# Allocation and prognosis of temporary mechanical circulatory support in unselected cardiogenic shock: Insights from the FRENSHOCK registry

Stéphane Manzo-Silberman, Vincent Bataille, Laurent Bonello, François Roubille, Bernard Levy, Pascal Lim, Guillaume Schurtz, Philippe Letocart, Karim Chaoui, Vincent Probst, et al.

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Stéphane Manzo-Silberman, Vincent Bataille, Laurent Bonello, François Roubille, Bernard Levy, et al. Allocation and prognosis of temporary mechanical circulatory support in unselected cardiogenic shock: Insights from the FRENSHOCK registry. Archives of cardiovascular diseases, 2025, 10.1016/j.acvd.2025.10.331. hal-05402261

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# Allocation and prognosis of temporary mechanical circulatory support in unselected cardiogenic shock: Insights from the FRENSHOCK registry

Stéphane Manzo-Silberman ¹, Vincent Bataille ², Laurent Bonello ³, François Roubille ⁴,
Bernard Levy ⁵, Pascal Lim ⁶, Guillaume Schurtz ⁷, Philippe Letocart ⁸, Karim Chaoui ⁹,
Vincent Probst ¹⁰, Emile Ferrari ¹¹, Olivier Delhaye ¹², Raphael Favory ¹³, Meyer Elbaz ¹⁴,
Edouard Gerbaud ¹⁵, Eric Bonnefoy ¹⁶, Etienne Puymirat ¹⁷, Guillaume Leurent ¹⁸,
Clement Delmas ¹⁹

¹ Sorbonne University, Institute of Cardiology, Hôpital Pitié-Salpêtrière, AP-HP, ACTION Study Group, 75013 Paris, France. Electronic address: stephane.manzosilberman@aphp.fr.

² Fédération des Services de Cardiologie, CHU de Toulouse, 31059 Toulouse, France; Association pour la Diffusion de la Médecine de Prévention, 31400 Toulouse, France.

³ Aix-Marseille Université, 13385 Marseille, France; Intensive Care Unit, Department of Cardiology, Assistance publique-Hôpitaux de Marseille, Hôpital Nord, 13385 Marseille, France; Mediterranean Association for Research and Studies in Cardiology (MARS Cardio), 13015 Marseille, France.

⁴ PhyMedExp, Cardiology Department, Université de Montpellier, Inserm, CNRS, INI-CRT, CHU de Montpellier, 34295 Montpellier, France.

⁵ Medical Intensive Care Unit, Brasbois, CHU de Nancy, 54000 Nancy, France.

⁶ Intensive Cardiac Care Unit, Cardiology Department, AP-HP, Hôpital Henri-Mondor, 94010 Créteil, France.

⁷ USIC Urgences, Centre Hémodynamique, Institut Cœur Poumon, Centre Hospitalier Universitaire Soins Intensifs de Cardiologie, CHU de Lille, University of Lille, Inserm U1167, 59000 Lille, France.

⁸ Intensive Care Unit, CH Jacques-Puel, 12027 Rodez, France.

⁹ Intensive Care Unit, CH de Cahors, 46000 Cahors, France.

¹⁰ CHU de Nantes, 44000 Nantes, France.

¹¹ Hôpital Pasteur, CHU de Nice, 06001 Nice, France; Université de Nice Sofia Antipolis, 06103 Nice, France.

¹² Hôpital Privé Le Blois Lille, 59003 Lille, France.

¹³ Lille Hopital Roger-Salengro, 59000 Lille, France.

¹⁴ Fédération des Services de Cardiologie, CHU de Toulouse, 31059 Toulouse, France.
**Keywords:**

Cardiogenic shock; Extracorporeal membrane oxygenation; Mechanical circulatory support; Microaxial flow pump; Prognosis.

**\*Corresponding author at:**

Institute of Cardiology, Hôpital Pitié-Salpêtrière, AP-HP, Sorbonne Université, 47-83, boulevard de l'Hôpital, 75651 Paris cedex 13, France.

**\*\*Co-corresponding author at:**

Intensive Cardiac Care Unit, Department of Cardiology, Toulouse University Hospital, 1, avenue Jean-Poulhès, TSA 50032, 31059 Toulouse cedex 9, France.

**E-mail addresses:**

stephane.manzosilberman@aphp.fr
(S. Manzo-Silberman),
delmas.clement@chu-toulouse.fr
(C. Delmas).

<footnote n="15">15 Intensive Cardiac Care Unit and Interventional Cardiology, CHU de Bordeaux, Hôpital Cardiologique de Haut Levêque, Institut Hospitalo-Universitaire Liryc, Electrophysiology and Heart Modeling Institute, 33604 Pessac, France; Bordeaux Cardio-Thoracic Research Centre, CRTCB, Inserm U1045, Bordeaux University, 33600 Pessac, France.</footnote>

<footnote n="16">16 Intensive Cardiac Care Unit, Cardiology Department, Hospice Civils de Lyon, Hôpital Lyon-Brom, 69500 Lyon, France.</footnote>

<footnote n="17">17 Intensive Cardiac Care Unit, Cardiology Department, AP-HP, Hôpital Européen Georges-Pompidou, 75015 Paris, France.</footnote>

<footnote n="18">18 Université Rennes 1, Department of Cardiology, CHU de Rennes, Inserm, LTSI, UMR 1099, 35000 Rennes, France.</footnote>

<footnote n="19">19 Fédération des Services de Cardiologie, CHU de Toulouse, 31059 Toulouse, France; Université Paul-Sabatier, Toulouse 3, 31000 Toulouse, France; Recherche Enseignement en Insuffisance Cardiaque Avancée Transplantation et Assistance (REICATRA), Institut Saint-Jacques, 31300 Toulouse, France. Electronic address: delmas.clement@chu-toulouse.fr.</footnote>
# Abstract

**Background:**

Patients in cardiogenic shock (CS) can benefit from temporary mechanical circulatory support (tMCS) but data in heterogeneous populations with diverse CS aetiologies are rare.

**Aims:**

To compare baseline characteristics, management and independent correlates of 30-day and 1-year mortalities between patients managed with and without tMCS for CS.

**Methods:**

The FRENSHOCK registry (NCT02703038) included 772 unselected patients with CS admitted in 49 French critical care units between April and October 2016.

