Cardiogenic shock future or investigational therapies
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] James Nasr[3]
Cardiogenic shock future or investigational therapies
Overview
Future and investigational therapies for cardiogenic shock include emerging mechanical circulatory support strategies, investigational pharmacologic agents, regionalized shock systems, artificial intelligence-based decision support, phenotype-based treatment selection, extracorporeal blood purification, regenerative therapies, xenotransplantation, and next-generation artificial heart platforms. These approaches are not established standard of care unless otherwise specified, and most require prospective validation before routine clinical use.[1][2]
The DanGer Shock trial provided randomized evidence that Impella CP reduced mortality in selected patients with STEMI-related cardiogenic shock, but its results should not be extrapolated to all cardiogenic shock etiologies, SCAI stages, post-cardiac arrest states, or institutional settings.[3] Current standard medical therapy, revascularization, temporary mechanical circulatory support indications, and procedural management are addressed in the medical therapy and surgery microchapters.
Investigational mechanical circulatory support strategies
Microaxial flow pump trials
Ongoing and planned trials are evaluating whether earlier or higher-flow microaxial left ventricular unloading improves outcomes in selected cardiogenic shock or high-risk revascularization populations.
| Trial or program | Population | Intervention | Clinical question |
|---|---|---|---|
| RECOVER IV | STEMI complicated by cardiogenic shock | Impella 5.5 placed before PCI | Whether early higher-flow LV unloading before PCI improves myocardial recovery and clinical outcomes in AMI-related cardiogenic shock.[4] |
| PROTECT IV | Complex coronary artery disease with severely reduced LVEF and excessive surgical risk | Impella CP-supported PCI versus PCI with or without IABP | Whether hemodynamic support improves long-term outcomes during high-risk PCI. This trial is not a cardiogenic shock trial but may inform prevention of periprocedural hemodynamic collapse.[5] |
DanGer Shock showed that Impella CP reduced 180-day all-cause mortality in selected STEMI-related cardiogenic shock patients without anoxic brain injury, but increased bleeding, limb ischemia, and renal replacement therapy.[3] Future microaxial pump trials must clarify optimal timing, device selection, vascular complication mitigation, and generalizability to NSTEMI-related shock, heart failure-related shock, post-cardiac arrest coma, and lower-volume centers.
LV unloading during VA-ECMO
VA-ECMO can increase LV afterload and may worsen LV distension, pulmonary edema, or myocardial recovery in selected patients. LV unloading with Impella during VA-ECMO, sometimes termed ECPELLA, is being evaluated as an investigational strategy.
The REVERSE trial is a single-center randomized trial with planned enrollment of 96 patients comparing VA-ECMO alone with VA-ECMO plus early Impella CP LV venting within 10 hours of ECMO initiation in cardiogenic shock from multiple etiologies. The primary endpoint is recovery from cardiogenic shock at 30 days, defined as survival free from mechanical circulatory support, transplant, or inotropic support.[4]
A meta-analysis of 7 observational studies including 1,054 patients found that ECPELLA was associated with lower short-term mortality than VA-ECMO alone (RR 0.89; 95% CI 0.80-0.99), but with higher rates of hemolysis, limb ischemia, and renal replacement therapy.[6] Randomized data are needed before routine ECPELLA can be considered evidence-based.
Routine VA-ECMO and ongoing ECMO trials
An individual-patient-data meta-analysis of four randomized VA-ECMO trials including 1,199 patients found no survival benefit for routine VA-ECMO in AMI-related cardiogenic shock at 6-month follow-up. Future MCS research should therefore focus on patient selection, LV unloading strategies, timing, complication mitigation, and non-AMI etiologies rather than routine VA-ECMO deployment.[7]
EURO SHOCK is an ongoing European randomized trial evaluating VA-ECMO in AMI-related cardiogenic shock and may provide additional data on patient selection, timing, and regional practice patterns. Its results should be interpreted alongside the negative ECLS-SHOCK trial and the individual-patient-data meta-analysis of randomized VA-ECMO trials.[7]
Heart failure-related cardiogenic shock
Most completed randomized MCS trials have focused on AMI-related cardiogenic shock. Randomized evidence remains limited for heart failure-related cardiogenic shock, despite its increasing prevalence at many centers.[2] Future trials should evaluate MCS timing, device selection, bridge-to-recovery, bridge-to-durable-LVAD, bridge-to-transplant, and bridge-to-decision strategies in heart failure-related shock.
