarditis. Eur Heart J, 2025.PMID 40878297