**Results:**

Among 770 patients with CS and available data, 135 (17.5%) received tMCS (63 extracorporeal life support, 35 intra-aortic balloon pump, 13 micro-axial flow pump and 24 combination), of whom 69.0% were implanted during the first 24hours. Patients with tMCS were less likely to present with histories of cardiac or peripheral artery diseases or chronic renal failure. An ischaemic or mechanical complication trigger for CS tripled the probability of receiving tMCS, while increased lactate doubled the probability. Thirty-day mortality was higher among patients with versus without tMCS (34.1% vs. 24.3%; P<0.001), but after adjustment for age and CS severity (LVEF and arterial lactates at admission, noradrenaline and invasive mechanical ventilation use), the difference was no longer significant (hazard ratio: 1.37, 95% confidence interval: 0.93-2.01). Among 30-day survivors, mortality was similar regardless of initial receipt of tMCS (P=0.312).

**Conclusion:**

In real-life practice, tMCS may not be associated with improvements in 30-day or 1-year mortality in an all-comers cohort of patients with CS. However, it should be noted that there were substantial differences in patient characteristics and management between patients who received tMCS and those who did not. Additional targeted studies should help to determine more precise algorithms for granting assistance within the complex and heterogeneous population of patients with CS.
# 1. Abbreviations

AMICS acute myocardial infarction with cardiogenic shock; CCU critical care unit; CS cardiogenic shock; ECLS extracorporeal life support; HR hazard ratio; IABP intra-aortic balloon pump; LVEF left ventricular ejection fraction; AFP micro-axial flow pump; MCS mechanical circulatory support; Padjage-adjusted P-value; PCI percutaneous coronary intervention; RCT randomized controlled trial; SCAI Society for Cardiovascular Angiography and Interventions; SD standard deviation; STEMI ST-segment elevation myocardial infarction; MCS temporary mechanical circulatory support; VAD ventricular assist device

# 2. Background

Cardiogenic shock (CS) is the systemic consequence of inadequate cardiac output and this primary cardiovascular disorder can result in multi-organ dysfunction and death related to tissue hypoperfusion [1]. It is characterized by diverse presentation and severity with multiple aetiologies that seem to be linked to prognosis [2]. Whereas prognosis has been greatly improved in several cardiac conditions, such as myocardial infarction [3], CS-associated early mortality is still very high (30–50%) [4–7]. So far, only the SHOCK trial, published 25 years ago, was positive on its secondary outcomes (6-month mortality) and demonstrated the place for early revascularization in the setting of acute myocardial infarction with CS (AMICS) [8].

Despite promising haemodynamic data with a reliable patho-physiological rationale for perfusion flow improvement [9] and encouraging studies [10,11], no randomized study has demonstrated a benefit for temporary mechanical circulatory support (tMCS) in patients with CS regardless of the type (extracorporeal life support [ECLS] or intra-aortic balloon pump [IABP]) [12–17]. Recently, the Dan GerShock trial showed a potential benefit of percutaneous micro-axial flow pump (mAFP) use in a specific sub-group of patients with AMICS (ST-segment elevation myocardial infarction [STEMI] < 24 hours previously without prolonged cardiac arrest or severe right ventricular failure) [18]. However, there was a high rate of associated complications and a neutral as-treated analysis [18].

Nevertheless, in practice, tMCS is still used in more severe CS presentation refractory to usual care [19] (stages C to E of the Society for Cardiovascular Angiography and Interventions [SCAI] classification [20]) based on their immediate haemodynamic beneficial effects, despite their potential costs and high rate of complications.

Data in more heterogeneous populations and CS of diverse aetiologies are still rare. Moreover, the profile of patients included in the randomized studies does not reflect all
patients affected by CS [21]. The aim of the current study was to compare the baseline characteristics, management and independent correlates of 30-day and 1-year mortalities between patients with CS who underwent tMCS and those who did not.

# 3. Methods

## 3.1. Patient population

This study is an ancillary study of the prospective multicentre observational FRENSHOCK registry (NCT02703038), conducted in metropolitan France between April and October 2016 in 49 critical care units (CCUs) (Text A.1), the primary objective of which was to describe the characteristics, management and outcomes of patients with CS [2,22]. The study included adult patients with at least one of the following: (1) haemodynamic criteria (systolic blood pressure < 90 mmHg and/or need of vasopressors or inotropes and/or low cardiac index < 2.2 L/min/m2); (2) left and/or right heart pressure elevation and (3) signs of organ malperfusion. Exclusion criteria were refusal or inability to consent and a diagnosis of CS refuted in favour of alternative diagnoses (septic shock, refractory cardiac arrest or post-cardiotomy CS).

Written consent was obtained for all patients. Data recording, handling and storage were reviewed and approved by the Comité Consultatif sur les Traitements de l'Information en matière de Recherche dans le domaine de la Santé (French Health Research Data Processing Advisory Committee; no15.897) and the Com-mission Nationale de l'Informatique et des Libertés (French Data Protection Agency; noDR-2016-109).

## 3.2. Data collection

Data on baseline characteristics – including demographics (age, sex, body mass index, employment status), risk factors, medical history and previous medications – were collected in the FREN-SHOCK study, as well as pre-CCU course and clinical, biological and echocardiographic data within the first 24 hours after admission. CS triggers, cardiac procedures, organ replacement therapies and in-hospital complications were collected. All-cause mortality, need for heart transplant or chronic ventricular assist device (VAD) at 30-day and 1-year follow-up were also collected [2,22].
As the SCAI CS classification was not available at the time of the FRENSHOCK registry, we retrospectively determined the maximum SCAI classification stage reached during hospitalization based on the total use of vasopressors, inotropes and tMCS devices as previously described [23]. Briefly, Stage A represented patients at risk for CS, which was not applicable to our study population. Stage B, Stage C, and Stage E included patients with hypoperfusion requiring initial intervention with either one drug or one mechanical circulatory support (MCS) device. Stage D referred to patients whose condition worsens despite initial intervention, necessitating additional drugs or MCS treatment. Lastly, Stage E identified patients who deteriorated further and required maximal support, defined as needing at least two tMCS devices and two drugs during hospitalization.

### 3.3. Mechanical circulatory support

Use, type of tMCS, purpose and timing of implantation, and need for escalation and type were collected. Patients who received any tMCS at any time after admission (tMCS group) were com-pared to patients who did not receive it (no tMCS group). Diverse tMCS types and combinations were included: IABP, ECLS and/or mAFP (Impella® devices CP or 5.0, Abiomed Europe GmbH, Aachen, Germany). The choice of tMCS and the possible combination/escalation was left to the discretion of the treating heart team and adjusted to the severity of the CS and local protocols.

### 3.4. Study endpoints and follow-up

Thirty-day and 1-year all-cause mortalities were studied as primary endpoints. The secondary endpoint was the composite of death or heart replacement therapies (heart transplantation or VAD).

