Left ventricular assist device support induces acute changes in myocardial electrolytes in heart failure.

The regulation of myocardial electrolyte concentrations is critical to proper cardiac function. Myocardial ischemia is associated with deranged ion transport. Left ventricular assist device (LVAD) therapy improves myocyte bioenergetics in chronic heart failure (CHF), which may manifest as electrolyte alterations; however, rapid electrolyte shifts may place critically ill patients at risk for arrhythmias upon initiation of LVAD support. We examine the effect of incremental increases in LVAD support on acute changes in myocardial arteriovenous electrolytes in CHF. CHF was induced in sheep via coronary microembolization. Four months later, sheep underwent acute LVAD implantation. LVAD support was incrementally increased (0%, 25%, 50%, 75% support). Paired arterial and coronary sinus blood samples were obtained at each increment and analyzed for K+, Ca2+, and Na+ concentrations. Arteriovenous electrolyte concentrations (mmol/l) were inverted in CHF before LVAD support: K+ (-0.08), Ca2+ (-0.04), and Na+ (0.04). These imbalances were corrected within 20 minutes and with as little as 25% LVAD support: K+ (0.06), Ca2+ (0.012), and Na+ (-0.80). The arteriovenous differences further widened as LVAD support was increased. In conclusion, LVAD support in CHF induces acute alterations in myocardial electrolytes. Rapid shifts myocardial arteriovenous electrolyte balances during LVAD support may in part explain the incidence of post-LVAD arrhythmias observed clinically in humans.