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New studies say restricting salt intake can reduce the risk of atrial fibrillation (AF) in certain patients, but cannot reduce the risks of morbidity and death in patients with heart failure.
There is a complex relationship between sodium intake and heart health outcomes in patients with cardiovascular disease, diabetes, and heart failure, according to recent research. One study suggests a J-shaped link between high sodium consumption and increased risk of atrial fibrillation (AF), urging a rethink of dietary habits. Meanwhile, another review challenges longstanding beliefs about sodium restriction in heart failure management, hinting at a nuanced approach that may impact patient quality of life. These findings prompt a deeper exploration into dietary recommendations and their implications for cardiovascular health.
Sodium intake beyond 6 grams per day was linked to a 10% increased AF risk for each additional gram consumed | Image credit: Melica – stock.adobe.com
New research says reducing salt intake can mitigate the risk of AF in patients with cardiovascular disease or diabetes.
Published in JAMA Network Open, the study revealed a J-shaped relationship between sodium intake and the risk of developing AF for these patients.1 The research is part of the Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) and Telmisartan Randomised Assessment Study in ACE Intolerant Subjects With Cardiovascular Disease (TRANSCEND).
This cohort study included 27,391 participants from the ONTARGET and TRANSCEND trials with vascular disease or high-risk diabetes, with a mean (SD) age of 66.3 (7.2) years and with most (70.5%) being male. Participants without a urine sample for sodium measurement, those with missing data, a history of AF, or AF detected within the first year of enrollment were excluded. The study analyzed sodium intake estimated from morning fasting urine samples using the Kawasaki formula.
Key findings revealed that over a mean (SD) follow-up period of 4.6 (1.0) years, The average sodium intake was 4.8 (1.6) grams per day, and 5.7% of participants developed incident AF. Within the J-shaped association between sodium intake and AF risk, the researchers also observed a significant increase in AF risk at high sodium intakes. Specifically, participants consuming 8 grams or more of sodium per day had a 32% higher risk of developing AF compared with those consuming 4 to 5.99 grams per day.
Additionally, sodium intake greater than 6 grams per day was linked to a 10% increased AF risk per additional gram of sodium consumed. However, the researchers found no evidence that consuming less sodium would reduce AF risk, other than that consuming less than 5 grams per day was not significantly associated with AF risk.
“Low sodium intake, at levels consumed by less than 3% of the population in our study, was associated with increased AF risk when early AF events were included,” the authors mentioned. “Low sodium intakes could lead to AF through orthostatic hypotension and activation of the renin-angiotensin-aldosterone system, as well as increased adrenaline excretion.”
Among individuals with hypertension, the link between sodium intake and incident AF was found to be independent of systolic blood pressure. Randomization to telmisartan or ramipril, alone or in combination, did not affect AF incidence in the overall population or among patients with hypertension. Additionally, the link between sodium consumption and AF was more pronounced among diuretic users, especially those without a history of hypertension. Despite similar sodium intakes, diuretic users were more frequently hospitalized for heart failure, suggesting a high prevalence of unreported or early asymptomatic heart failure, which likely influenced their AF risk. Future research should explore if sodium-reducing interventions could lower AF incidence in individuals with subclinical heart failure.
“These data suggest that lowering sodium intake for AF prevention is best targeted at individuals who consume high-sodium diets,” the authors concluded.
Meanwhile, another recent paper published in the European Journal of Clinical Investigation suggested that sodium intake restrictions do not reduce the risks of morbidity or mortality for patients with heart failure, though some symptoms may improve.2
For decades, it was standard practice to recommend reducing salt intake for patients with heart failure, based on the belief that neurohumoral activation and fluid retention made sodium restriction beneficial. However, a narrative review of literature from 2000 to 2023 found that strict sodium restriction does not significantly reduce mortality or hospitalization rates for heart failure patients, and that there is no proven clinical benefit from strict sodium intake, with or without restricted fluid intake.
Paolo Raggi, MD, cardiology consultant at the University of Alberta Hospital and sole author of this review, analyzed a range of studies, including some small randomized trials and a large trial that was stopped early due to futility.
