Sodium excretion and risk of developing coronary heart disease

M.M. Joosten, R.T. Gansevoort, K.J. Mukamal, H. Lambers Heerspink, J.M. Geleijnse, E.J.M. Feskens, G. Navis, S.J.L. Bakker

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

Background—Despite compelling evidence for sodium’s adverse effects on blood pressure, it remains uncertain whether excess sodium intake is a risk factor for coronary heart disease (CHD) in the overall population and in potentially more susceptible subgroups. Methods and Results—We prospectively followed 7543 adults aged 28 to 75 years and free of cardiovascular and kidney disease in 1997/1998 of the Prevention of Renal and Vascular End-stage Disease (PREVEND) study. Sodium excretion was measured in two 24-hour urine collections at baseline. Potential susceptibility factors were blood pressure and plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP). Median 24-hour sodium excretion was 137 mmol (Q1–Q3, 106–171 mmol). During a median follow-up of 10.5 (Q1–Q3: 9.9–10.8) years, 452 CHD events occurred. In the entire cohort, there was no association between each 1-g/d (43 mmol/24 h) increment in sodium excretion and CHD risk (adjusted hazard ratio, 1.07; 95% confidence interval, 0.98–1.18; P=0.15). However, the association of sodium excretion with CHD risk tended to be modified by mean arterial pressure (Pinteraction=0.08) and was modified by NT-proBNP (Pinteraction=0.002). When stratified, each 1-g/d increment in sodium excretion was associated with an increased risk for CHD in subjects with hypertension (adjusted hazard ratio, 1.14; 95% confidence interval, 1.01–1.28; n=2363) and in subjects with NT-proBNP concentrations above the sex-specific median (adjusted hazard ratio, 1.16; 95% confidence interval, 1.03–1.30; n=3771). Conclusions—Overall, there was no association between sodium excretion and risk of CHD. The association between sodium excretion and CHD risk was modified by NT-proBNP. Higher sodium excretion was associated with an increased CHD risk among subjects with increased NT-proBNP concentrations or with hypertension.
LanguageEnglish
Pages1121-1128
JournalCirculation
Volume129
DOIs
Publication statusPublished - 2014

Fingerprint

Coronary Disease
Sodium
Brain Natriuretic Peptide
Confidence Intervals
Blood Pressure
Hypertension
Urine Specimen Collection
Kidney Diseases
Chronic Kidney Failure
Blood Vessels
Arterial Pressure
Cardiovascular Diseases
Population

Keywords

  • modest salt reduction
  • blood-pressure
  • potassium intake
  • cardiovascular-disease
  • dietary-sodium
  • urinary sodium
  • natriuretic-peptide
  • hypertension prevention
  • randomized-trials
  • public-health

Cite this

Joosten, M. M., Gansevoort, R. T., Mukamal, K. J., Lambers Heerspink, H., Geleijnse, J. M., Feskens, E. J. M., ... Bakker, S. J. L. (2014). Sodium excretion and risk of developing coronary heart disease. Circulation, 129, 1121-1128. https://doi.org/10.1161/CIRCULATIONAHA.113.004290
Joosten, M.M. ; Gansevoort, R.T. ; Mukamal, K.J. ; Lambers Heerspink, H. ; Geleijnse, J.M. ; Feskens, E.J.M. ; Navis, G. ; Bakker, S.J.L. / Sodium excretion and risk of developing coronary heart disease. In: Circulation. 2014 ; Vol. 129. pp. 1121-1128.
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abstract = "Background—Despite compelling evidence for sodium’s adverse effects on blood pressure, it remains uncertain whether excess sodium intake is a risk factor for coronary heart disease (CHD) in the overall population and in potentially more susceptible subgroups. Methods and Results—We prospectively followed 7543 adults aged 28 to 75 years and free of cardiovascular and kidney disease in 1997/1998 of the Prevention of Renal and Vascular End-stage Disease (PREVEND) study. Sodium excretion was measured in two 24-hour urine collections at baseline. Potential susceptibility factors were blood pressure and plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP). Median 24-hour sodium excretion was 137 mmol (Q1–Q3, 106–171 mmol). During a median follow-up of 10.5 (Q1–Q3: 9.9–10.8) years, 452 CHD events occurred. In the entire cohort, there was no association between each 1-g/d (43 mmol/24 h) increment in sodium excretion and CHD risk (adjusted hazard ratio, 1.07; 95{\%} confidence interval, 0.98–1.18; P=0.15). However, the association of sodium excretion with CHD risk tended to be modified by mean arterial pressure (Pinteraction=0.08) and was modified by NT-proBNP (Pinteraction=0.002). When stratified, each 1-g/d increment in sodium excretion was associated with an increased risk for CHD in subjects with hypertension (adjusted hazard ratio, 1.14; 95{\%} confidence interval, 1.01–1.28; n=2363) and in subjects with NT-proBNP concentrations above the sex-specific median (adjusted hazard ratio, 1.16; 95{\%} confidence interval, 1.03–1.30; n=3771). Conclusions—Overall, there was no association between sodium excretion and risk of CHD. The association between sodium excretion and CHD risk was modified by NT-proBNP. Higher sodium excretion was associated with an increased CHD risk among subjects with increased NT-proBNP concentrations or with hypertension.",
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Joosten, MM, Gansevoort, RT, Mukamal, KJ, Lambers Heerspink, H, Geleijnse, JM, Feskens, EJM, Navis, G & Bakker, SJL 2014, 'Sodium excretion and risk of developing coronary heart disease', Circulation, vol. 129, pp. 1121-1128. https://doi.org/10.1161/CIRCULATIONAHA.113.004290

Sodium excretion and risk of developing coronary heart disease. / Joosten, M.M.; Gansevoort, R.T.; Mukamal, K.J.; Lambers Heerspink, H.; Geleijnse, J.M.; Feskens, E.J.M.; Navis, G.; Bakker, S.J.L.