Investigational pharmacologic and adjunctive myocardial salvage therapies
Istaroxime
Istaroxime is an investigational intravenous agent with inotropic and lusitropic effects. It inhibits sodium-potassium ATPase and stimulates SERCA2a activity, potentially improving contractility and diastolic relaxation without the tachycardia and arrhythmia burden typical of conventional catecholaminergic inotropes.[8][9]
The SEISMiC trial randomized 60 patients with acute heart failure-related pre-cardiogenic shock and reported hemodynamic improvement with istaroxime compared with placebo.[10] A subsequent phase 2 trial extending infusion to 60 hours in acute heart failure-related pre-cardiogenic shock found increased systolic blood pressure, increased cardiac output, decreased pulmonary wedge pressure, decreased heart rate, and no significant malignant arrhythmia signal on Holter monitoring.[11]
Istaroxime remains investigational. Phase 3 trials are needed to determine whether short-term hemodynamic benefits translate into improved survival, reduced mechanical circulatory support use, renal recovery, or durable functional outcomes.
Levosimendan
Levosimendan is a calcium sensitizer and phosphodiesterase III inhibitor available in some countries but not approved in the United States. Its mechanism is independent of adrenergic receptors, but evidence in cardiogenic shock remains insufficient for routine use. The SURVIVE trial in acute decompensated heart failure found no significant 1-month or 6-month survival advantage compared with dobutamine.[1]
The LevoHeartShock trial is evaluating levosimendan versus placebo in cardiogenic shock using a composite endpoint that includes 30-day mortality, VA-ECMO, or renal replacement therapy.[1] Until outcome benefit is shown, levosimendan should be considered investigational or regionally available rather than standard cardiogenic shock therapy.
Inotrope versus placebo: CAPITAL DOREMI 2
The CAPITAL DOREMI 2 trial is a multicenter, double-blind, placebo-controlled trial randomizing patients with SCAI stage C or D cardiogenic shock to single-agent inotrope therapy with milrinone or dobutamine versus placebo during the initial 12-hour resuscitation period. The trial tests whether inotrope therapy itself improves outcomes in cardiogenic shock, an assumption not previously established in a rigorous placebo-controlled randomized trial.[12]
CAPITAL DOREMI 2 follows the original CAPITAL DOREMI trial, which compared milrinone with dobutamine in cardiogenic shock and found no significant difference in the primary composite outcome, establishing equipoise between these two inotropes and motivating the subsequent placebo-controlled design.[13]
Adrecizumab
Adrecizumab is a non-neutralizing anti-adrenomedullin antibody intended to modulate vascular tone and endothelial function. The randomized ACCOST-HH trial of 77 cardiogenic shock patients found no significant difference in short-term cardiovascular organ support or mortality with adrecizumab.[1] At present, adrecizumab has no established role in cardiogenic shock treatment outside research settings.
Supersaturated oxygen therapy
Supersaturated oxygen therapy delivers hyperoxemic blood to the infarct-related coronary territory after reperfusion and is being studied as a myocardial salvage strategy in large anterior STEMI. Its relevance to cardiogenic shock is indirect: reducing infarct size could theoretically reduce progression to LV failure and shock, but it is not an established therapy for cardiogenic shock itself.
Systems-of-care innovations
Regionalized cardiogenic shock networks
Regionalized cardiogenic shock systems use hub-and-spoke models analogous to STEMI and trauma networks. Proposed hub centers maintain 24/7 multidisciplinary shock teams, advanced temporary MCS capability, cardiac surgery, durable LVAD and transplant programs, and transfer or mobile retrieval pathways. Spoke centers use standardized recognition, stabilization, and transfer protocols.[14][15]
Early implementation data support feasibility. The French cardiac-RESCUE pilot demonstrated safe mobile ECMO team deployment across a 22-center network, and a regionalized US network reported comparable risk-adjusted outcomes regardless of whether patients initially presented to a spoke or hub hospital.[15] The 2025 ACC Expert Consensus Statement supports standardized interdisciplinary care and hospital-level classification for regional cardiogenic shock systems.[2]
Formal prospective evaluation of regionalized cardiogenic shock systems remains an important research priority.