Follow-up was completed on the last medical interview date, the last examination date or the date when the endpoint event occurred. At 1 year, follow-up was performed using the sequential procedures previously described [24].
### 3.5. Statistical analysis

Continuous variables are reported as mean ± standard deviation (SD) or medians and interquartile ranges (IQRs) when appropriate. Categorical variables are reported as numbers and percentages.

The two groups (tMCS and no tMCS) were compared using the Student's t-test or non-parametric Mann & Whitney test for continuous variables, and using _2or Fisher's exact tests for categorical variables. Age-adjusted P-values (Padj) were computed using a logistic regression model with group (tMCS vs. no tMCS) as the dependent variable and age as an independent variable. Factors independently associated with the placement of tMCS were identified using stepwise backward multiple logistic regression, considering baseline characteristics and parameters at admission found to be associated with placement of tMCS with P < 0.15 in univariate analyses.

Finally, survival analyses were conducted using the Kaplan-Meier method to study 30-day and 1-year prognosis. Survival curves were compared using the log-rank test and age-adjusted hazard ratios (HRs) were computed using a Cox proportional hazards model. P < 0.05 was considered as statistically significant. All analyses were performed using Stata Statistical Software (Stata-Corp, 2023; Stata Statistical Software: Release 18. College Station, TX: StataCorp LLC).

