Physicians' Academy for Cardiovascular Education

More than 3.7 g sodium per day has a negative effect on cardiac mechanics

Association of Estimated Sodium Intake With Adverse Cardiac Structure and Function

From the HyperGEN Study

Selvaraj S, a Luc Djoussé MA, Aguilar FG, et al. - J Am Coll Cardiol 2017;70:715–24


Recent recommendations regarding sodium intake goals of 1.5 to 2.3 g/day have been challenged by data showing a J-shaped relationship between estimated sodium intake (ESI) and the risk of death and cardiovascular (CV) events [1,2]. Although other studies suggest that ESI is linearly related with mortality, there are only a few data examining the association between low sodium intake and CV events [3].

In this study, the relationship between ESI and indices expressing systolic strain and myocardial relaxation was evaluated in 2,996 individuals without heart failure (HF), using data from the large population based cross-sectional study HyperGEN, which aimed at characterizing and identifying the genetic basis of familial hypertension [4]. Included were participants with a diagnosis of hypertension <60 years and at least 1 sibling willing to participate in the study. A random sample of normotensive individuals was also recruited. Stratification was based on ESI (≥3.7 g/day = spline 1 vs. >3.7 g/day = spline 2).

Urinary electrolytes were measured from overnight urine collections and extrapolated to 24-h urinary sodium and potassium excretion using the method of Tanaka [5]. The 24-h urinary sodium was used as a surrogate of sodium intake.

Indices of cardiac structure and function, like for example left ventricular (LV) ejection fraction (LVEF), LV mass index, the early diastolic (E) and late/atrial diastolic (A) trans-mitral velocities, the E/A ratio, the isovolumic relaxation time and E deceleration time as well as the peak longitudinal and circumferential strain and the average speckle-tracking derived e’ (STe’) velocities, were calculated based on echocardiographic images.

Main results


In contrast to an ESI of <3.7 g/day, an ESI of ≥3.7 g/day was associated with adverse strain and STe’, SBP and serum aldosterone explained a significant proportion of the indirect effects between ESI and strain and STe’. These results support the hypothesis of the adverse CV effects of high sodium intake.

Editorial comment

In his editorial article [6], Marwick discusses the limitations of the study published by Selvaraj et al, including:

  • The echocardiographic methodology is characterized as being an ‘archaeological echocardiography’ approach, since echo-images stored on videotapes may show lower values of strain and velocity.
  • The link between aldosterone and the effect of sodium intake on myocardial function implies that fibrosis might have been the reason for the myocardial change.
  • The subjects with higher salt intake were more likely to have hypertension, obesity, dyslipidemia and diabetes mellitus.

The author concludes: ‘The observed effects of salt on myocardial function may be very relevant in some groups. The evidence provided in the paper by Selvaraj et al. supports renewed attention to the potential benefits of controlling salt intake, especially in individuals with a risk of myocardial dysfunction. Because of the pervasive presence of sodium in the Western diet, there is some urgency in clarifying this information. The next logical step might be to investigate the merits of salt reduction, and related contributors such as dietary fiber in patients with LV dysfunction, the precursor to heart failure.’


Show references

Find this article online at JACC