Shock team standardization
Dedicated shock teams are no longer purely investigational at many centers, but optimal team composition, activation criteria, quality metrics, transfer thresholds, and de-escalation protocols remain areas of active study. Observational data associate shock teams with lower adjusted cardiac ICU mortality, greater pulmonary artery catheter use, greater advanced MCS use, and shorter cardiac ICU length of stay.[2] Prospective multicenter validation is needed to determine which protocol elements drive outcome improvement.
Artificial intelligence and machine learning
AI and machine learning tools may support early detection, risk stratification, treatment selection, MCS candidacy assessment, and real-time decision support in cardiogenic shock. These tools remain investigational unless prospectively validated and integrated safely into clinical workflows.
A systematic review of machine learning-based cardiogenic shock prediction models reported a collective AUC-ROC of approximately 0.82, with important predictors including Killip class, ECG rhythm, creatinine, potassium, and renal dysfunction markers.[16] More recent models for STEMI and AMI populations have reported AUC values above 0.90 in retrospective or temporally validated cohorts.[17][18]
The OPtiMCS deep learning model was developed to guide personalized MCS use in cardiogenic shock patients undergoing PCI and reported high discrimination for outcomes including 30-day mortality, 1-year mortality, acute kidney injury, bleeding, and stroke.[19]
Current limitations include retrospective derivation, limited external validation, uncertain calibration across centers, susceptibility to dataset shift, limited workflow integration, and interpretability concerns. No AI-based cardiogenic shock treatment-selection tool has been validated in a prospective randomized trial.
Phenotype-based and precision medicine approaches
Cardiogenic shock is a heterogeneous syndrome rather than a single disease. Future management may shift from uniform protocols toward early phenotype-guided and endotype-guided treatment selection.[20][21]
| Approach | Potential use | Current limitation |
|---|---|---|
| Hemodynamic phenotyping | Distinguish LV failure, RV failure, biventricular failure, vasodilatory-mixed shock, congestion, and low filling pressure states to guide vasoactive and device selection. | Requires timely invasive or advanced noninvasive assessment and has not been prospectively tested as a treatment-randomization strategy. |
| Biomarker-based phenotyping | Identify cardiorenal, inflammatory, congestive, noncongested, and cardiometabolic patterns with different prognoses and possible treatment responses. | Clusters are not yet linked to validated treatment algorithms. |
| Multi-omics endotyping | Integrate genomics, transcriptomics, metabolomics, proteomics, hemodynamic waveforms, ECG data, and imaging to identify mechanistic endotypes. | Largely conceptual and not ready for bedside decision-making. |
The SCAI staging system provides a validated severity framework, but SCAI stage, hemodynamic phenotype, biomarker cluster, and mechanistic endotype are distinct concepts. No phenotype- or endotype-guided cardiogenic shock treatment strategy has been validated in a prospective clinical trial.[2]
Extracorporeal blood purification and cytokine hemoadsorption
Systemic inflammatory activation is common in cardiogenic shock and may be amplified by exposure of blood to artificial surfaces in extracorporeal circuits. Cytokine hemoadsorption has been proposed as an adjunctive therapy to reduce inflammatory mediator burden.
A retrospective cohort of critically ill patients with systemic inflammatory response syndrome treated with CytoSorb coupled with renal replacement therapy showed reductions in interleukin-6 and vasopressor requirements, but the population was heterogeneous and not specific to cardiogenic shock.[22] In a porcine model of refractory ischemic cardiogenic shock supported with VA-ECMO, CytoSorb reduced IL-10 levels but did not significantly improve hemodynamics or biochemical parameters over 4 hours.[23]
The ECMOsorb trial is evaluating VA-ECMO with CytoSorb versus VA-ECMO alone in cardiogenic shock, with improvement in inotropic score at 72 hours as the primary endpoint.[24]
Cytokine hemoadsorption remains investigational in cardiogenic shock. No randomized trial has demonstrated improved survival or durable clinical outcomes, and nonselective mediator or medication removal remains a concern.[25]
Regenerative and cell-based therapies
Regenerative and cell-based therapies aim to improve myocardial repair after severe myocardial injury. These therapies remain investigational and are not established treatments for acute cardiogenic shock or post-shock ventricular dysfunction.