## 4. Results

### 4.1. Patient characteristics

Of 777 patients in the FRENSHOCK cohort, five were duplicates and two were excluded from the current analysis due to missing records on tMCS. Among the remaining 770 patients, 135 received tMCS (17.5%). The cohort was mainly male (71.6%), with a mean ± SD age of 65.7 ± 14.9 years. Patients in the tMCS group were younger (56.9 ± 14.7 vs. 67.6 ± 14.3 years; P < 0.001; Table 1). After adjustment for age, the cardiovascular risk profiles of the two groups were generally similar, but patients in the tMCS group presented with a lower rate of cardiac disease history (37.3% vs. 60.0%; Padj < 0.001), peripheral artery disease (4.4% vs. 13.4%; Padj < 0.030) and chronic renal failure (8.1% vs. 24.1%; Padj < 0.008). Accordingly, medication use before admission was lower in the tMCS group, including beta blockers, vitamin K antagonists and furosemide.
<table><caption>**Table 1**
Baseline and CS characteristics according to tMCS use in the FRENSHOCK registry.</caption><thead><tr><th></th><th>No tMCS<br>(n=635)</th><th>tMCS<br>(n=135)</th><th>P</th><th>P<sub>adj</sub><sup>a</sup></th></tr></thead><tbody><tr><td>Male</td><td>450 (70.9)</td><td>101 (74.8)</td><td>0.356</td><td>0.545</td></tr><tr><td>Age (years)</td><td>67.6 ± 14.3</td><td>56.9 ± 14.7</td><td>&lt; 0.001</td><td>—</td></tr><tr><td>Body mass index (kg/m<sup>2</sup>)</td><td>25.7 ± 5.4</td><td>26.5 ± 6.2</td><td>0.160</td><td>0.334</td></tr><tr><td>Risk factors</td><td></td><td></td><td></td><td></td></tr><tr><td>Current smoker</td><td>159/611 (26.0)</td><td>47/127 (37.0)</td><td>0.012</td><td>0.759</td></tr><tr><td>Diabetes mellitus</td><td>181/634 (28.5)</td><td>34/134 (25.4)</td><td>0.457</td><td>0.349</td></tr><tr><td>Arterial hypertension</td><td>315 (49.6)</td><td>47/134 (35.1)</td><td>0.002</td><td>0.848</td></tr><tr><td>Dyslipidaemia</td><td>237 (37.3)</td><td>38/134 (28.4)</td><td>0.049</td><td>0.880</td></tr><tr><td>Medical history</td><td></td><td></td><td></td><td></td></tr><tr><td>History of cardiac disease</td><td>381 (60.0)</td><td>50/134 (37.3)</td><td>&lt; 0.001</td><td>&lt; 0.001</td></tr><tr><td>Ischaemic</td><td>200 (31.5)</td><td>28/134 (20.9)</td><td>0.015</td><td>0.567</td></tr><tr><td>Hypertrophic</td><td>10 (1.6)</td><td>1/134 (0.7)</td><td>0.700</td><td>0.297</td></tr><tr><td>Idiopathic</td><td>68 (10.7)</td><td>10/134 (7.5)</td><td>0.258</td><td>0.173</td></tr><tr><td>Toxic</td><td>32 (5.0)</td><td>2/134 (1.5)</td><td>0.101</td><td>0.038</td></tr><tr><td>Multisite pacing</td><td>58/634 (9.1)</td><td>5 (3.7)</td><td>0.036</td><td>0.174</td></tr><tr><td>Defibrillator</td><td>110/634 (17.4)</td><td>17 (12.6)</td><td>0.176</td><td>0.145</td></tr><tr><td>CABG</td><td>57/634 (9.0)</td><td>4 (3.0)</td><td>0.019</td><td>0.135</td></tr><tr><td>PCI</td><td>144/634 (22.7)</td><td>21 (15.6)</td><td>0.066</td><td>0.776</td></tr><tr><td>Peripheral artery disease</td><td>85/634 (13.4)</td><td>6 (4.4)</td><td>0.003</td><td>0.030</td></tr><tr><td>Ischaemic stroke</td><td>53/634 (8.4)</td><td>9 (6.7)</td><td>0.512</td><td>0.955</td></tr><tr><td>Chronic renal failure</td><td>153/634 (24.1)</td><td>11 (8.1)</td><td>&lt; 0.001</td><td>0.008</td></tr><tr><td>COPD</td><td>46/634 (7.3)</td><td>4 (3.0)</td><td>0.066</td><td>0.252</td></tr><tr><td>Active neoplasia</td><td>48/634 (7.6)</td><td>3 (2.2)</td><td>0.023</td><td>0.061</td></tr><tr><td>Previous medications</td><td></td><td></td><td></td><td></td></tr><tr><td>Aspirin</td><td>238/634 (37.5)</td><td>49/134 (36.6)</td><td>0.833</td><td>0.173</td></tr><tr><td>P2Y12 inhibitor</td><td>96/634 (15.1)</td><td>29/134 (21.6)</td><td>0.064</td><td>0.007</td></tr><tr><td>Statin</td><td>246/634 (38.8)</td><td>38/134 (28.4)</td><td>0.023</td><td>0.718</td></tr><tr><td>Betablocker</td><td>277/634 (43.7)</td><td>37/134 (27.6)</td><td>0.001</td><td>0.014</td></tr><tr><td>Vitamin K antagonist</td><td>152/634 (24.0)</td><td>13/134 (9.7)</td><td>&lt; 0.001</td><td>0.009</td></tr><tr><td>Direct oral anticoagulant</td><td>49/634 (7.7)</td><td>7/134 (5.2)</td><td>0.311</td><td>0.429</td></tr><tr><td>ACEI or ARB or ARNI</td><td>253/634 (39.9)</td><td>38/134 (28.4)</td><td>&lt; 0.001</td><td>0.243</td></tr><tr><td>Furosemide</td><td>338/634 (53.3)</td><td>37/134 (27.6)</td><td>&lt; 0.001</td><td>&lt; 0.001</td></tr><tr><td>Aldosterone antagonist</td><td>92/634 (14.5)</td><td>16/134 (11.9)</td><td>0.437</td><td>0.254</td></tr><tr><td>Triggers</td><td></td><td></td><td></td><td></td></tr><tr><td>Ischaemic</td><td>212 (33.4)</td><td>77 (57.0)</td><td>&lt; 0.001</td><td>&lt; 0.001</td></tr><tr><td>Mechanical</td><td>16 (2.5)</td><td>8 (5.9)</td><td>0.053</td><td>0.009</td></tr><tr><td>Ventricular arrhythmia</td><td>75 (11.8)</td><td>23 (17.0)</td><td>0.098</td><td>0.196</td></tr><tr><td>Atrial arrhythmia</td><td>92 (14.5)</td><td>16 (11.9)</td><td>0.423</td><td>0.399</td></tr><tr><td>Conductive disorders</td><td>18 (2.8)</td><td>0 (0.0)</td><td>0.055</td><td>—</td></tr><tr><td>Infectious</td><td>83 (13.1)</td><td>12 (8.9)</td><td>0.180</td><td>0.180</td></tr><tr><td>Non-compliance</td><td>29 (4.6)</td><td>1 (0.7)</td><td>0.037</td><td>0.064</td></tr><tr><td>Iatrogenic</td><td>55 (8.7)</td><td>6 (4.4)</td><td>0.099</td><td>0.053</td></tr><tr><td>Other</td><td>89 (14.0)</td><td>13 (9.6)</td><td>0.172</td><td>0.007</td></tr><tr><td>None/undefined</td><td>103 (16.2)</td><td>8 (5.9)</td><td>0.002</td><td>0.008</td></tr><tr><td>Admission unit</td><td></td><td></td><td>0.355</td><td>0.784</td></tr><tr><td>Intensive cardiac care unit</td><td>347/489 (71.0)</td><td>67/101 (66.3)</td><td></td><td></td></tr><tr><td>Intensive care unit</td><td>142/489 (29.0)</td><td>34/101 (33.7)</td><td></td><td></td></tr><tr><td>Clinical presentation at admission</td><td></td><td></td><td></td><td></td></tr><tr><td>Heart rate (bpm)</td><td>94 ± 30 (n=634)</td><td>102 ± 27 (n=133)</td><td>0.007</td><td>0.086</td></tr><tr><td>SBP (mmHg)</td><td>102 ± 25 (n=634)</td><td>99 ± 24 (n=134)</td><td>0.248</td><td>0.100</td></tr><tr><td>DBP (mmHg)</td><td>63 ± 17 (n=634)</td><td>63 ± 17 (n=133)</td><td>0.856</td><td>0.141</td></tr><tr><td>Sinus rhythm</td><td>317/632 (50.2)</td><td>81/134 (60.4)</td><td>0.030</td><td>0.234</td></tr><tr><td>Mottling</td><td>202/543 (37.2)</td><td>54/115 (47.0)</td><td>0.051</td><td>0.026</td></tr><tr><td>Cardiac arrest</td><td>52 (8.2)</td><td>27 (20.0)</td><td>&lt; 0.001</td><td>0.002</td></tr><tr><td>Left heart failure signs</td><td>451/634 (71.1)</td><td>101/134 (75.4)</td><td>0.322</td><td>0.294</td></tr><tr><td>Right heart failure signs</td><td>331/633 (52.3)</td><td>46/133 (34.6)</td><td>&lt; 0.001</td><td>0.001</td></tr><tr><td>Blood tests at admission</td><td></td><td></td><td></td><td></td></tr><tr><td>Sodium (mmol/L)</td><td>135 ± 6 (n=625)</td><td>135 ± 6 (n=133)</td><td>0.693</td><td>0.522</td></tr><tr><td>eGFR (mL/min/1.73 m<sup>2</sup>)</td><td>47.6 ± 25.7 (n=617)</td><td>59.2 ± 28.9 (n=132)</td><td>&lt; 0.001</td><td>0.139</td></tr><tr><td>Bilirubin (mg/L)</td><td>17 (10-31) (n=449)</td><td>13 (8-21) (n=93)</td><td>0.013</td><td>0.007</td></tr><tr><td>Haemoglobin (g/dL)</td><td>12.5 ± 2.3 (n=619)</td><td>12.7 ± 2.6 (n=133)</td><td>0.272</td><td>0.898</td></tr><tr><td>Arterial blood lactates (mmol/L)</td><td>3.0 (2.0-4.0) (n=557)</td><td>3.4 (2.1-6.0) (n=125)</td><td>&lt; 0.001</td><td>&lt; 0.001</td></tr><tr><td>ASAT (IU/L)</td><td>81 (38-273) (n=454)</td><td>145 (46-522) (n=92)</td><td>0.009</td><td>0.007</td></tr><tr><td>ALAT (IU/L)</td><td>54 (25-170) (n=465)</td><td>82 (45-214) (n=92)</td><td>0.010</td><td>0.106</td></tr><tr><td>Echocardiographic evaluation</td><td></td><td></td><td></td><td></td></tr><tr><td>LVEF (%)</td><td>26.9 ± 13.4 (n=629)</td><td>23.3 ± 12.9 (n=132)</td><td>0.006</td><td>0.087</td></tr><tr><td>Severe mitral regurgitation</td><td>91/605 (15.0)</td><td>16/126 (12.7)</td><td>0.499</td><td>0.357</td></tr><tr><td>Severe aortic stenosis</td><td>35/625 (5.6)</td><td>1/132 (0.8)</td><td>0.018</td><td>0.165</td></tr><tr><td>Severe aortic regurgitation</td><td>9/620 (1.5)</td><td>1/133 (0.8)</td><td>1.000</td><td>0.416</td></tr><tr><td>SCAI Shock Score</td><td>(n=634)</td><td></td><td>&lt; 0.001</td><td>&lt; 0.001</td></tr></tbody></table>
<table><caption>Table 1 (Continued)</caption><thead><tr><th></th><th>No tMCS<br>(n=635)</th><th>tMCS<br>(n=135)</th><th>P</th><th>P<sub>adj</sub><sup>a</sup></th></tr></thead><tbody><tr><td>B</td><td>63 (9.9)</td><td>0 (0.0)</td><td></td><td></td></tr><tr><td>C</td><td>272 (42.9)</td><td>5 (3.7)</td><td></td><td></td></tr><tr><td>D</td><td>299 (47.2)</td><td>106 (78.5)</td><td></td><td></td></tr><tr><td>E</td><td>0 (0.0)</td><td>24 (17.8)</td><td></td><td></td></tr></tbody></table>

