Dietary Sodium Reduction in Heart Failure: A Challenge to the Cochrane Review

One of the conclusions of the study by Taylor et al., “Reduced Dietary Salt for the Prevention of Cardiovascular Disease: A Meta-Analysis of Randomized Controlled Trials (Cochrane Review)”,1 was that dietary that sodium reduction in heart failure (HF) is associated with cardiovascular morbidity and mortality. We question this conclusion which was based on a single HF study,2 that we assert is not sufficiently generalizable to be included in this analysis. The study by Paterna et al.2 met the inclusion criteria for this Cochrane Review since it was a randomized trial of two levels of dietary sodium which evaluated cardiovascular morbidity and mortality over a 6 month period. They included 232 HF patients one month following hospitalization for decompensation. The intervention was 80 mmol (1.8 g) vs. 120 mmol (2.8 g) dietary sodium/day. Patients in both groups were prescribed 500–1000 mg of furosemide daily and a 1 l fluid restriction. Patients following the sodium-reduced diet had a greater risk of hospitalization and mortality. Patients in both groups developed hypotension, elevation in serum creatinine, and hypokalemia. Although dietary sodium was the only difference between the two study groups, we argue that other aspects of treatment likely confounded any clinical effects of dietary sodium. HF is a sodium avid state, largely due to impaired renal sodium handling. Sodium balance in HF is maintained by an interplay of neurohumoral blockade which improves renal sodium handling, diuretics which directly increase natriuresis, and dietary sodium restriction. Although all patients in the study by Paterna et al. were taking angiotensin-converting enzyme inhibitors, only 9% were taking β-blockers. Furthermore, patients were prescribed very high doses of loop diuretics, which exceeded dosages typically used in clinical practice as well as maximum doses recommended by HF practice guidelines.3 The patients in the low sodium group were likely exposed to hypovolemia based on the combination of very high diuretic dosage, and both sodium and water restriction. This is likely based on the observations of low blood pressure and increased creatinine in this investigation. We therefore suggest that a more correct interpretation of Paterna et al. is that sodium restriction is dangerous in HF patient who are also receiving very high doses of loop diuretics and fluid restriction. The results of the study by Paterna et al. have limited generalizability to broad HF populations who are on conventional dosages of diuretics, and are also receiving β-blocker therapy. In the absence of other randomized controlled trials, practice guidelines for HF should continue to encourage prudent sodium intake, and individualized and cautious use of diuretics to maintain euvolemia.3 The authors declared no conflict of interest.

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