Dynamic changes in serum chloride concentrations during worsening of heart failure and its recovery following conventional diuretic therapy: A single-center study.

Abstract

Background and aimsFew data are available regarding the dynamic changes in the serum chloride concentrations in heart failure (HF) pathophysiology. The aim of the present study was to investigate changes in the serum chloride concentration under worsening HF and its recovery following conventional diuretic therapy.MethodsBlood test data, including measurements of serum albumin/solutes and b‐type natriuretic peptide, at both worsening and recovery of HF status, were obtained from 47 patients with definite HF.ResultsAmbulatory patients with HF were enrolled and followed up at the outpatient clinic of Nishida Hospital between June 2003 and March 2009. From clinically stable to worsening HF, the serum sodium concentration increased from (mean ± SD) 139 ± 4.1 to 141 ± 5.07 mEq/L (P < 0.05, two‐way analysis of variance) and the serum chloride concentration increased from 101 ± 5.36 to 104 ± 5.44 mEq/L (P < 0.01) among all patients. After resolution of worsening HF by treatment with conventional diuretics, both the serum sodium concentration and serum chloride concentration decreased significantly to 138 ± 5.12 and 99.5 ± 5.33 mEq/L, respectively (P < 0.0001 for each). The absolute changes in the serum sodium concentration from clinically stable HF to worsening HF appeared to be lesser than those in the serum chloride concentration (1.70 ± 4.34 vs 2.72 ± 6.02 mEq/L, P = 0.079, t test), but this was not statistically significant. Absolute changes in the serum sodium concentration from worsening HF to its recovery following treatment with conventional diuretics were lesser than those in the serum chloride concentration (−2.87 ± 4.38 vs −4.45 ± 5.23 mEq/L, P = 0.0068, t test).ConclusionUnder conventional diuretic therapy, greater changes occur in the serum chloride concentration than in the serum sodium concentration under HF state transitions, suggesting that chloride dynamics might contribute more to HF pathophysiology under such therapeutic circumstance.