The CHART-1 trial, the largest cell therapy trial in heart failure, used cardiopoietic mesenchymal stem cells delivered by transendocardial injection. The primary hierarchical composite endpoint was not statistically significant, though exploratory analyses suggested possible benefit in selected patients with advanced LV dilation.[26] The ixCELL-DCM trial suggested a reduction in clinical events in ischemic cardiomyopathy, but a confirmatory trial was not pursued.[26]
Stem cell therapy has not demonstrated consistent clinically meaningful benefit in adequately powered trials. Barriers include low cell retention, inconsistent efficacy, immune or inflammatory responses, variable delivery methods, and uncertain durability.[27]
Cell-free regenerative approaches, including mesenchymal stem cell-derived exosomes and extracellular vesicles, may avoid some limitations of direct cell delivery such as poor retention and immune rejection. These approaches remain preclinical or early clinical and have no established role in cardiogenic shock.
Xenotransplantation and total artificial heart
Cardiac xenotransplantation and next-generation total artificial heart platforms are investigational or highly specialized strategies for selected patients with refractory end-stage heart failure or biventricular failure.
Cardiac xenotransplantation using genetically modified pig hearts has progressed from preclinical models to compassionate-use human cases. The first pig-to-human heart transplant in 2022 achieved approximately 60-day survival. A second compassionate-use pig-to-human heart transplant was performed in 2025, with ongoing evaluation of outcomes and immunosuppressive strategies.[28][29]
Major barriers include immune rejection, coagulation dysregulation, graft overgrowth, infection risk, zoonotic safety, and intensive immunosuppression requirements.[28][29]
Total artificial hearts may be used as bridge-to-transplant in selected patients with biventricular failure. Next-generation systems aim to improve durability, reduce thromboembolic risk, reduce infection risk, and expand feasibility beyond bridge-to-transplant use. Device size, anticoagulation, infection, thrombosis, hemolysis, and durability remain important limitations.[30][31]
Areas of uncertainty
- No completed randomized trial has established a mechanical circulatory support strategy for heart failure-related cardiogenic shock.
- Optimal timing of temporary mechanical circulatory support, including pre-PCI versus post-PCI placement, remains uncertain.
- ECPELLA has an observational survival signal but lacks definitive randomized outcomes evidence.
- Routine VA-ECMO has not shown survival benefit in AMI-related cardiogenic shock, but trial design, patient selection, LV unloading, and non-AMI shock populations remain active research areas.
- It remains unknown whether inotropes improve clinical outcomes compared with placebo in cardiogenic shock.
- Istaroxime has promising phase 2 hemodynamic data but no phase 3 outcomes evidence.
- Phenotype- and endotype-guided therapy is conceptually appealing but lacks prospective validation.
- AI and machine learning tools require prospective validation, calibration testing, interpretability safeguards, and workflow integration before clinical deployment.
- Cytokine hemoadsorption has not demonstrated survival or durable clinical benefit in cardiogenic shock.
- Regenerative therapies, including exosome-based approaches, have not shown consistent benefit in adequately powered cardiovascular outcome trials.
Common pitfalls
- Presenting investigational therapies as standard of care before outcomes data are available
- Extrapolating DanGer Shock to all cardiogenic shock etiologies, SCAI stages, post-arrest states, or institutional settings
- Assuming that improved hemodynamics with a drug or device proves survival benefit
- Treating ECPELLA as evidence-based despite primarily observational data
- Overlooking the absence of randomized mechanical support evidence in heart failure-related cardiogenic shock
- Adopting AI or machine learning tools without prospective validation, workflow testing, or calibration assessment
- Confusing SCAI stage, hemodynamic phenotype, biomarker cluster, and molecular endotype
- Assuming regenerative therapies are clinically ready for cardiogenic shock or post-shock ventricular recovery
References
- ↑ 1.0 1.1 1.2 1.3 Lüsebrink E, Binzenhöfer L, Adamo M; et al. (2024). "Cardiogenic Shock". Lancet. 404 (10466): 2006–2020. doi:10.1016/S0140-6736(24)01818-X.
- ↑ 2.0 2.1 2.2 2.3 2.4 Sinha SS, Morrow DA, Kapur NK, Kataria R, Roswell RO (2025). "2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Evaluation and Management of Cardiogenic Shock". Journal of the American College of Cardiology. 85 (16): 1618–1641. doi:10.1016/j.jacc.2025.02.018.
