Dr Anderson began his talk by defining cardiorenal syndrome (CRS) as a pathophysiological disorder of the heart and kidney, whereby acute or chronic dysfunction of one organ may induce acute or chronic dysfunction in the other. The focus of his study was CRS-1, cardiorenal syndrome characterised by rapid worsening of cardiac function, such as acute decompensation of heart failure, leading to acute renal injury.1 A feedback loop of neurohormonal and molecular signalling ensues between the kidney and heart, further promoting organ damage. The rate of decline in renal function predicts mortality in these patients, even after adjusting for baseline kidney function. The current standard of care for acute decompensated heart failure (ADHF) is a loop diuretic. If the loop diuretic is not effective in removing excess fluid volume, it is followed by or combined with additional diuretics, vasoactives, ultrafiltration and ultimately renal replacement therapy (RRT). Heart failure patients with CRS who are on RRT have poorer outcomes, as they are often declined for advanced therapies, such as a left ventricular assist device (LVAD).
Dr Anderson’s research hypothesis is that cardiac unloading with an Impella transvalvular mechanical support device in CRS-1 patients can have a favourable impact on neurohormonal activation and haemodynamics to mitigate the need for RRT. Potential benefits of Impella support include increasing cardiac output and haemodynamic stability, decreased neural sympathetic drive, renal unloading (resulting in decreased central venous pressure [CVP]), decreased renin–angiotensin–aldosterone system activation and decreased inflammatory response.
A retrospective chart review of 13 CRS-1 patients diagnosed with ADHF and acute kidney injury, who received the Impella 5.0 or Impella 5.5 device prior to RRT, demonstrated positive outcomes. All 13 patients survived with no serious adverse events and were successfully bridged to LVAD, transplant or native heart recovery, with none requiring RRT. Impella support improved haemodynamics with decreased CVP, maintenance of mean arterial pressure (MAP) and increased mixed venous oxygen saturation (SVO2) to normal levels. Normalisation of SVO2 levels indicate overall improved end-organ perfusion. Several patients were weaned off vasoactives/inotropes by day 7 of treatment. Impella support also improved renal function with significantly increased 24-hour urine output at days 1 and 7 of treatment, and significantly decreased blood urea nitrogen levels by day 7.
Dr Anderson concluded that Impella support safely improves cardiac and renal function and prevents progressive renal deterioration in ADHF patients diagnosed with CRS-1 who are refractory to diuretics and inotropes. A putative mechanism includes unloading the renal circulation by decreasing CVP and maintaining MAP. Impella may also be an effective bridge therapy to improve the candidacy of CRS-1 patients for LVAD or transplant by preventing the need for RRT. Future directions include a larger, prospective study with longer-term follow-up to confirm findings and understand whether observed improvements in renal function persist, especially in heart recovery patients.