Data are expressed as mean ± standard deviation, number (%) or median (interquartile range). ACEI: angiotensin-converting enzyme inhibitor; ALAT: alanine aminotransferase; ARB: angiotensin-receptor blocker; ARNI: angiotensin receptor-neprilysin inhibitor; ASAT: aspartate aminotransferase; CABG: coronary artery bypass graft; COPD: chronic obstructive pulmonary disease; CS: cardiogenic shock; DBP: diastolic blood pressure; eGFR: estimated glomerular filtration rate; LVEF: left ventricular ejection fraction; PCI: percutaneous coronary intervention; SBP: systolic blood pressure; SCAI: Society for Cardiovascular Angiography and Interventions; tMCS: temporary mechanical circulatory support.

## 4.2. Presentation and initial management

Patients in the tMCS group mainly had an ischaemic trigger (57.0%), compared with only 33.4% of the no tMCS group (Padj< 0.001; Table 1). Similarly, mechanical triggers were more common in the tMCS group (5.9% vs. 2.5%; Padj= 0.009), but patients with an unrecognized CS trigger were less likely to receive tMCS (5.9% vs. 16.2%; Padj= 0.008). Patients in the tMCS group mainly had SCAI D (78.5%) or SCAIE (17.5%) severity levels, while those in the no tMCS group were distributed more evenly between levels C (42.9%) and D (47.2%), with no level E and 9.9% level B (Table 1).

At admission, resuscitated cardiac arrest and mottling were more prevalent in the tMCS group, and lactates were higher (Table 1). Interestingly, left ventricular ejection fraction (LVEF) and severe valvular disease did not differ significantly between groups after age adjustment.

As reported in Table 2, tMCS use was associated with mechanical and ischaemic CS triggers (OR: 3.17, 95% CI: 1.00–9.99; P = 0.049 and OR: 2.95, 95% CI: 1.87–4.64; P < 0.001, respectively). tMCS use was also associated with more severe tissue malperfusion, as indicated by the highest tertile of lactate levels (OR: 2.49, 95% CI: 1.41–4.39; P = 0.002). Conversely, peripheral artery disease (OR: 0.34, 95% CI: 0.13–0.86; P = 0.022) and ongoing furosemide treatment (OR: 0.51, 95% CI: 0.32–0.81; P = 0.004) were associated with a lower use of tMCS.

## 4.3. tMCS type, combination and delay

Among the 135 patients with tMCS, 111 (82.2%) only had one tMCS type: 63 (46.7%) ECLS, 13 (9.6%) Impella® and 35 (25.9%) IABP. The remaining 24 had a combination of at least two types of tMCS as an escalation strategy or for left ventricular unloading under ECLS support for 22 patients (details in Table A.1).

<footnote>a Age-adjusted.</footnote>
tMCS devices were placed on the same day as admission in 69.0% of patients. tMCS was mainly used as a bridge to recovery strategy (64%) in 63.8%. A comparison of the characteristics of tMCS recipients according to the timing of implantation is provided in Table A.2. Patients in whom a tMCS was implanted during the first 24 hours were more frequently smokers (43.2% vs. 20.0%; P = 0.012) and more often presented with an ischaemic CS trigger (67.4% vs. 35.0%; P = 0.001), but were less likely to have a history of previous cardiac disease (22.5% vs. 70.0%; P < 0.001) and were taking less cardiac medication at admission. Patients with early tMCS also presented with a higher mean ± SD heart rate (105 ± 29 vs. 95 ± 22 bpm; P = 0.048), more cardiac arrest (28.1% vs. 5.0%; P = 0.003) and less right heart failure signs (28.4% vs. 47.5%; P = 0.035).

<table><caption>**Table 2**
Factors associated with use of tMCS in the FRENSHOCK registry.</caption><thead><tr><th></th><th>OR (95% CI)</th><th>P</th></tr></thead><tbody><tr><td>Age (per 1-year increase)</td><td>0.95 (0.94-0.96)</td><td>&lt; 0.001</td></tr><tr><td>Peripheral artery disease</td><td>0.34 (0.13-0.86)</td><td>0.022</td></tr><tr><td>Ischaemic trigger</td><td>2.95 (1.87-4.64)</td><td>&lt; 0.001</td></tr><tr><td>Mechanical trigger</td><td>3.17 (1.00-9.99)</td><td>0.049</td></tr><tr><td>Ongoing anti-P2Y12 treatment</td><td>1.88 (1.09-3.25)</td><td>0.023</td></tr><tr><td>Ongoing furosemide treatment</td><td>0.51 (0.32-0.81)</td><td>0.004</td></tr><tr><td>Initial LVEF (per 1% increase)</td><td>0.97 (0.96-0.99)</td><td>0.003</td></tr><tr><td>Lactates</td><td></td><td></td></tr><tr><td>Tertile 1</td><td>Reference</td><td></td></tr><tr><td>Tertile 2</td><td>1.79 (1.03-3.11)</td><td>0.040</td></tr><tr><td>Tertile 3</td><td>2.49 (1.41-4.39)</td><td>0.002</td></tr></tbody></table>

CI: confidence interval; LVEF: left ventricular ejection fraction; OR: odds ratio; tMCS: temporary mechanical circulatory support.

## 4.4. In-hospital outcomes

Patients in the tMCS group were more likely to receive norepinephrine (75.4% vs. 48.7%; Padj< 0.001), epinephrine (29.1% vs. 8.9%; Padj< 0.001) or a combination of catecholamines (69.4% vs. 40.8%; Padj< 0.001) than those in the no tMCS group, but similarly likely to receive dobutamine (Table 3). Coronary angiography and subsequent percutaneous coronary intervention (PCI) were more often performed in the tMCS group (67.4% vs. 48.2%; Padj< 0.001 and 43.0% vs. 26.3%; Padj< 0.001, respectively).