The American Heart Association recommends a daily sodium intake of less than 1.5 grams, while the World Health Organization suggests less than 2 grams per day for everyone. These guidelines are primarily based on the influential DASH-sodium trial and other studies showing benefits in controlling hypertension and reducing cardiovascular events. However, there is no consensus among experts on the ideal daily sodium intake, as highlighted by conflicting interpretations of the same evidence in major cardiovascular journals. Some studies suggest a J-shaped curve for sodium intake, where both very high and very low intakes are associated with increased mortality, yet others dispute these findings due to perceived biases in study designs.
According to Raggi, small randomized clinical trials have shown no significant reduction in mortality or hospitalization from sodium restriction, though some quality of life improvements were noted. These past findings suggest that while severe sodium restriction may not significantly impact survival, a moderate intake of 2 to 3 grams per day might be a more practical and beneficial approach.
Of note, the review highlighted a personal case of a patient with heart failure who experienced fluid overload due to high sodium intake from ramen noodles, illustrating the practical challenges of reducing sodium consumption. Some research has suggested that substituting sodium with potassium may offer a more effective and sustainable strategy for improving cardiovascular outcomes compared with just restricting sodium intake. Additionally, while salt substitutes might help control hypertension, their use in patients with heart failure is limited due to the risk of hyperkalemia.
On the other end of the spectrum, prior research has suggested that consuming too little salt could have an adverse effect on patients with heart failure with preserved ejection fraction (HFpEF).3
A subanalysis of the TOPCAT trial published in 2022 examined the impact of strict salt-intake guidelines on patients with HFpEF. Contrary to prevailing assumptions, participants with a self-reported cooking salt score greater than 0 showed a 24% collective reduced risk of cardiovascular death, heart failure hospitalization, and sudden cardiac arrest compared with those with a score of 0. These patients also had a 26% reduced risk of HF hospitalization specifically. The observed decreases in all-cause mortality and cardiovascular death were found not to be statistically significant, with reductions of 16% and 22%, respectively.
These findings challenge the efficacy of severe salt restriction in improving outcomes for HFpEF patients, highlighting potential harm from overly strict dietary recommendations and advocating for reconsideration of current clinical advice.
“Overstrict dietary salt intake restriction could harm patients with HFpEF and is associated with worse prognosis,” the researchers wrote. “Physicians should reconsider giving this advice to patients with HFpEF.”
When considering fluid restriction for patients with heart failure, it's important to understand the distribution of body water. Most water is outside the vascular system, with only about 10% being intravascular.2 In heart failure, both intravascular and interstitial volumes increase, leading to edema. While fluid restriction seems logical to manage heart failure, evidence supporting this approach is limited.
“Pathophysiologically, it may not matter if the oral intake of fluid is restricted from an average of 2000 mL per day to 800 mL per day,” Raggi wrote in his review. “In fact, the fluid shifts that affect the compensated state in heart failure take place between the splanchnic venous reservoir and the extravascular space, driven by both osmolar concentrations and neuro-adrenergic stimuli.”
The European Society of Cardiology has suggested fluid restriction for select patients but provided no specific guidelines on the degree or patient type. Additionally, small trials have found no significant benefits from strict fluid and sodium restrictions in patients with acute decompensated heart failure. While some studies have shown improvements in symptoms and quality of life, the evidence is inconsistent, and Raggi wrote that larger, more comprehensive trials are needed.
Raggi concluded that a moderate daily sodium intake of 3 to 4.5 grams seems sensible to enhance quality of life and functional abilities in patients with heart failure, although it is unlikely to affect life expectancy or hospitalization rates. He wrote those experiencing frequent hospitalizations due to fluid overload may benefit from reducing their sodium intake to between 2 and 3 grams per day.
“All patients with heart failure should favour fresh fruits and vegetables, and preferably prepare their own meals, rather than eating prepared meals that typically contain large amounts of sodium,” Raggi wrote. “The debate on tight sodium restriction in heart failure continues to appear in major medical journals, yet it would seem that after many years of controversy the time has come to close it.”
References
The Importance of Examining and Preventing Atrial Fibrillation