- ↑ 3.0 3.1 Møller JE, Engstrøm T, Jensen LO; et al. (2024). "Microaxial Flow Pump or Standard Care in Infarct-Related Cardiogenic Shock". The New England Journal of Medicine. 391 (13): 1220–1230. doi:10.1056/NEJMoa2312572.
- ↑ 4.0 4.1 Pahuja M, Johnson A, Kabir R; et al. (2022). "Randomized Trials of Percutaneous Microaxial Flow Pump Devices: JACC State-of-the-Art Review". Journal of the American College of Cardiology. 80 (21): 2028–2049. doi:10.1016/j.jacc.2022.08.807.
- ↑ Mangner N, Sharma SK, O'Connor C; et al. (2025). "Mechanical Circulatory Support in High-Risk Elective PCI: Rationale and Design of the PROTECT IV Trial". EuroIntervention. doi:10.4244/EIJ-D-25-00486.
- ↑ Bhatia K, Jain V, Hendrickson MJ; et al. (2022). "Meta-Analysis Comparing Venoarterial Extracorporeal Membrane Oxygenation With or Without Impella in Patients With Cardiogenic Shock". The American Journal of Cardiology. 181: 94–101. doi:10.1016/j.amjcard.2022.06.059.
- ↑ 7.0 7.1 Thiele H, Møller JE, Henriques JPS; et al. (2024). "Temporary Mechanical Circulatory Support in Infarct-Related Cardiogenic Shock: An Individual Patient Data Meta-Analysis of Randomised Trials With 6-Month Follow-Up". Lancet. 404 (10457): 1019–1028. doi:10.1016/S0140-6736(24)01448-X.
- ↑ Florek K, Zimoch W, Biegus J (2026). "Istaroxime - Update of Data in Early Cardiogenic Shock and Decompensated Heart Failure". Expert Opinion on Investigational Drugs. doi:10.1080/13543784.2026.2618978.
- ↑ Francis GS, Bartos JA, Adatya S (2014). "Inotropes". Journal of the American College of Cardiology. 63 (20): 2069–2078. doi:10.1016/j.jacc.2014.01.016.
- ↑ Metra M, Chioncel O, Cotter G; et al. (2022). "Safety and Efficacy of Istaroxime in Patients With Acute Heart Failure-Related Pre-Cardiogenic Shock". European Journal of Heart Failure. 24 (10): 1967–1977. doi:10.1002/ejhf.2629.
- ↑ Biegus J, Mebazaa A, Metra M; et al. (2025). "Safety and Efficacy Intravenous Istaroxime Up to 60 Hours for Patients With Pre-Cardiogenic Shock". The Journal of Heart and Lung Transplantation. doi:10.1016/j.healun.2025.05.013.
- ↑ Parlow S, Santo PD, Sterling LH; et al. (2023). "Inotrope Versus Placebo Therapy in Cardiogenic Shock: Rationale and Study Design of the CAPITAL DOREMI2 Trial". American Heart Journal. 262: 83–89. doi:10.1016/j.ahj.2023.04.010.
- ↑ Mathew R, Di Santo P, Jung RG; et al. (2021). "Milrinone as Compared with Dobutamine in the Treatment of Cardiogenic Shock". The New England Journal of Medicine. 385 (6): 516–525. doi:10.1056/NEJMoa2026845.
- ↑ van Diepen S, Katz JN, Albert NM; et al. (2017). "Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association". Circulation. 136 (16): e232–e268. doi:10.1161/CIR.0000000000000525.
- ↑ 15.0 15.1 Tehrani BN, Sherwood MW, Rosner C; et al. (2022). "A Standardized and Regionalized Network of Care for Cardiogenic Shock". JACC: Heart Failure. 10 (10): 768–781. doi:10.1016/j.jchf.2022.04.004.
- ↑ Aleman R, Patel S, Sleiman J; et al. (2021). "Cardiogenic Shock and Machine Learning: A Systematic Review on Prediction Through Clinical Decision Support Softwares". Journal of Cardiac Surgery. 36 (11): 4153–4159. doi:10.1111/jocs.15934.
- ↑ Stamate E, Culea-Florescu AL, Miron M; et al. (2025). "AI-Based Predictive Models for Cardiogenic Shock in STEMI: Real-World Data for Early Risk Assessment and Prognostic Insights". Journal of Clinical Medicine. 14 (11): 3698. doi:10.3390/jcm14113698.