In-hospital complications were significantly more prevalent in the tMCS group except for stroke (Table 3). Patients in the tMCS group were four times more likely to have bleeding (34.9% vs. 8.6%; Padj< 0.001), seven times more likely to require blood transfusion (28.8% vs. 4.1%; Padj< 0.001), six times more likely to have clinically relevant haemolysis (18.8% vs. 3.0%; Padj< 0.001) and more than 10 times more likely to have limb ischaemia (3.1% vs. 0.2%; Padj< 0.021). Moreover, patients in the tMCS group had a higher rate of sepsis with a positive blood test (28.8% vs. 9.9%; Padj< 0.001).
<table><caption>**Table 3**
In-hospital management, left ventricular function assessment and discharge mode according to the use of tMCS in the FRENSHOCK registry.</caption><thead><tr><th></th><th>No tMCS<br>(n=635)</th><th>tMCS<br>(n=135)</th><th>P</th><th>P<sub>adj</sub><sup>a</sup></th></tr></thead><tbody><tr><td><strong>Medications used</strong></td><td></td><td></td><td></td><td></td></tr><tr><td>Diuretics</td><td>532/633 (84.0)</td><td>100/134 (74.6)</td><td>0.009</td><td>0.041</td></tr><tr><td>Dobutamine</td><td>513/633 (81.0)</td><td>118/134 (88.1)</td><td>0.053</td><td>0.075</td></tr><tr><td>Norepinephrine</td><td>308/633 (48.7)</td><td>101/134 (75.4)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Epinephrine</td><td>56/633 (8.9)</td><td>39/134 (29.1)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Norepinephrine + dobutamine</td><td>258/633 (40.8)</td><td>93/134 (69.4)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Levosimendan</td><td>38/633 (6.0)</td><td>19/134 (14.2)</td><td>0.001</td><td>0.008</td></tr><tr><td>Antiarrhythmic</td><td>237/633 (37.4)</td><td>61/134 (45.5)</td><td>0.081</td><td>0.046</td></tr><tr><td>Transfusion</td><td>71/632 (11.2)</td><td>57/134 (42.5)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td><strong>Organ replacement therapies</strong></td><td></td><td></td><td></td><td></td></tr><tr><td>Mechanical circulatory support</td><td></td><td></td><td></td><td></td></tr><tr><td>IABP</td><td>-</td><td>48 (35.6)</td><td>-</td><td>-</td></tr><tr><td>Impella</td><td>-</td><td>26 (19.3)</td><td>-</td><td>-</td></tr><tr><td>ECLS</td><td>-</td><td>85 (63.0)</td><td>-</td><td>-</td></tr><tr><td>Renal replacement therapy</td><td>79 (12.4)</td><td>43 (31.9)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Mechanical ventilation</td><td>296 (46.8)</td><td>113 (84.3)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Invasive mechanical ventilation</td><td>186 (29.4)</td><td>105 (78.4)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td><strong>Invasive cardiology</strong></td><td></td><td></td><td></td><td></td></tr><tr><td>Coronary angiography</td><td>306 (48.2)</td><td>91 (67.4)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Culprit lesion</td><td>184/240 (76.7)</td><td>71/76 (93.4)</td><td>0.001</td><td>0.004</td></tr><tr><td>Any PCI</td><td>167 (26.3)</td><td>58 (43.0)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Right heart catheterization</td><td>92 (14.5)</td><td>29 (21.6)</td><td>0.040</td><td>0.511</td></tr><tr><td>Pacemaker implantation</td><td>32/600 (5.3)</td><td>3/131 (2.3)</td><td>0.139</td><td>0.301</td></tr><tr><td>Defibrillator implantation</td><td>29/600 (4.8)</td><td>8/131 (6.1)</td><td>0.431</td><td>0.627</td></tr><tr><td><strong>Complications</strong></td><td></td><td></td><td></td><td></td></tr><tr><td>Bleeding</td><td>52/608 (8.6)</td><td>44/126 (34.9)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Blood transfusion</td><td>25/605 (4.1)</td><td>36/125 (28.8)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Stroke</td><td>29/610 (4.8)</td><td>7/127 (5.5)</td><td>0.719</td><td>0.638</td></tr><tr><td>Haemolysis<sup>b</sup></td><td>18/606 (3.0)</td><td>24/128 (18.8)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Sepsis with positive blood test</td><td>60/604 (9.9)</td><td>38/132 (28.8)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Limb ischaemia</td><td>1/602 (0.2)</td><td>4/130 (3.1)</td><td>&lt;0.001</td><td>0.021</td></tr><tr><td><strong>At discharge</strong></td><td></td><td></td><td></td><td></td></tr><tr><td>LVEF (%)</td><td>34.0 ± 13.7 (n=374)</td><td>40.9 ± 17.3 (n=64)</td><td>&lt;0.001</td><td>0.006</td></tr><tr><td>Change in LVEF (%)</td><td>6.8 ± 12.1 (n=371)</td><td>18.0 ± 20.5 (n=81)</td><td>&lt;0.001</td><td>&lt;0.001</td></tr><tr><td>Length of stay in CCU (days)</td><td>11 (7-21) (n=372)</td><td>20 (8-29) (n=67)</td><td>&lt;0.001</td><td>0.001</td></tr><tr><td>Length of stay in hospital (days)</td><td>16 (11-25) (n=369)</td><td>24 (15-52) (n=66)</td><td>&lt;0.001</td><td>0.001</td></tr><tr><td>Discharge mode</td><td>0.156</td><td>0.078</td><td></td><td></td></tr><tr><td>Home</td><td>150 (41.1)</td><td>21 (31.8)</td><td></td><td></td></tr><tr><td>Rehabilitation or transferred</td><td>215 (58.9)</td><td>45 (68.2)</td><td></td><td></td></tr><tr><td><strong>Treatments among in-hospital survivors</strong></td><td></td><td></td><td></td><td></td></tr><tr><td>ACEI or ARB or ARNI</td><td>303/460 (65.9)</td><td>49/83 (59.0)</td><td>0.230</td><td>0.272</td></tr><tr><td>Betablocker</td><td>258/460 (56.1)</td><td>48/83 (57.8)</td><td>0.768</td><td>0.923</td></tr><tr><td>Aldosterone antagonist</td><td>144/460 (31.3)</td><td>26/83 (31.3)</td><td>0.997</td><td>0.554</td></tr><tr><td>Furosemide</td><td>312/460 (67.8)</td><td>34/83 (41.0)</td><td>&lt;0.001</td><td>0.001</td></tr><tr><td>Registration on transplant waiting list</td><td>21/514 (4.1)</td><td>19/108 (17.6)</td><td>&lt;0.001</td><td>0.004</td></tr></tbody></table>

Data are expressed as mean ± standard deviation, number (%) or median (interquartile range). ACEI: angiotensin-converting enzyme inhibitor; ARB: angiotensin-receptor blocker; CCI: critical care unit; ECLS: extracorporeal life support; IABP: intra-aortic balloon pump; LVEF: left ventricular ejection fraction; PCI: percutaneous coronary intervention; tMCS: temporary mechanical circulatory support.