In: Circulation, Vol. 129, 2014, p. 1121-1128.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Sodium excretion and risk of developing coronary heart disease

AU - Joosten, M.M.

AU - Gansevoort, R.T.

AU - Mukamal, K.J.

AU - Lambers Heerspink, H.

AU - Geleijnse, J.M.

AU - Feskens, E.J.M.

AU - Navis, G.

AU - Bakker, S.J.L.

PY - 2014

Y1 - 2014

N2 - Background—Despite compelling evidence for sodium’s adverse effects on blood pressure, it remains uncertain whether excess sodium intake is a risk factor for coronary heart disease (CHD) in the overall population and in potentially more susceptible subgroups. Methods and Results—We prospectively followed 7543 adults aged 28 to 75 years and free of cardiovascular and kidney disease in 1997/1998 of the Prevention of Renal and Vascular End-stage Disease (PREVEND) study. Sodium excretion was measured in two 24-hour urine collections at baseline. Potential susceptibility factors were blood pressure and plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP). Median 24-hour sodium excretion was 137 mmol (Q1–Q3, 106–171 mmol). During a median follow-up of 10.5 (Q1–Q3: 9.9–10.8) years, 452 CHD events occurred. In the entire cohort, there was no association between each 1-g/d (43 mmol/24 h) increment in sodium excretion and CHD risk (adjusted hazard ratio, 1.07; 95% confidence interval, 0.98–1.18; P=0.15). However, the association of sodium excretion with CHD risk tended to be modified by mean arterial pressure (Pinteraction=0.08) and was modified by NT-proBNP (Pinteraction=0.002). When stratified, each 1-g/d increment in sodium excretion was associated with an increased risk for CHD in subjects with hypertension (adjusted hazard ratio, 1.14; 95% confidence interval, 1.01–1.28; n=2363) and in subjects with NT-proBNP concentrations above the sex-specific median (adjusted hazard ratio, 1.16; 95% confidence interval, 1.03–1.30; n=3771). Conclusions—Overall, there was no association between sodium excretion and risk of CHD. The association between sodium excretion and CHD risk was modified by NT-proBNP. Higher sodium excretion was associated with an increased CHD risk among subjects with increased NT-proBNP concentrations or with hypertension.

AB - Background—Despite compelling evidence for sodium’s adverse effects on blood pressure, it remains uncertain whether excess sodium intake is a risk factor for coronary heart disease (CHD) in the overall population and in potentially more susceptible subgroups. Methods and Results—We prospectively followed 7543 adults aged 28 to 75 years and free of cardiovascular and kidney disease in 1997/1998 of the Prevention of Renal and Vascular End-stage Disease (PREVEND) study. Sodium excretion was measured in two 24-hour urine collections at baseline. Potential susceptibility factors were blood pressure and plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP). Median 24-hour sodium excretion was 137 mmol (Q1–Q3, 106–171 mmol). During a median follow-up of 10.5 (Q1–Q3: 9.9–10.8) years, 452 CHD events occurred. In the entire cohort, there was no association between each 1-g/d (43 mmol/24 h) increment in sodium excretion and CHD risk (adjusted hazard ratio, 1.07; 95% confidence interval, 0.98–1.18; P=0.15). However, the association of sodium excretion with CHD risk tended to be modified by mean arterial pressure (Pinteraction=0.08) and was modified by NT-proBNP (Pinteraction=0.002). When stratified, each 1-g/d increment in sodium excretion was associated with an increased risk for CHD in subjects with hypertension (adjusted hazard ratio, 1.14; 95% confidence interval, 1.01–1.28; n=2363) and in subjects with NT-proBNP concentrations above the sex-specific median (adjusted hazard ratio, 1.16; 95% confidence interval, 1.03–1.30; n=3771). Conclusions—Overall, there was no association between sodium excretion and risk of CHD. The association between sodium excretion and CHD risk was modified by NT-proBNP. Higher sodium excretion was associated with an increased CHD risk among subjects with increased NT-proBNP concentrations or with hypertension.

KW - modest salt reduction

KW - blood-pressure

KW - potassium intake

KW - cardiovascular-disease

KW - dietary-sodium

KW - urinary sodium

KW - natriuretic-peptide

KW - hypertension prevention

KW - randomized-trials

KW - public-health

U2 - 10.1161/CIRCULATIONAHA.113.004290

DO - 10.1161/CIRCULATIONAHA.113.004290

M3 - Article

VL - 129

SP - 1121

EP - 1128

JO - Circulation

T2 - Circulation

JF - Circulation

SN - 0009-7322

ER -