By Van Selby, MD
Assistant Professor of Medicine, UCSF Cardiology Division, Advanced Heart Failure Section, San Francisco
Dr. Selby reports no financial relationships relevant to this field of study.
SYNOPSIS: In an observational study of outpatients with NYHA class II or III heart failure, dietary sodium restriction (< 2500 mg/day) was associated with increased risk of death or heart failure hospitalization.
SOURCE: Doukky R, et al. Impact of dietary sodium restriction on heart failure outcomes. JACC Heart Fail 2016 2016;4:24-35.
Dietary sodium restriction is perhaps the most common self-care recommendation patients with chronic heart failure (HF) receive. However, data evaluating the effectiveness of sodium restriction are sparse, and the few studies that do exist have shown conflicting results.
To evaluate the relationship between dietary sodium restriction and clinical outcomes in chronic HF, Doukky et al analyzed data from the HF Adherence and Retention Trial (HART), a multicenter study of 902 patients with New York Heart Association (NYHA) functional class II or III systolic or diastolic HF. Patients were followed for a median of 36 months, and sodium intake was assessed using a food frequency questionnaire. Patients were classified as either sodium restricted (< 2500 mg/d) or unrestricted (≥ 2500 mg/d), and propensity score matching was used to address possible confounders. The primary outcome was the composite of death or HF hospitalization.
Sodium restriction was associated with a significantly higher risk of death or HF hospitalization (42.3% vs 26.2%; hazard ratio [HR], 1.85; P = 0.004). The difference was primarily due to higher rates of HF hospitalization (HR, 1.82;P = 0.015), though there was also a nonsignificant increase in the rate of death (P = 0.074). Subgroup analyses found the increased risk associated with sodium restriction was particularly high in patients not taking angiotensin-converting-enzyme inhibitors or angiotensin receptor blockers (HR, 5.78; P = 0.002) and patients with milder NYHA class II symptoms (HR, 2.36; P = 0.003). Sodium restriction was not associated with any significant effect on quality of life, 6-minute walk distance, or symptom severity. The authors concluded that dietary sodium restriction may have a detrimental effect on outcome in patients with symptomatic chronic HF. They stress that a randomized clinical trial is warranted to resolve the issue.
COMMENTARY
Excessive sodium intake is associated with fluid retention, and many episodes of acute decompensated HF are often attributed to “sodium binges” in patients with stable chronic HF. For decades, sodium restriction has been a cornerstone of appropriate HF management, and the benefits of sodium restriction were so obvious that a trial evaluating its effectiveness seemed unnecessary. Current U.S. guidelines recommend patients with symptomatic HF restrict sodium intake to between 2000-3000 mg/day.
More recently, investigators are evaluating the effectiveness of sodium restriction more rigorously, and the results have been mixed. Several small studies have shown a clear benefit, with decreased signs and symptoms of HF as well as improved event-free survival. However, other studies have shown no clear benefit associated with sodium restriction, especially in patients with milder (class I-II) HF. The Doukky study is important for two reasons. First, the patients were recruited from a large, multicenter clinical trial. Second, the study evaluated an objective clinical outcome and found increased adverse outcomes among sodium-restricted patients.
Why would sodium restriction be harmful? Small studies have shown that sodium restriction increases neurohormonal activation by worsening intravascular volume depletion. Sodium restriction may also worsen hemodynamics, with a decrease in cardiac index and increase in systemic vascular resistance. In the Doukky study, patients not receiving angiotensin-converting-enzyme inhibitors or angiotensin receptor blockers showed an especially high risk of adverse events with sodium restriction, suggesting the effect is mediated through neurohormonal pathways. Interestingly, sodium restriction was associated with a greater increase in adverse outcomes among patients with milder, class II symptoms. This is similar to what has been reported in other studies. It is possible that more symptomatic (class III) patients are particularly prone to hypervolemia, and, therefore, sodium restriction is beneficial for preventing worsening fluid overload. Class II patients, on the other hand, experience the detrimental neurohormonal activation from sodium restriction without seeing the benefits related to hypervolemia.
Limitations include the retrospective design, small sample size, and use of a food frequency questionnaire to measure dietary sodium intake. The authors used propensity matching to eliminate confounders, but it is still possible the sodium-restricted patients comprised a sicker group overall. This study offers no information regarding the utility of sodium restriction during hospitalization for acute HF.
Despite these limitations, the Doukky study adds to a growing body of research suggesting dietary sodium restriction may not be beneficial, perhaps even harmful in chronic HF. In response to this increasing evidence, the most recent European guidelines have removed any formal recommendation regarding sodium restriction, and the 2013 American Heart Association/American College of Cardiology guidelines downgraded the strength of their longstanding recommendation regarding dietary sodium restriction from class I (recommended) to class IIa (reasonable). Given the prevalence of chronic HF and the widespread use of recommendations regarding dietary sodium intake, many in the field echo the authors’ call for a randomized trial to rigorously evaluate the effectiveness of these recommendations. Until then, there is no clear evidence to support aggressive sodium restriction in chronic HF, especially in patients with mild disease.