CRT-600.10 Combining VA-ECMO and Impella (EC-Pella) Before Reperfusion Mitigates Left Ventricular Loading and Injury Due to VA-ECMO in Acute Myocardial Infarction

Everett, Kay; Swain, Lija; Reyelt, Lara; Majumdar, Monica; Qiao, Xiaoying; Bhave, Shreyas; Warner, Mary Grace; Mahmoudi, Ebrahim; Surks, Will; Aryaputra, Tejasvi; Goel, Siya; Kapur, Navin K.

doi:10.1016/j.jcin.2022.01.213

Cited by 5 publications

(10 citation statements)

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“…4,8,33 We have further reported that VA-ECMO–induced mitochondrial dysfunction occurs despite actively reducing LV afterload with an Impella pump before VA-ECMO initiation. 32 Combined with our current findings that VA-ECMO triggers mitochondrial damage within 6 hours in uninjured swine, these findings are consistent with several other preclinical reports showing that VA-ECMO or veno-veno ECMO promotes mitochondrial injury in a manner that is independent of hemodynamic stress. 34 Prior attempts to mitigate ECMO-induced mitochondrial injury include approaches such as autologous mitochondrial transplantation.…”

Section: Discussionsupporting

confidence: 93%

“…We recently reported that despite reducing LV stroke work, pressure-volume area, and systemic blood pressure, VA-ECMO disrupts mitochondrial integrity and ETC function in preclinical models of AMI. 8,32 In several preclinical and clinical reports, VA-ECMO has been shown to reduce cardiac filling pressures and systemic blood pressure, which may reflect reduced total circulating volume or systemic vasorelaxation. 4,8,33 We have further reported that VA-ECMO–induced mitochondrial dysfunction occurs despite actively reducing LV afterload with an Impella pump before VA-ECMO initiation.…”

Section: Discussionmentioning

confidence: 99%

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Novel Role for Cardiolipin as a Target of Therapy to Mitigate Myocardial Injury Caused by Venoarterial Extracorporeal Membrane Oxygenation

Swain,

Bhave,

Qiao

et al. 2024

Circulation

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BACKGROUND: Cardiolipin is a mitochondrial-specific phospholipid that maintains integrity of the electron transport chain (ETC) and plays a central role in myocardial ischemia/reperfusion injury. Tafazzin is an enzyme that is required for cardiolipin maturation. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) use to provide hemodynamic support for acute myocardial infarction has grown exponentially, is associated with poor outcomes, and is under active clinical investigation, yet the mechanistic effect of VA-ECMO on myocardial damage in acute myocardial infarction remains poorly understood. We hypothesized that VA-ECMO acutely depletes myocardial cardiolipin and exacerbates myocardial injury in acute myocardial infarction. METHODS: We examined cardiolipin and tafazzin levels in human subjects with heart failure and healthy swine exposed to VA-ECMO and used a swine model of closed-chest myocardial ischemia/reperfusion injury to evaluate the effect of VA-ECMO on cardiolipin expression, myocardial injury, and mitochondrial function. RESULTS: Cardiolipin and tafazzin levels are significantly reduced in the left ventricles of individuals requiring VA-ECMO compared with individuals without VA-ECMO before heart transplantation. Six hours of exposure to VA-ECMO also decreased left ventricular levels of cardiolipin and tafazzin in healthy swine compared with sham controls. To explore whether cardiolipin depletion by VA-ECMO increases infarct size, we performed left anterior descending artery occlusion for a total of 120 minutes followed by 180 minutes of reperfusion in adult swine in the presence and absence of MTP-131, an amphipathic molecule that interacts with cardiolipin to stabilize the inner mitochondrial membrane. Compared with reperfusion alone, VA-ECMO activation beginning after 90 minutes of left anterior descending artery occlusion increased infarct size (36±8% versus 48±7%; P <0.001). VA-ECMO also decreased cardiolipin and tafazzin levels, disrupted mitochondrial integrity, reduced electron transport chain function, and promoted oxidative stress. Compared with reperfusion alone or VA-ECMO before reperfusion, delivery of MTP-131 before VA-ECMO activation reduced infarct size (22±8%; P =0.03 versus reperfusion alone and P <0.001 versus VA-ECMO alone). MTP-131 restored cardiolipin and tafazzin levels, stabilized mitochondrial function, and reduced oxidative stress in the left ventricle. CONCLUSIONS: We identified a novel mechanism by which VA-ECMO promotes myocardial injury and further identify cardiolipin as an important target of therapy to reduce infarct size and to preserve mitochondrial function in the setting of VA-ECMO for acute myocardial infarction.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Novel Role for Cardiolipin as a Target of Therapy to Mitigate Myocardial Injury Caused by Venoarterial Extracorporeal Membrane Oxygenation

