P332 A CASE OF METABOLIC ACIDOSIS AFTER INITIATION OF SGLT2–I THERAPY IN HEART FAILURE WITH REDUCED EJECTION FRACTION

Abstract

Abstract In July 2022 C.M., a 58–year–old woman, was admitted to our Heart Failure Outpatient Clinic. Patient with permanent AF undergoing DOAC therapy, previous double mitral and tricuspid valve replacement with bioprosthesis. As comorbidities she had stage IIIb CKD, previous ischemic stroke without outcome, multifactorial anaemia, asthma, ulcerative rectocolitis non–responsive to biological therapy. Since April 2022 progressive reduction in exercise tolerance with dyspnoea for previously well–tolerated exertion, with finding of severe left ventricular systolic dysfunction (FE 25%) due to widespread hypokinesia previously unknown. In September angiographic control confirmed the absence of coronary artery disease. Amiodarone therapy was started for frequent runs of VT. Cardiac MRI confirmed FE 27% with fibrosis of the interventricular septum and lower basal wall of non–ischemic appearance. In view of the clinical–instrumental findings, a single–chamber ICD pacemaker was implanted and the therapy for heart failure with reduced FE was optimised with the introduction of Sacubitril/Valsartan (later discontinued due to hypotension), MRA and SGLT2–I (Empagliflozin). Due to the persistence of labile haemodynamic compensation, an indication was given to perform three cycles of Levosimendan infusion at our Day Hospital. The routine EGA taken during the first infusion cycle showed metabolic acidosis in the absence of significant worsening of renal function (Fig. 1) with mild hypobicarbonatemia and electrolytes in the normal range. On the assumption that the acidosis was secondary to the introduction of SGLT2–I (about two months earlier), Empagliflozin was discontinued. One week after discontinuation, the control EGA (Fig. 1) showed resolution of the acidosis, with a substantially stable glomerular filtrate, so that discontinuation of the drug was confirmed. Conclusions In the literature there are reviews and case reports of euglycaemic diabetic ketoacidosis (euDKA) in DM2 patients on SGLT2–I therapy although there are currently only hypotheses regarding the pathophysiological mechanism. The possibility of inducing acidosis with hypobicarbonatemia in the absence of worsening renal function is unclear. A ‘Fanconi–like‘ mechanism could be hypothesised with induction of type 2 tubular acidosis with bicarbonate loss due to glycosuria.