Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): The Danish Heart Foundation Unrestricted research grant from Abiomed Background No strong evidence exists regarding the treatment of cardiogenic shock (CS) caused by acute right ventricular (RV) failure which has mainly consisted of vasoactive drugs. There is expert agreement that treatment with the recently developed Impella RP is feasible, but no previous studies have compared vasoactive treatment strategies with the Impella RP in terms of cardiac unloading and end-organ perfusion. Hypothesis Treatment with the Impella RP device will be associated with lower RV myocardial workload (pressure-volume area) compared to vasoactive treatment strategies and can furthermore be achieved without compromising organ perfusion. Methods CS was induced by a stepwise injection of polyvinyl alcohol microspheres into the right coronary artery in twenty adult female Danish landrace pigs weighing 75-80 kg. After induction of CS, the pigs were allocated to one of the two interventions for 180 minutes: 1) vasoactive therapy comprised a continuous infusion of norepinephrine (0.1 µg/kg/min) for the first 30 minutes, supplemented by an infusion of milrinone (0.4 µg/kg/min) for the remaining 150 minutes or 2) immediate insertion of and treatment with the Impella RP. The results are presented as median [Q1;Q3]. Results Treatment with the Impella RP was associated with a lower RV workload compared to the vasoactive group, while no difference was observed with regards to left ventricular workload among intervention groups, Figure 1. Renal venous oxygen saturation increased to a similar degree following both interventions compared to the state of CS. A trend towards a higher cerebral venous oxygen saturation was observed with norepinephrine compared to Impella RP (Impella RP 51 [47;61] % vs Norepinephrine 62 [57;71] % ; p = 0.07), which became significantly higher with the addition of milrinone (Impella RP 45 [32;63] % vs Norepinephrine +Milrinone 73 [66;81] %; p = 0.002). Conclusion In this large animal model of profound CS caused by predominantly RV failure the Impella RP unloaded the failing RV. The vasoactive treatment, however, caused a higher cerebral venous oxygen saturation, while both interventions increased renal venous oxygen saturation to a similar degree. Abstract Figure 1
Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): The Danish Heart Foundation Odense University Hospital and Rigshospitalets Research Council. Background Acute myocardial infarction complicated by cardiogenic shock (AMICS) comprises a heterogenous population with high mortality. Insight in timing and cause of death may improve understanding of the condition and aid individualization of treatment. Purpose To determine the cause and timing of death in patients admitted with AMICS. Methods This was a retrospective, multi-center observational cohort study based on 1716 AMICS patients treated during the period of 2010-2017, of whom 904 died prior to hospital discharge from either of two tertiary cardiac centers in Denmark providing advanced care for cardiogenic shock for 3.9 million inhabitants. Patients admitted with AMICS were identified through national registries and review of individual patient charts. Only patients dying during hospitalization were eligible. Cause of death was categorized as caused by progressive cardiac failure, multi organ failure or due to neurological damage. Time to death was calculated in hours from first medical contact to death. Results Among 904 patients with AMICS who died prior to hospital discharge (median age 72 years [IQR: 63 - 79], 70% men), 342 (38%) patients had suffered an out-of-hospital cardiac arrest (OHCA). The most frequent cause of death was primary cardiac (54%), whereas 24% died of neurologic injury and 20% of multi-organ failure. Time to death was 13 hours [IQR: 5, 43] for cardiac failure; 140 hours [IQR: 95, 209] in neurological injury; and 137 hours [IQR: 59, 321] in multi-organ failure, p<0.001. The causes of death in patients presenting with OHCA were neurological injury in 57%, as opposed to 4% among patients not presenting with OHCA, p<0.001. No specific phenotype on admission characterized patients with OHCA who died from neurological injury or cardiac causes. Conclusion In patients with AMICS, cause of death was mainly primary cardiac failure followed by neurological injury and multi-organ failure. Median time from first medical contact to death was only 13 hours in patients dying from cardiac causes. The risk of dying of neurological injury was low in patients without OHCA.
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