Background: Impella 5.5 (Abiomed; Danvers, MA) (IMP5) is a commonly used, surgically implanted, tMCS device that requires systemic anticoagulation and purge solution to avoid pump failure. To avoid heparin-induced thrombocytopenia (HIT) from unfractionated heparin (UFH) use, our program has explored the utility of bivalirudin (BIV) for systemic anticoagulation and sodium bicarbonatedextrose purge solution (SBPS) in IMP5.5. Methods: This single center, retrospective study included 34 patients supported on IMP5.5 with BIV based AC and SBPS between December 1st 2020 to December 1st 2021.The efficacy and safety end points were incidence of development of HIT, Tissue Plasminogen Activator (tPA) use for suspected pump thrombosis, stroke, and device failure as well as clinically significant bleeding. Results:The median duration of IMP5.5 support was 9.8 days (IQR: 6-15). Most patients were bridged to HTX (58%) followed by recovery (27%) and LVAD implantation (15%). Patients were therapeutic on bivalirudin for 64% of their IMP5.5 support. One patient (2.9%) suffered from ischemic stroke and 26.5% (9) patients developed clinically significant bleeding. tPA was administered to 7(21%) patients. One patient in the entire cohort developed HIT. Conclusions:Our experience supports the use of systemic BIV and SBPS as a method to avoid heparin exposure in a patient population predisposed to the development of HIT.

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BackgroundVA-ECMO with concomitant Impella support (ECpella) is an emerging treatment modality for cardiogenic shock (CS). Survival outcomes by CS etiology with ECpella support have not been well-described.MethodsThis study was a retrospective, single-center analysis of patients with cardiogenic shock due to acute myocardial infarction (AMI-CS) or decompensated heart failure (ADHF-CS) supported with ECpella from December 2020 to January 2023. Primary outcomes included 90-day survival post-discharge and destination after support. Secondary outcomes included complications post-ECpella support.ResultsA total of 44 patients were included (AMI-CS,n =20, and ADHF-CS,n= 24). Patients with AMI-CS and ADHF-CS had similar survival 90 days post-discharge (p= .267) with similar destinations after ECpella support (p =.220). Limb ischemia and acute kidney injury occurred more frequently in patients presenting with AMI-CS (p=.013;p= .030). Patients with initial Impella support were more likely to survive ECpella support and be bridged to transplant (p=.033) and less likely to have a cerebrovascular accident(p=.016). Sub-analysis of ADHF-CS patients into acute-on-chronic decompensated heart failure and de novo heart failure demonstrated no difference in survival or destination.ConclusionECpella can be used to successfully manage patients with CS. There is no difference in survival or destination for AMI-CS and ADHF-CS in patients with ECpella support. Patients with initial Impella support are more likely to survive ECpella support and bridge to transplant. Future multicenter studies are required to fully analyze the differences between AMI-CS and ADHF-CS with ECpella support.Clinical PerspectivesWhat is New?ECpella support is a feasible support strategy for allcomers in severe cardiogenic shock. This study demonstrates that ECpella can be utilized not only as a salvage therapy and venting strategy for those in cardiogenic shock on VA-ECMO, but also can be utilized as a method for additional cardiac support for patients with initial Impella support. There were no differences in survival between cardiogenic shock secondary to acute myocardial infarction and cardiogenic secondary to acute decompensated heart failure.What are the clinical implications?Although ECpella patients that received initial Impella support have higher success in bridging to heart transplant, allcomers on ECpella support should be evaluated for advanced therapies early in their clinical course. Further studies are required to ascertain the differences in pathophysiology between cardiogenic shock secondary to acute myocardial infarction and cardiogenic secondary to acute decompensated heart failure and determine appropriate support strategies for differing cardiogenic shock phenotypes.

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