आईएसएसएन: 2155-9880
Hajime Kataoka
We recently proposed a unifying hypothesis of the “chloride theory” for Heart Failure (HF) pathophysiology, which states that changes in the serum chloride concentration are the primary determinant of changes in the plasma volume and neurohormonal activity under worsening HF and its resolution. The proposed hypothesis is based on speculative interactions between changes in the serum chloride concentration and neurohormonal systems, but it has been unclear whether these interactions are physiologically applicable to clinical HF states. Thus, here we review the current literature to provide scientific rationale for the “ chloride theory ” to explain the activity of neurohormonal systems, mainly the renin-angiotensin-aldosterone system and the antidiuretic hormone axis. Many published clinical studies provide support for the “chloride theory” in real-world HF pathophysiology during both HF worsening ant recovery.