At discharge, patients in the tMCS group presented with a significantly higher mean ± SD LVEF (40.9% ± 17.3 vs. 34.0% ± 13.7; Padj= 0.006) and had a larger in-hospital improvement in LVEF(+18.0% vs. +6.8%; Padj< 0.001) (Table 3). Median (IQR) lengths of stay, both in the CCU and the hospital, were significantly longer for patients in the tMCS group (20 [8–29] vs. 11 [7–21] days; Padj= 0.001 and 24 [15–52] vs. 16 [11–25] days; Padj=0.001). Patients in the tMCS group were numerically less likely to be discharged home than those without tMCS (31.8% vs. 41.1%; Padj= 0.078) and more likely to be registered on the transplant waiting list during hospitalization (17.6% vs. 4.1%; Padj= 0.004) (Table 3).

Regarding medications at discharge, we did not find any significant differences between groups apart from a less frequent prescription of furosemide in the tMCS group (41.0% vs. 67.8%; Padj= 0.001).

<footnote>a Age-adjusted.</footnote>

<footnote>b Clinically relevant.</footnote>

<footnote>c From admission to discharge.</footnote>
4.5. 30-day and 1-year outcomes

At 30 days, we found that mortality was significantly higher in the tMCS vs. no tMCS group (34.1% vs. 24.3%; P = 0.019; Fig. 1A). After adjustment for age, the difference remained significant (Padj< 0.001). The composite 30-day endpoint combining death, heart transplant and VAD was also higher in the tMCS group (48.2% vs. 27.6%; P < 0.001; Fig. 1B). However, after adjustment for age and CS severity (LVEF and arterial lactates at admission, noradrenaline and invasive mechanical ventilation use), the difference was no longer significant (HR: 1.37, 95% CI: 0.93–2.01).

<figure><img src="image_2.png" /><figcaption>Fig. 1. Kaplan-Meier curves according to the in-hospital use of tMCS for A. 30-day all-cause mortality and B. 30-day composite of all-cause death, heart transplant or VAD. CI: confidence interval; HR: hazard ratio; tMCS: temporary mechanical circulatory support; VAD: chronic ventricular assist device.</figcaption></figure>

In this landmark Kaplan-Meier analysis of 1-year mortality, patients who required tMCS
showed significantly higher early (≤ 1 month) mortality (P = 0.019), but similar longer-
term(1–12 months) survival compared with those managed without MCS (P = 0.312) (Fig. 2).
<figure><img src="image_3.png" /><figcaption>**Fig. 2.** Early (30-day) and long-term (1-year) all-cause mortality by Kaplan-Meier landmark analysis according to the in-hospital use of tMCS. tMCS: temporary mechanical circulatory support.</figcaption></figure>

**4.6. Sensitivity analysis**

After excluding the 35 patients for whom only an IABP was used, comparison of 30-day mortality between the two groups did not change (P = 0.008), nor did the 30-day mortality, heart transplantation or VAD rate: the tMCS group still showed a higher event rate (P < 0.001) compared to the no tMCS group (data not shown).

**5. Discussion**

The main findings of this analysis of the FRENSHOCK registry areas follows (Central Illustration): (1) in real-life practice, tMCS was used in 17.5% of a large unselected CS population in tertiary and non-tertiary centres; (2) the aetiology of CS influenced the use of tMCS, with ischaemic CS more prone to received tMCS; (3) resuscitated cardiac arrest, mottling and high lactate levels increased the use of tMCS; (4) ECLS was the most often used support; (5) tMCS devices were mostly placed early, during the first 24 hours of admission, as a bridge to recovery strategy; and (6) the use of tMCS did not improve 30-day or 1-year prognosis and was associated with a higher rate of in-hospital complications.5.1. tMCS allocation The 17.5% use of tMCS in the FRENSHOCK cohort represents a relatively high percentage of tMCS employment due to the unselected CS population. Von Lewinski et al. [25] reported 19% of MCS use in their cohort, including 69% of AMICS, as compared with only one third of ischaemic CS triggers in our population. Interestingly, in an international
multicentre retrospective cohort of non-acute ischaemic CS, Schrage et al. reported a very high rate of tMCS (ECLS and/or mAFP) use of 43% [26], highlighting a different use in a much more specific context. Patients were included in expert CS centres and were mainly SCAI C (51.6%), decompensated ischaemic cardiomyopathy (63.0%) and higher rate of already optimal therapy as implantable defibrillator (26.0%) and/or resynchronization therapy (13.7%) than in our population. These real-life cohorts are currently the only sources of data for non-AMICS patients since non-AMICS patients were often excluded from previous randomized studies [26,27], explaining why allocation of tMCS remains controversial in this specific subgroup. This real-life practice high-lighted the intriguing balance between patient's profiles and CS severity that intervene in the choice process of tMCS allocation.

In unselected AMICS, the routine use of ECLS was not associated with a 30-day mortality improvement compared to the standard of care (209 vs. 208 patients) in a population of severe CS (lactate6.9 mmol/L) with frequent cardiac arrest (77.7%) and prolonged resuscitation (median time 20 min) in the ECLS SHOCK trial [15]. However, the use of a percutaneous mAFP (Impella CP®) was associated with a significant reduction in all-cause mortality at 180days (45.8% vs. 58.5%; P = 0.04) at the cost of a higher incidence of adverse events (24.0% vs. 6.2%) compared with the standard of care in 355 STEMI-related CS undergoing PCI in the recent DanGer Shock trial [17]. Differences in included patients (exclusion of prolonged cardiac arrest, only STEMI patients), timing of inclusion (before PCI 84.8% vs. 21.1%), CS-associated management and device may explain these opposite results [28,29] and do not make a direct comparison of the two devices (mAFP and ECLS) possible. Once again, these results highlight the challenges associated with performing randomized controlled trials (RCTs) of tMCS in patients experiencing AMICS [30].

In the absence of positive RCTs to support the decision to implant tMCS and despite more rigorous CS classification [5], the decision-making process includes conflicting criteria: patients should be severe enough to require circulatory support but strong enough to overcome potential complications [31]. Our study perfectly reflects this ambiguous situation and thus provides innovative information on the very heterogeneous population of unselected CS undergoing tMCS implantation. In this setting, stratification and the chosen risk prediction model can lead to opposite conclusions [32]. Thanks to improved determination of characteristics directly related to the patient, the best tMCS candidates who will derive the maximum expected benefit could be selected [33].

