Rethinking Sodium Restriction in Systolic Heart Failure

The only thing certain in life is change. This is certainly true of medicine in general and dietary information in particular. Salt restriction recommendations for heart failure, once considered a core foundational practice tantamount to diuretics for fluid overload, are now being questioned.

European and North American heart failure management guidelines recommend sodium restriction for patients with systolic and diastolic heart failure with preserved ejection fraction. Available data now suggest that sodium restriction may actually increase mortality among patients with systolic heart failure. As a generalist, perhaps I was not aware of this raging debate among the subspecialists, but now would be a great time to pay attention and try to understand what is being said.

Pharmacist James J DiNicolantonio of Wegmans Pharmacy, Ithaca, NY, and colleagues recently published a systematic review evaluating the impact of a restricted sodium diet in patients with systolic heart failure. The authors included randomized controlled clinical trials enrolling adults with systolic heart failure (ejection fraction < 40%) evaluating studies restricting salt through a dietary intervention or recommending reduced salt intake.

Six studies with 2,747 subjects were included in the analysis. Studies reported that all subjects consumed the same diet, except for the level of sodium, which ranged from low (< 1.8 g/day) to normal (2.8 g/day). Trials measured 24-hour urinary sodium levels.

Compared with a normal sodium diet, a low sodium diet increased the risk for mortality (RR 1.95; 1.66 to 2.29), sudden cardiac death (RR 1.72; 1.21 to 2.44), heart failure (RR 2.23; 1.77 to 2.81), and heart failure readmissions (RR 2.10; 1.67 to 2.64) (Heart doi:10.1136/heartjnl-2012-302337).

The trials showed that a normal sodium intake improved ejection fraction, renal function, hydration status, aldosterone/renin activity, heart rate, BNP, TNF-alpha, IL-6 and prevented hyponatremia. These data may suggest that harm is caused at lower levels of sodium intake due to the counter-regulatory mechanisms addressing hypovolemia. Indeed, hyponatremia is an independent risk predictor of mortality.

This article is likely to generate more discussion. Many of us will likely “wait and see” how large organizations such as the American Heart Association are going to respond to or challenge this information. Let’s hope they can convince us with open minds and thoughtful analysis rather than reflexive defense of traditional paradigms.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflict of interest. The opinions expressed are solely those of the author. Contact him at [email protected].

The only thing certain in life is change. This is certainly true of medicine in general and dietary information in particular. Salt restriction recommendations for heart failure, once considered a core foundational practice tantamount to diuretics for fluid overload, are now being questioned.

European and North American heart failure management guidelines recommend sodium restriction for patients with systolic and diastolic heart failure with preserved ejection fraction. Available data now suggest that sodium restriction may actually increase mortality among patients with systolic heart failure. As a generalist, perhaps I was not aware of this raging debate among the subspecialists, but now would be a great time to pay attention and try to understand what is being said.

Pharmacist James J DiNicolantonio of Wegmans Pharmacy, Ithaca, NY, and colleagues recently published a systematic review evaluating the impact of a restricted sodium diet in patients with systolic heart failure. The authors included randomized controlled clinical trials enrolling adults with systolic heart failure (ejection fraction < 40%) evaluating studies restricting salt through a dietary intervention or recommending reduced salt intake.

Six studies with 2,747 subjects were included in the analysis. Studies reported that all subjects consumed the same diet, except for the level of sodium, which ranged from low (< 1.8 g/day) to normal (2.8 g/day). Trials measured 24-hour urinary sodium levels.

Compared with a normal sodium diet, a low sodium diet increased the risk for mortality (RR 1.95; 1.66 to 2.29), sudden cardiac death (RR 1.72; 1.21 to 2.44), heart failure (RR 2.23; 1.77 to 2.81), and heart failure readmissions (RR 2.10; 1.67 to 2.64) (Heart doi:10.1136/heartjnl-2012-302337).

The trials showed that a normal sodium intake improved ejection fraction, renal function, hydration status, aldosterone/renin activity, heart rate, BNP, TNF-alpha, IL-6 and prevented hyponatremia. These data may suggest that harm is caused at lower levels of sodium intake due to the counter-regulatory mechanisms addressing hypovolemia. Indeed, hyponatremia is an independent risk predictor of mortality.

This article is likely to generate more discussion. Many of us will likely “wait and see” how large organizations such as the American Heart Association are going to respond to or challenge this information. Let’s hope they can convince us with open minds and thoughtful analysis rather than reflexive defense of traditional paradigms.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflict of interest. The opinions expressed are solely those of the author. Contact him at [email protected].

The only thing certain in life is change. This is certainly true of medicine in general and dietary information in particular. Salt restriction recommendations for heart failure, once considered a core foundational practice tantamount to diuretics for fluid overload, are now being questioned.

European and North American heart failure management guidelines recommend sodium restriction for patients with systolic and diastolic heart failure with preserved ejection fraction. Available data now suggest that sodium restriction may actually increase mortality among patients with systolic heart failure. As a generalist, perhaps I was not aware of this raging debate among the subspecialists, but now would be a great time to pay attention and try to understand what is being said.

Pharmacist James J DiNicolantonio of Wegmans Pharmacy, Ithaca, NY, and colleagues recently published a systematic review evaluating the impact of a restricted sodium diet in patients with systolic heart failure. The authors included randomized controlled clinical trials enrolling adults with systolic heart failure (ejection fraction < 40%) evaluating studies restricting salt through a dietary intervention or recommending reduced salt intake.

Six studies with 2,747 subjects were included in the analysis. Studies reported that all subjects consumed the same diet, except for the level of sodium, which ranged from low (< 1.8 g/day) to normal (2.8 g/day). Trials measured 24-hour urinary sodium levels.

Compared with a normal sodium diet, a low sodium diet increased the risk for mortality (RR 1.95; 1.66 to 2.29), sudden cardiac death (RR 1.72; 1.21 to 2.44), heart failure (RR 2.23; 1.77 to 2.81), and heart failure readmissions (RR 2.10; 1.67 to 2.64) (Heart doi:10.1136/heartjnl-2012-302337).

The trials showed that a normal sodium intake improved ejection fraction, renal function, hydration status, aldosterone/renin activity, heart rate, BNP, TNF-alpha, IL-6 and prevented hyponatremia. These data may suggest that harm is caused at lower levels of sodium intake due to the counter-regulatory mechanisms addressing hypovolemia. Indeed, hyponatremia is an independent risk predictor of mortality.

This article is likely to generate more discussion. Many of us will likely “wait and see” how large organizations such as the American Heart Association are going to respond to or challenge this information. Let’s hope they can convince us with open minds and thoughtful analysis rather than reflexive defense of traditional paradigms.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflict of interest. The opinions expressed are solely those of the author. Contact him at [email protected].