News Release

Study assesses association between urinary salt excretion and risk of cardiovascular events or death

Peer-Reviewed Publication

JAMA Network

For persons with cardiovascular disease or diabetes, urinary sodium excretion (a surrogate for salt intake) at higher levels or at lower levels compared to mid-range values was associated with an increased risk of cardiovascular events (for higher levels) or cardiovascular death and hospitalization for congestive heart failure (for lower levels), according to a study in the November 23/30 issue of JAMA. Also, higher estimated urinary potassium excretion was associated with a reduced risk of stroke.

There is uncertainty regarding the optimal daily intake of sodium. Findings from prospective cohort studies, evaluating the association between sodium intake and cardiovascular (CV) events, have been conflicting. "Clarifying the optimal daily intake of sodium is particularly important in patients with established CV disease, where it has been inadequately studied. Patients with CV disease may be especially vulnerable to the CV effects of high and low sodium intake and are most likely to receive recommendations on restricting sodium intake," according to background information in the article. The authors add that the optimal level of daily potassium intake, a proposed modifier of the association between sodium intake and CV disease, has not been established.

Martin J. O'Donnell, M.B., Ph.D., and Salim Yusuf, D.Phil., F.R.C.P.C., F.R.S.C., of McMaster University, Hamilton, Ontario, Canada, and colleagues examined the association between sodium and potassium excretion (markers of intake) and CV events and mortality. The study consisted of an observational analyses of 2 cohorts (n = 28,880) included in the ONTARGET and TRANSCEND trials (November 2001-March 2008 from initial recruitment to final follow-up). The researchers estimated 24-hour urinary sodium and potassium excretion from a morning fasting urine sample. Multivariable models were used to determine the association of urinary sodium and potassium with CV events (myocardial infarction [MI; heart attack], stroke, and hospitalization for congestive heart failure (CHF) and mortality.

At study entry, the average estimated 24-hour excretion for sodium was 4.77 g and 2.19 g for potassium. After a median (midpoint) follow-up of 56 months, the composite outcome occurred in 4,729 (16.4 percent) participants. The researchers found that after multivariable analysis, compared with baseline sodium excretion of 4 to 5.99 g per day (n = 14,156 [15.2 percent with the composite outcome]), higher baseline sodium excretion (18.4 percent for 7-8 g/d and 24.1 percent for greater than 8 g/d) and lower sodium excretion (18.2 percent for 2-2.99 g/d and 20.2 percent for less than 2g/d) were associated with an increased risk of the composite of CV death, heart attack, stroke, and hospitalization for CHF.

Compared with the reference group, higher baseline sodium excretion was associated with an increased risk of CV death (9.7 percent for 7-8 g/day; and 11.2 percent for greater than 8 g/day), MI (6.8 percent for greater than 8 g/day), stroke (6.6 percent for greater than 8 g/day), and hospitalization for CHF (6.5 percent for greater than 8 g/day). Lower sodium excretion was associated with an increased risk of CV death (8.6 percent for 2-2.99 g/day; 10.6 percent for less than 2 g/day), and hospitalization for CHF (5.2 percent for 2-2.99 g/day) on multivariable analysis. Compared with an estimated potassium excretion of less than 1.5 g per day, higher potassium excretion was associated with a reduced risk of stroke on multivariable analysis.

The researchers note that previous individual prospective cohort studies have either reported a positive association, no association, or an inverse relationship between sodium intake and CV mortality. "Discrepant findings of previous studies are likely due to differences in ranges of sodium intake, study populations, methods of measurement, and failure to explore a nonlinear association."

"Compared with moderate sodium excretion, we found an association between high sodium excretion and CV events and low sodium excretion and CV death and hospitalization for CHF, which emphasizes the urgent need to establish a safe range for sodium intake in randomized controlled trials. Higher urinary potassium excretion was associated with lower stroke risk and is a potential intervention that merits further evaluation for stroke prevention."

(JAMA. 2011;306[20]:2229-2238. Available pre-embargo to the media at www.jamamedia.org)

Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

Editorial: Urinary Sodium and Cardiovascular Disease Risk

In an accompanying editorial, Paul K. Whelton, M.B., M.D., M.Sc., of the Tulane University School of Public Health and Tropical Medicine, New Orleans, comments on the importance of reducing salt intake.

"Most U.S. adults consume levels of sodium far in excess of physiologic need, and the vast majority of that excess is added during the processing of foods. A progressive reduction in the addition of sodium to food products could represent one of the 'lifestyle' changes with the greatest potential for intervention success. This shift to a more natural diet would concurrently lead to an absolute increase in dietary potassium content and also lead to an improved sodium-potassium ratio, which may be more desirable than change of either electrolyte on its own. The scientific underpinning for the health benefits from sodium reduction is strong, and the available evidence does not support deviating from the stated goal of reducing the exposure to dietary sodium in the general population."

(JAMA. 2011;306[20]:2262-2264. Available pre-embargo to the media at http://www.jamamedia.org)

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Editor's Note: Please see the article for additional information, including financial disclosures, funding and support, etc.

To contact Martin J. O'Donnell, M.B., Ph.D., call Veronica McGuire at 905-525-9140, ext. 22169; or email vmcguir@mcmaster.ca. To contact editorial author Paul K. Whelton, M.B., M.D., M.Sc., email Arthur Nead at anead@tulane.edu.


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