Increased potassium requirement after LVAD implantation- may reflect increased RAAS activity

Introduction

Despite haemodynamics improvement LVAD implantation was found to be associated with an increased actvitity of the systemic renine –angiotensin-aldosteron axis (RAAS) as well local intrarenal RAAS axis that may lead to hypokalemia due toincreased urinary potassium excretion. We hypothetised that the phenomenon might be the source of hypokalemia after LVAD implantation.

Methods

Data of 20 consecutive LVAD patients were analysed retrospectively. Potassium requirement was expressed as ratio of daily potassium intake [mg] to daily furosemide dose [mg] and recorded at three time points: preLVAD, about 3 months and 1 year after LVAD implantation. Torasmide was converted to furosemide in 1:2 ratio.

Results

There were no significant difference in serum potassium level before LVAD implantation and 3 months and 1 year afterwards. However to maintain similar level of potassium one year after LVAD implantation its supplementation increased by over 80% ( from an average total dose of 1885 baseline to 3385 mg 1 year after LVAD, p=0,046) along with only 15% increase in furosemide dose (from 132mg to 151 mg, p=ns). Thus ratio of potassium to furosemid intake increased over 50% (Fig. 1A, p=0,033). At the same time there was mild and insignificant increase in creatinine level while utilisation of ACE-I, ARB or ARNI and MRA remain stable (Fig 1B, C, D). Similar results were found among patients without ARNI_ARB or ACE-I before LVAD implantation and regardless of the presence of the aortic valve opening after surgery.

Conclusion

LVAD patients require significantly greater potassium supplementation to maintain preLVAD level despite comparable RAAS inhibition.

This may reflect increased RAAS activity due to loss of pulsatility.For image description, please refer to the figure legend and surrounding text.