WASHINGTON, DC — An estimated sodium intake exceeding 3.7 g/day was associated with echocardiographic measures of subclinical cardiac remodeling and dysfunction in a population-based study[1].
Most of the significant association was not explained by dietary sodium effects on systolic blood pressure, according to the investigators, who propose that sodium effects on aldosterone and therefore myocardial fibrosis may also be involved.
Cardiac dysfunction was identified by speckle-tracking echocardiographic analysis of myocardial strain and the e’ velocity metric for diastolic function, explained lead author Dr Senthil Selvaraj (Brigham and Women’s Hospital and Harvard Medical School, Boston, MA) to theheart.org | Medscape Cardiology by email.
High sodium intake, estimated by 24-hour urinary sodium excretion, also was associated with adverse left atrial and LV structural remodeling in the analysis, based on 2996 subjects followed by echo in the Hypertension Genetic Epidemiology Network (HyperGEN) study.
“Our data may offer mechanistic insight into why high sodium intake is associated with worse cardiovascular outcomes, including heart failure,” the group writes in their report published in the August 8, 2017 issue of the Journal of the American College of Cardiology.
Causation or Association?
High dietary sodium might not actually cause abnormal myocardial strain and e’ velocities; rather, “it may be a marker of a higher-risk patient with poor dietary habits in general,” the group writes. But, “if causal, elevated estimated sodium intake may be multifactorially related to worse systolic strain and impaired diastolic relaxation.”
The findings have implications for dietary guidelines, management of hypertensive patients, and the conduct of hypertension clinical trials, according to Selvaraj.
Given the population-based nature of the study, he said, “extrapolation to any given patient is difficult, and there may be significant variability with each patient. However, we believe our results to be applicable in a broad sense to the population studied, predominantly hypertensive patients,” although the study included patients without hypertension.
Interestingly, “In an exploratory analysis, we did find that the relationship of elevated sodium intake with poor strain was much more prominent in participants with low potassium intake,” Selvaraj said. That is consistent with well-recognized evidence that high potassium intake “may counteract the adverse effects of sodium intake in the general population.”
Because echocardiography has been used in research to track the success of antihypertensive therapy on LV hypertrophy, similarly following patients on salt-restricted diets in practice might be feasible, he speculated. “With respect to dietary sodium, it is possible that strain and diastolic function could also be monitored as a metric of success as well.”
“It is entirely plausible that the association of subclinical dysfunction with daily sodium intake exists because sodium is a marker of other dietary characteristics, rather than having a causative role,” agreed Dr Thomas H Marwick (Baker Heart and Diabetes Institute, Melbourne, Australia) in an accompanying editorial[2].
“More Than Just a Curiosity”
But the study’s primary finding of a link between sodium intake and myocardial mechanics, Marwick writes, “is more than just a curiosity; myocardial strain is an important predictor of adverse outcome, probably stronger than ejection fraction, especially at normal or nearly normal ejection fractions. In this context, an effect on myocardial function, independent of BP, could be a powerful argument to instigate reduced salt intake in individuals at risk of subclinical dysfunction, including those with hypertension and type 2 diabetes.”
The study used the cohort’s M-mode, two-dimensional, and Doppler echo data that had been stored in an analog format; digital storage wasn’t widely used at the time. Images were then digitized to allow speckle-tracking analysis, an accepted technique that, the authors acknowledge and Marwick cautions, likely underestimated actual strain and velocity readings.
The cohort’s mean blood pressure was 126 mm Hg systolic and 72 mm Hg diastolic, mean estimated glomerular filtration rate was 87 mL/min/1.73 m2, median estimated sodium intake was 3.73 g/day, and median estimated potassium intake was 1.55 g/day.
Doppler, 2D, and Speckle-Tracking Echo Parameters by Estimated Sodium Intake in HyperGEN Cohort
| Parameter | < 3.7 g/day, n=1457 |
>3.7 g/day, n=1,539 | P |
|---|---|---|---|
| LV end-diastolic volume, mL | 125 | 133 | <0.001 |
| LV end-systolic volume, mL | 49 | 53 | <0.001 |
| LV mass index, g/m2 | 82 | 85 | <0.001 |
| Left atrial diameter, cm | 3.4 | 3.5 | <0.001 |
| LVEF, % | 62 | 61 | 0.03 |
| E/A ratio | 1.28 | 1.20 | 0.001 |
| e’ , cm/s | 3.8 | 3.6 | <0.001 |
| E/e’ ratio | 22.5 | 22.9 | 0.41 |
| Longitudinal strain, % | 14.6 | 14.4 | 0.09 |
A=late/atrial diastolic transmitral velocity
E=early diastolic transmitral velocity
e’=early diastolic tissue velocity (derived from speckle tracking)
In analysis adjusted for age, sex, smoking status, alcohol intake, daily walking distance, diuretic use, estimated glomerular filtration rate, LV mass, LVEF, wall-motion abnormalities, speckle-tracking analysis, and image quality, estimated sodium intake >3.7 g/day was associated with:
-
Larger left atrial and LV dimensions (P<0.05).
-
Lower LVEF (P<0.05).
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Worsened longitudinal strain (P=0.009) and circumferential strain (P=0.045).
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Lower e’ velocity (P=0.015).
Sodium intake of <3.7 g/day wasn’t significantly related to those parameters.
Strain by echocardiography correlates with myocardial fibrosis, myocyte hypertrophy, and abnormal calcium flux in myocytes, the authors explain; e’ is a tissue-Doppler measure of diastolic relaxation for which lower values suggest dysfunction.
Sodium and Aldosterone
Closer analysis, the group writes, “suggested that systolic blood pressure explained 14% and 20% of the indirect effects between estimated sodium intake and longitudinal strain and e’ velocity, respectively, whereas serum aldosterone explained 19% of the indirect effects between estimated sodium intake and longitudinal strain.”
The possible role of aldosterone in the observed sodium-cardiac function link “brings the possibility that the observed myocardial change could be related to fibrosis. Autonomous aldosterone secretion (producing inappropriate aldosterone levels for sodium status) may be present in 30% of hypertensive subjects,” Marwick observed.
“Although aldosterone may not be directly implicated in this case (there appears to be no difference in aldosterone levels between the high- and low-salt excreters), there may be an indirect effect because the adverse effects of aldosterone are not apparent in the absence of sodium.”
The study was funded by grants from the National Institutes of Health. Selvaraj had no relevant financial relationships. Disclosures for the coauthors are listed in the paper.
Marwick reports that he has no relevant financial relationships.
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