Michel M Joosten1, Ron T Gansevoort, Kenneth J Mukamal, Hiddo J Lambers Heerspink, Johanna M Geleijnse, Edith J M Feskens, Gerjan Navis, Stephan J L Bakker. 1. Top Institute Food and Nutrition, Wageningen, The Netherlands (M.M.J., J.M.G., E.J.M.F., S.J.L.B.); University of Groningen, University Medical Center Groningen, Department of Internal Medicine, Groningen, The Netherlands (M.M.J., R.T.G., G.N., S.J.L.B.); Beth Israel Deaconess Medical Center, Department of Medicine, Boston, MA (M.M.J.,K.J.M.); University of Groningen, University Medical Center Groningen, Department of Clinical Pharmacology, Groningen, The Netherlands (H.J.L.H.); and Wageningen University, Division of Human Nutrition, Wageningen, The Netherlands (J.M.G., E.J.M.F.).
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.
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.
Authors: Carly E Dougher; Dena E Rifkin; Cheryl Am Anderson; Gerard Smits; Martha S Persky; Geoffrey A Block; Joachim H Ix Journal: Am J Clin Nutr Date: 2016-06-29 Impact factor: 7.045
Authors: Jelmer K Humalda; David J A Goldsmith; Ravi Thadhani; Martin H de Borst Journal: Nephrol Dial Transplant Date: 2015-01-20 Impact factor: 5.992
Authors: Charlotte A Keyzer; Hiddo J Lambers-Heerspink; Michel M Joosten; Petronella E Deetman; Ron T Gansevoort; Gerjan Navis; Ido P Kema; Dick de Zeeuw; Stephan J L Bakker; Martin H de Borst Journal: Clin J Am Soc Nephrol Date: 2015-10-08 Impact factor: 8.237