Swain,

Bhave,

Qiao

et al. 2024

Circulation

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“…Amongst other indications, treatment of clinical complications were a more common indication for unloading than invasive hemodynamic parameters or echocardiographic parameters (Table 2). When hemodynamic metrics were used, the thresholds for PCWP and LVEDP were a median (IQR) of 20 mmHg (18)(19)(20)(21)(22)(23)(24)(25), and 18 mmHg (16-25) respectively, whilst for LVOT VTI this was a median (IQR) of 8 cm (5-10). Only 21 (11%) respondents reported working in a center with a guideline to protocolize unloading decisions.…”

Section: Indications For Unplanned Unloadingmentioning

confidence: 99%

“…Hemodynamic goals were used less frequently to optimize unloading. 40% aimed for a PCWP of 18mmHg (IQR [15][16][17][18][19][20], in contrast only 18 (9%) respondents used pulmonary artery diastolic pressure target of 22.5 mmHg (IQR 20-25), whilst 37 (19.3%) targeted a LVEDP of 15 mmHg (IQR 11.5-21).…”

Section: Unloading Targetsmentioning

confidence: 99%

Left ventricular unloading in patients supported with veno-arterial extra corporeal membrane oxygenation; an international EuroELSO survey

Ezad,

Ryan,

Barrett

et al. 2024

Perfusion

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Introduction Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) improves end-organ perfusion in cardiogenic shock but may increase afterload, which can limit cardiac recovery. Left ventricular (LV) unloading strategies may aid cardiac recovery and prevent complications of increased afterload. However, there is no consensus on when and which unloading strategy should be used. Methods An online survey was distributed worldwide via the EuroELSO newsletter mailing list to describe contemporary international practice and evaluate heterogeneity in strategies for LV unloading. Results Of 192 respondents from 43 countries, 53% routinely use mechanical LV unloading, to promote ventricular recovery and/or to prevent complications. Of those that do not routinely unload, 65% cited risk of complications as the reason. The most common indications for unplanned unloading were reduced arterial line pulsatility (68%), pulmonary edema (64%) and LV dilatation (50%). An intra-aortic balloon pump was the most frequently used device for unloading followed by percutaneous left ventricular assist devices. Echocardiography was the most frequently used method to monitor the response to unloading. Conclusions Significant variation exists with respect to international practice of ventricular unloading. Further research is required that compares the efficacy of different unloading strategies and a randomized comparison of routine mechanical unloading versus unplanned unloading.

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“…Table 3 relates relevant risks via phase of care, noting the almost five-fold increase in mortality associated with postoperative tMCS institution when compared to preoperative institution. Insight into the mechanism(s) and impact of earlier institution of tMCS and unloading [73] are evolving in parallel to ongoing clinical efforts in high-risk percutaneous coronary interventions, such as the PROTECT IV [74] randomized clinical trial [as well as evolving experimental data on unloading the left ventricle prior to acute myocardial infarction (AMI) [75][76][77].…”

Section: Risk Assessmentmentioning

confidence: 99%

Temporary mechanical circulatory support & enhancing recovery after cardiac surgery

Lobdell,

Grant,

Salenger

2023

Current Opinion in Anaesthesiology

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Purpose of review This review highlights the integration of enhanced recovery principles with temporary mechanical circulatory support associated with adult cardiac surgery. Recent findings Enhanced recovery elements and efforts have been associated with improvements in quality and value. Temporary mechanical circulatory support technologies have been successfully employed, improved, and the value of their proactive use to maintain hemodynamic goals and preserve long-term myocardial function is accruing. Summary Temporary mechanical circulatory support devices promise to enhance recovery by mitigating the risk of complications, such as postcardiotomy cardiogenic shock, organ dysfunction, and death, associated with adult cardiac surgery.

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CRT-600.10 Combining VA-ECMO and Impella (EC-Pella) Before Reperfusion Mitigates Left Ventricular Loading and Injury Due to VA-ECMO in Acute Myocardial Infarction

Cited by 5 publications

References 0 publications

Novel Role for Cardiolipin as a Target of Therapy to Mitigate Myocardial Injury Caused by Venoarterial Extracorporeal Membrane Oxygenation

Novel Role for Cardiolipin as a Target of Therapy to Mitigate Myocardial Injury Caused by Venoarterial Extracorporeal Membrane Oxygenation

Left ventricular unloading in patients supported with veno-arterial extra corporeal membrane oxygenation; an international EuroELSO survey

Temporary mechanical circulatory support & enhancing recovery after cardiac surgery

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