Abstract 15773: Sodium Restriction Activates the Renin-angiotensin-aldosterone System but Fails to Improve Heart Failure or Survival in Experimental Dilated Cardiomyopathy
Introduction: Dilated cardiomyopathy (DCM) causes progressive heart failure (HF), which affects millions of Americans. Dietary sodium restriction is recommended by AHA/ACC guidelines to reduce the progression of HF. Still, clinical data for sodium restriction show conflicting results and the health benefit for HF patients is controversial.
Methods and results: We examined the dose-dependent effects of sodium restriction on survival and HF using a translationally relevant mouse model of DCM. Male littermate mice were randomly assigned to three groups (n=40-50/group) receiving identical diets with different sodium concentrations: normal (0.3%), reduced 0.1% and low sodium (0.05%). Median survival among all three groups was not significantly different (137, 142 vs. 144 days; p>0.05). Systolic function (ejection fraction), measured at the late stage of HF (120 days), was similar in the low vs. normal sodium groups. Lung water retention was not different among the groups. Sodium restriction was associated with dose-associated increases in cGMP levels (66±11, 83±22, 124±17 pmol/mL; p<0.001) levels. Increasing sodium restriction also caused dose-dependent increases in active plasma renin levels (37±6.0< 42±9< 55±7 arbitrary units; p=0.01). Aldosterone levels were significantly increased in the low sodium group (520±44, 552±71, 1278±101 pg/mL; p<0.0001). Still, kidney function (BUN, creatinine) remained normal in the low versus normal sodium groups.
Conclusion: In experimental dilated cardiomyopathy, sodium restriction failed to improve survival, heart systolic function and HF. Increasing sodium restriction was associated with dose-related increases in biomarkers associated with worsening HF such as cGMP, renin and aldosterone. These data indicate that sodium restriction has dubious value in halting the progression of HF and mortality in experimental dilated cardiomyopathy.
Author Disclosures: R. Tripathi: None. R. Sullivan: None. M. Fan: None. N. Houng: None. I.P. Gladysheva: None. G.L. Reed: None.
- © 2016 by American Heart Association, Inc.