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      The impact of ECPELLA on haemodynamics and global oxygen delivery: a comprehensive simulation of biventricular failure

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          Abstract

          Background

          ECPELLA, a combination of veno-arterial (VA) extracorporeal membrane oxygenation (ECMO) and Impella, a percutaneous left ventricular (LV) assist device, has emerged as a novel therapeutic option in patients with severe cardiogenic shock (CS). Since multiple cardiovascular and pump factors influence the haemodynamic effects of ECPELLA, optimising ECPELLA management remains challenging. In this study, we conducted a comprehensive simulation study of ECPELLA haemodynamics. We also simulated global oxygen delivery (DO 2) under ECPELLA in severe CS and acute respiratory failure as a first step to incorporate global DO 2 into our developed cardiovascular simulation.

          Methods and results

          Both the systemic and pulmonary circulations were modelled using a 5-element resistance‒capacitance network. The four ventricles were represented by time-varying elastances with unidirectional valves. In the scenarios of severe LV dysfunction, biventricular dysfunction with normal pulmonary vascular resistance (PVR, 0.8 Wood units), and biventricular dysfunction with high PVR (6.0 Wood units), we compared the changes in haemodynamics, pressure–volume relationship (PV loop), and global DO 2 under different VA-ECMO flows and Impella support levels.

          Results

          In the simulation, ECPELLA improved total systemic flow with a minimising biventricular pressure–volume loop, indicating biventricular unloading in normal PVR conditions. Meanwhile, increased Impella support level in high PVR conditions rendered the LV–PV loop smaller and induced LV suction in ECPELLA support conditions. The general trend of global DO 2 was followed by the changes in total systemic flow. The addition of veno-venous ECMO (VV-ECMO) augmented the global DO 2 increment under ECPELLA total support conditions.

          Conclusions

          The optimal ECPELLA support increased total systemic flow and achieved both biventricular unloading. The VV-ECMO effectively improves global DO 2 in total ECPELLA support conditions.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s40635-024-00599-7.

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          Most cited references55

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          Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock.

          The leading cause of death in patients hospitalized for acute myocardial infarction is cardiogenic shock. We conducted a randomized trial to evaluate early revascularization in patients with cardiogenic shock. Patients with shock due to left ventricular failure complicating myocardial infarction were randomly assigned to emergency revascularization (152 patients) or initial medical stabilization (150 patients). Revascularization was accomplished by either coronary-artery bypass grafting or angioplasty. Intraaortic balloon counterpulsation was performed in 86 percent of the patients in both groups. The primary end point was mortality from all causes at 30 days. Six-month survival was a secondary end point. The mean age of the patients was 66+/-10 years, 32 percent were women and 55 percent were transferred from other hospitals. The median time to the onset of shock was 5.6 hours after infarction, and most infarcts were anterior in location. Ninety-seven percent of the patients assigned to revascularization underwent early coronary angiography, and 87 percent underwent revascularization; only 2.7 percent of the patients assigned to medical therapy crossed over to early revascularization without clinical indication. Overall mortality at 30 days did not differ significantly between the revascularization and medical-therapy groups (46.7 percent and 56.0 percent, respectively; difference, -9.3 percent; 95 percent confidence interval for the difference, -20.5 to 1.9 percent; P=0.11). Six-month mortality was lower in the revascularization group than in the medical-therapy group (50.3 percent vs. 63.1 percent, P=0.027). In patients with cardiogenic shock, emergency revascularization did not significantly reduce overall mortality at 30 days. However, after six months there was a significant survival benefit. Early revascularization should be strongly considered for patients with acute myocardial infarction complicated by cardiogenic shock.
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            • Article: not found

            The sympathetic nervous system in heart failure physiology, pathophysiology, and clinical implications.

            Heart failure is a syndrome characterized initially by left ventricular dysfunction that triggers countermeasures aimed to restore cardiac output. These responses are compensatory at first but eventually become part of the disease process itself leading to further worsening cardiac function. Among these responses is the activation of the sympathetic nervous system (SNS) that provides inotropic support to the failing heart increasing stroke volume, and peripheral vasoconstriction to maintain mean arterial perfusion pressure, but eventually accelerates disease progression affecting survival. Activation of SNS has been attributed to withdrawal of normal restraining influences and enhancement of excitatory inputs including changes in: 1) peripheral baroreceptor and chemoreceptor reflexes; 2) chemical mediators that control sympathetic outflow; and 3) central integratory sites. The interface between the sympathetic fibers and the cardiovascular system is formed by the adrenergic receptors (ARs). Dysregulation of cardiac beta(1)-AR signaling and transduction are key features of heart failure progression. In contrast, cardiac beta(2)-ARs and alpha(1)-ARs may function in a compensatory fashion to maintain cardiac inotropy. Adrenergic receptor polymorphisms may have an impact on the adaptive mechanisms, susceptibilities, and pharmacological responses of SNS. The beta-AR blockers and the inhibitors of the renin-angiotensin-aldosterone axis form the mainstay of current medical management of chronic heart failure. Conversely, central sympatholytics have proved harmful, whereas sympathomimetic inotropes are still used in selected patients with hemodynamic instability. This review summarizes the changes in SNS in heart failure and examines how modulation of SNS activity may affect morbidity and mortality from this syndrome.
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              • Article: not found

              Load independence of the instantaneous pressure-volume ratio of the canine left ventricle and effects of epinephrine and heart rate on the ratio.

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                Author and article information

                Contributors
                saku.keita@ncvc.go.jp
                Journal
                Intensive Care Med Exp
                Intensive Care Med Exp
                Intensive Care Medicine Experimental
                Springer International Publishing (Cham )
                2197-425X
                16 February 2024
                16 February 2024
                December 2024
                : 12
                : 13
                Affiliations
                [1 ]Department of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center Research Institute, ( https://ror.org/01v55qb38) 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565 Japan
                [2 ]Department of Research Promotion and Management, National Cerebral and Cardiovascular Center Research Institute, ( https://ror.org/01v55qb38) Suita, Japan
                [3 ]NTTR-NCVC Bio Digital Twin Centre, National Cerebral and Cardiovascular Center Research Institute, ( https://ror.org/01v55qb38) Suita, Japan
                [4 ]Department of Anesthesiology and Critical Care Medicine, Graduate School of Medical Sciences, Kyushu University, ( https://ror.org/00p4k0j84) Fukuoka, Japan
                Author information
                http://orcid.org/0000-0002-6856-9362
                Article
                599
                10.1186/s40635-024-00599-7
                10869331
                38361021
                83387416-a63f-4f93-8d67-40f43d95a661
                © The Author(s) 2024

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 4 December 2023
                : 18 January 2024
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001691, Japan Society for the Promotion of Science;
                Award ID: 22K08222
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100009619, Japan Agency for Medical Research and Development;
                Award ID: 23hk0102085h0002
                Award ID: 23uk1024007h0001
                Award Recipient :
                Funded by: Ministry of Internal Affairs and Communications
                Award ID: JP225006004
                Award Recipient :
                Funded by: Intramural Research Fund for Cardiovascular Diseases of National Cerebral and Cardiovascular Center
                Award ID: 21-2-7
                Award ID: 21-2-9
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100002241, Japan Science and Technology Agency;
                Award ID: JPMJPF2018
                Award Recipient :
                Categories
                Research Articles
                Custom metadata
                © European Society of Intensive Care Medicine and Springer Nature Switzerland AG 2024

                simulation,cardiogenic shock,va-ecmo,impella,ecpella,haemodynamics,oxygen delivery

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