- ↑ Du S, Li W, Wang Y; et al. (2026). "Development and Validation of an in-Hospital Cardiogenic Shock Prediction Model for AMI Patients Based on Machine Learning". BMC Cardiovascular Disorders. 26 (1): 253. doi:10.1186/s12872-026-05562-w.
- ↑ Amin AP, Bach RG, Brilakis ES; et al. (2026). "A Deep Learning Model to Guide Personalized Mechanical Circulatory Support Use in Cardiogenic Shock Patients Undergoing PCI". JACC: Advances. 5 (1): 102379. doi:10.1016/j.jacadv.2025.102379.
- ↑ Mebazaa A, Soussi S (2023). "Precision Medicine in Cardiogenic Shock: We Are Almost There!". JACC: Heart Failure. 11 (10): 1316–1319. doi:10.1016/j.jchf.2023.06.024.
- ↑ Jentzer JC, Pöss J, Schaubroeck H; et al. (2023). "Advances in the Management of Cardiogenic Shock". Critical Care Medicine. 51 (9): 1222–1233. doi:10.1097/CCM.0000000000005919.
- ↑ Persic V, Jerman A, Malgaj Vrecko M; et al. (2022). "Effect of CytoSorb Coupled With Hemodialysis on Interleukin-6 and Hemodynamic Parameters in Patients With Systemic Inflammatory Response Syndrome". Journal of Clinical Medicine. 11 (24): 7500. doi:10.3390/jcm11247500.
- ↑ Piccoli J, Ehrlich T, Ferraro F; et al. (2025). "Early Impact of CytoSorb Adsorber on Proinflammatory Cytokine Plasmatic Levels in a Porcine Model of Refractory Cardiogenic Shock Supported With VA-ECMO". BMC Cardiovascular Disorders. 26 (1): 50. doi:10.1186/s12872-025-05438-5.
- ↑ Haertel F, Lehmann T, Heller T; et al. (2023). "Impact of a VA-ECMO in Combination With an Extracorporeal Cytokine Hemadsorption System in Critically Ill Patients With Cardiogenic Shock: Design and Rationale of the ECMOsorb Trial". Journal of Clinical Medicine. 12 (15): 4893. doi:10.3390/jcm12154893.
- ↑ Mitzner S, Kogelmann K, Ince C; et al. (2023). "Adjunctive Hemoadsorption Therapy With CytoSorb in Patients With Septic/Vasoplegic Shock: A Best Practice Consensus Statement". Journal of Clinical Medicine. 12 (23): 7199. doi:10.3390/jcm12237199.
- ↑ 26.0 26.1 Normand C, Kaye DM, Povsic TJ, Dickstein K (2019). "Beyond Pharmacological Treatment: An Insight Into Therapies That Target Specific Aspects of Heart Failure Pathophysiology". Lancet. 393 (10175): 1045–1055. doi:10.1016/S0140-6736(18)32216-5.
- ↑ Noorabadi P, Shahabi Rabori V, Jamali S, Jafari N, Saberiyan M (2025). "An Overview on Cardiac Regeneration Revolution: Exploring the Promise of Stem Cell Therapies". Molecular Biology Reports. 52 (1): 511. doi:10.1007/s11033-025-10580-6.
- ↑ 28.0 28.1 Reichart B, Cooper DKC, Längin M; et al. (2023). "Cardiac Xenotransplantation: From Concept to Clinic". Cardiovascular Research. 118 (18): 3499–3516. doi:10.1093/cvr/cvac180.
- ↑ 29.0 29.1 Reichart B, Längin M, Denner J; et al. (2021). "Pathways to Clinical Cardiac Xenotransplantation". Transplantation. 105 (9): 1930–1943. doi:10.1097/TP.0000000000003588.
- ↑ Rihal CS, Naidu SS, Givertz MM; et al. (2015). "2015 SCAI/ACC/HFSA/STS Clinical Expert Consensus Statement on the Use of Percutaneous Mechanical Circulatory Support Devices in Cardiovascular Care". Journal of the American College of Cardiology. 65 (19): e7–e26. doi:10.1016/j.jacc.2015.03.036.
- ↑ Smadja DM (2023). "Stem Cell Therapy, Artificial Heart or Xenotransplantation: What Will Be New Regenerative Strategies in Heart Failure During the Next Decade?". Stem Cell Reviews and Reports. 19 (3): 694–699. doi:10.1007/s12015-022-10476-z.