Pathophysiological Insights into Persistent Hyponatremia after LVAD Implantation

Abstract

Background Persistent hyponatremia after LVAD implantation is not uncommon in patients with end-stage heart failure (HF) and maybe associated with adverse outcomes. The etiology of hyponatremia in HF patients is multifactorial including - low cardiac output state, volume expansion, impaired free water excretion due to renal insufficiency and use of loop diuretics. It is generally thought that with restoration of hemodynamics hyponatremia would resolve after LVAD implantation. We sought to determine the etiology of persistent hyponatremia after LVAD implantation. Methods We performed a retrospective analysis of patients with end-stage HF who received a continuous-flow LVAD and subsequently underwent right heart catheterization (RHC) to assess invasive hemodynamics and for speed optimization. Data was collected concurrently on invasive hemodynamics, medication usage and basic metabolic panel. Hyponatremia was defined as serum sodium level 12 mmHg, volume depletion defined by RAP 0.75 (moderate) and >1.0 (severe), partially unloaded left ventricle (LV) defined by PCWP > 15, use of angiotensin converter enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB), use of loop diuretics and renal function measured by estimated glomerular filtration rate (GFR). Each of the factors were compared between patients with hyponatremia and normal sodium levels. Results We included 143 patients in our study. RHC was performed within 6 months from LVAD implantation in 70% of the population, the median time was 199 days. Patients with hyponatremia had a mean sodium of 130.5 mEq/L compared to 139.8 mEq/L in patients with normonatremia, p-value table 1 ). One-year mortality and all-cause readmissions (from time of RHC) were both higher in the hyponatremia group, p-values of 0.012 and 0.023 respectively. Discussion Persistent hyponatremia after LVAD implantation does not appear to be related to low cardiac output state, volume expansion or depletion, RV dysfunction, use of ACEI or ARBs, loop diuretics or renal function. Hyponatremia may be an independent marker of adverse outcomes after LVAD implantation.