Selected Talk: Left Ventricular Unloading Acutely Reduces Right Ventricular Preload in Patients with Acute Decompensated Heart Failure and Cardiogenic Shock

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Acute decompensated heart failure (ADHF) and cardiogenic shock (CS) are signs of deterioration in patients experiencing heart failure (HF). The proportion of patients with CS who also have ADHF is increasing, and mortality rates have remained high over the past few decades at 30–50%.1 Unfortunately, right ventricular (RV) dysfunction in these patients is associated with worse survival.2 The priority goals of managing these patients are supporting the systemic circulation, relieving decongestion and minimising myocardial workload. Ventricular unloading has emerged as a means of offering myocardial protection, but it remains to be determined whether maximum left ventricular (LV) unloading can improve RV performance in ADHF-CS. Up until now, understanding in this domain has been limited to computational analyses (i.e. simulations using computational modelling with patient haemodynamic data). Dr Everett’s study aimed to address this by directly collecting these data from human patients with ADHF and testing the hypothesis.

The hypothesis of the present study was that maximal transvalvular LV unloading decreases RV pressures and pressure–volume area (PVA) in patients with ADHF-CS. Dr Everett relied upon a clinical case series that has enrolled six patients to date. All six patients had ADHF and refractory CS and underwent Impella 5.5 implantation as a bridge to transplant or durable ventricular assist device. Invasive haemodynamics, including the biventricular pressure–volume loops, were performed at baseline and between 5 and 15 min after Impella activation to assess biventricular function. Analysis was performed on both the aggregate patient cohort and per patient.

The mean (±SD) age of patients was 57.3 ± 5.9 years and 83% were male. Patients had, on average, three vasoactive agents, and 33% required pulmonary vasodilators. Mean (±SD) LV ejection fraction was 10.0 ± 4.2% and LV end-diastolic diameter was 6.0 ± 0.7 cm. Baseline haemodynamics showed significant biventricular congestion and high vascular resistance in all patients.

Dr Everett presented the study results, which showed a significant reduction in end-diastolic pressures (EDP) of both the LV and RV after Impella 5.5 activation in the acute setting (p<0.05). Dr Everett proposed that these findings show that LV unloading of patients with ADHF-CS can achieve a reduction in biventricular filling pressures. Further, all patients saw a significant reduction in LV PVA during Impella 5.5 activation. There was a more diverse response in RV PVA, with four (67%) patients experiencing a significant reduction during the acute setting with Impella activation; one patient experienced no change and one patient experienced an increase in RV PVA (p<0.05).

Examination of pressure–volume loops showed that four of the six patients experienced a significant coupled reduction in LV and RV volumes, pressures and PVA. The two patients who experienced unchanged or increased RV volumes and PVA both required inhaled pulmonary vasodilators due to refractory LV failure. All patients tolerated the procedure well without complications and, by the end of the study, three patients had been weaned off vasoactive medications.

Dr Everett closed her presentation by summarising the findings of her study that identified a reduction in biventricular filling pressures, decrease in LV PVA, variable RV response and PVA reduction in selected patients with ADHF-CS in response to Impella 5.5 activation. These findings support the hypothesis that maximal transvalvular LV unloading may improve biventricular performance in ADHF-CS. Dr Everett added that in ADHF-CS patients with refractory RV failure, additional devices to address right-side decongestion or additional time on support may be required. She acknowledged the limitations of her study, including its small sample size and single-centre basis. However, additional enrolment of patients with and without refractory RV failure is ongoing, and this study will inform better identification of patients who require biventricular support.


  1. Abraham J, Blumer V, Burkhoff D, et al. Heart failure-related cardiogenic shock: pathophysiology, evaluation and management considerations: review of heart failure-related cardiogenic shock. J Card Fail 2021;27:1126–40. 
    Crossref | Pubmed
  2. Jain P, Thayer KL, Abraham J, et al. Right ventricular dysfunction is common and identifies patients at risk of dying in cardiogenic shock. J Card Fail 2021;27:1061–72. 
    Crossref | Pubmed