While hyponatremia is a strong prognostic marker for adverse outcomes in heart failure, treatments aimed at correcting serum sodium levels have not yet proven to improve survival, leaving its role as a mediator versus a marker uncertain.
Hyponatremia correction should not yet guide heart failure therapy; leaves open whether it is a modifiable mediator or prognostic marker.
Hyponatremia is a common clinical condition among hospitalized heart failure patients, related with increased morbidity and mortality. The pathophysiological mechanisms that relate heart failure with hyponatremia are complex, involving beyond renal dysfunction, neurohormonal activation, as well as diuretic treatment. The pituitary hormone vasopressin seems to play a central role leading to renal water retention and hyponatremia. Although therapeutic strategies (water restriction, hormone inhibition) have shown to increase serum sodium concentration and improve symptoms, no beneficial effect has been detected on clinical outcome. This fact, urges the need for the conduction of further clinical trials, in order to determine the real causality between short- and long-term outcome and serum sodium concentration in heart failure patients .
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Chrysohoou et al. (2012) studied this question.
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