## 5.2. tMCS timing and combination

Implantation of tMCS appeared early in the care pathway strategy in our cohort, mainly during the first 2 days. The prompt mechanical support use in CS is now a cornerstone of
treatment. Early implementation of the device may optimize the benefit of its support and thus improve survival with both ECLS [34] and a MFP[35] and even their combination [36], as suggested by recent RCT protocols in AMICS in DanGer Shock [18]. DanGer Shock stressed initiation as early as possible, even before PCI or during the index catheterization as had already been suggested in a meta-analysis [37]. In a recent retrospective study of patients with CS treated with ECLS, the timing of device implantation within 24 hours after CS onset was not associated with mortality [38]. Our cohort reflects the earlier use of tMCS in ischaemic-triggered CS compared to other CS aetiologies, mainly decompensated chronic cardiomyopathy, for which circulatory support was often delayed by more than 48 hours, accounting for more insidious onset of the shock than in the case of AMICS [39]. Preferential choice of ECLS as tMCS reflected the habits of the teams in France but also the budgetary constraints, which the Impella® device still faces in our country in the absence of dedicated reimbursement. In an Austrian cohort, Von Lewinski et al. reported similar use between ECLS and mAFP [25].

### 5.3. Prognosis

In this all-comers CS cohort, the 30-day mortality rate was higher in the tMCS group than in the standard therapy alone group in non-adjusted analysis (34.1% for tMCS and 24.3% for no-tMCS). Comparison of the 30-day all-cause mortality rates with those observed in the randomized study of the highly selected AMICS population of the Danger Shock [18] (39.6% for a MFP and 46.6% for control) and those of ECLS Shock studies [15] (47.8% for ECLS vs 49.0% in control) [28], highlights the very low mortality rate in our standard group and the quite comparable rate for the tMCS group. These results can be explained by the broad spectrum of CS aetiologies of our unselected CS population, their less severe presentation (lactate at admission 3.4 mmol/L in our cohort vs. 4.6 and 6.9 mmol/L, respectively, for DanGer Shock and ECLS SHOCK patients) and the inherent limitation of our observational design, but probably also confirmed the very specific entity of AMICS.

This underscores the need for careful, critical analysis of the various populations analysed and the different study results. Well-defined criteria, combined with a clear and precise treatment protocol, will enable us to develop strategies that are beneficial in terms of mortality reduction. A fortiori in the case of CS, an extremely heterogeneous entity in terms of aetiology, adaptive response and level of haemodynamic and organ damage, striv-ing for a univalent approach seems increasingly illusory. For this challenging setting of CS with heterogeneous aetiologies, various patient profiles, stages of heart failure and end-organ impact, the role of the multidisciplinary heart team is crucial in advocating the best tailored strategy [40]. Defining the target population must be the first key step in an algorithm predefined by expert multidisciplinary teams. This algorithm must then be adapted to the different endotypes, based on the results of reliable large randomized studies [41,42].
## 5.4. Limitations

Some of the limitations of the FRENSHOCK registry have been already reported [2,24,43]. The major limitation is that data from patients who died before informed consent was obtained were not collected and recorded in the database. This could be a source of bias, resulting in an underestimation of severity and mortality. Further, detailed aetiology of CS was not recorded in the electronic report form, thus limiting a more detailed analysis of CS triggers and their role in tMCS allocation. Likewise, biological data were the ones first available for the patient upon inclusion. In some cases, due to the severity of the shock, patients were already being treated by inotropic support, introducing another bias as the real baseline biological samples were not feasible/available. Another limitation that may reduce the robustness of the conclusions and restrict their generalizability comes from the choice to consider the different tMCS (ECLS, mAFP and IABP) together despite their differences in terms of flow rate, mechanism of action, degree of invasiveness and side effects. This choice is an obvious limitation, but the size of our population did not allow separate analysis.

Finally, our study was designed and patients were included before the publication and consensual adoption of the SCAI score [20]. We assigned post-hoc SCAI scoring [6] for better readability and comparability of the analyses reported. However, this retro-spective classification should be interpreted with caution as use of tMCS served as a severity criterion as well as targeted therapeutics. The ‘judge and party’ roles of tMCS have been acknowledged and reflects the complexity of CS evaluation and treatment.

# 6. Conclusions

This all-comers cohort of CS of various aetiologies provides an original insight into the real-world use of tMCS. Early use of tMCS was not associated with improved 30-day or 1-year mortality, but it should be remembered that patients were selected for tMCS or not depending on their characteristics. However, this heterogeneous population reflects the real-life profiles of patients encountered in practice. Compared to RCTs, we acknowledge lower mortality rates with similar complication rates in an unselected CS population. With the complexity of CS recognized, and the need for in-depth phenotyping highlighted, it appears vital not only to define decision-making algorithms precisely, but also to tailor the therapeutic tools employed (Central Illustration).
<figure><img src="image_4.png" /></figure>

**Central Illustration.** Allocation and prognosis of tMCS in unselected CS: Insights from the FRENSHOCK registry. CCU: critical care unit; CI: confidence interval; CS: cardiogenic shock; ECLS: extracorporeal life support; IABP: intra-aortic balloon pump; LVEF: left ventricular ejection fraction; mAFP: micro-axial flow pump; OR: odds ratio; PCI: percutaneous coronary intervention; tMCS: temporary mechanical circulatory support; VAD: ventricular assist device.

## Sources of funding

This study was sponsored by the Fédération Française de Cardiologie and funded by unrestricted grants from Daiichi-Sankyo, Orion pharma and Maquet SAS.

## Disclosure of interest

S.M.-S. has received consulting fees from Bayer, Organon and Exeltis; lecture fees from Bayer, BMS, Exeltis and Organon; and has served on the adjudication board for a study for Biotronik.G.L. reports proctoring activity, lecture and consultant fees from Abbott Medical and Edwards Life science. E.G. reports, outside the submitted work, personal fees and/or non-financial support from Terumo, Novo Nordisk, Abbott Medical, Servier and AOP Orphan Pharmaceuticals France. C.D. has received consulting fees from Abiomed, Abbott and Moderna; lecture fees from Abiomed, Abott, AstraZeneca, Bayer, Orion and Servier. All authors declare that they have no competing interest.
Acknowledgements

FRENSHOCK is a registry of the French Society of Cardiology, managed by its Emergency and Acute Cardiovascular Care Working Group. Our thanks go to all the devoted personnel of Société française de cardiologie who actively participate in the upkeep of the registry, especially Nicole Naccache, Elodie Drouet and TessaBergot. The authors are deeply indebted to all the physicians who took care of the patients at the participating institutions (complete list of investigators in Text A.1).

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