Andrew Mente1, Martin O'Donnell2, Sumathy Rangarajan3, Gilles Dagenais4, Scott Lear5, Matthew McQueen6, Rafael Diaz7, Alvaro Avezum8, Patricio Lopez-Jaramillo9, Fernando Lanas10, Wei Li11, Yin Lu12, Sun Yi12, Lei Rensheng13, Romaina Iqbal14, Prem Mony15, Rita Yusuf16, Khalid Yusoff17, Andrzej Szuba18, Aytekin Oguz19, Annika Rosengren20, Ahmad Bahonar21, Afzalhussein Yusufali22, Aletta Elisabeth Schutte23, Jephat Chifamba24, Johannes F E Mann25, Sonia S Anand26, Koon Teo3, S Yusuf26. 1. Population Health Research Institute, Hamilton Health Sciences, Hamilton, ON, Canada; Department of Clinical Epidemiology and Biostatistics, Hamilton, ON, Canada. Electronic address: andrew.mente@phri.ca. 2. Population Health Research Institute, Hamilton Health Sciences, Hamilton, ON, Canada; Department of Medicine, Hamilton, ON, Canada; HRB-Clinical Research Facility, NUI Galway, Ireland. 3. Population Health Research Institute, Hamilton Health Sciences, Hamilton, ON, Canada. 4. Laval University Heart and Lungs Institute, Quebec City, QC, Canada. 5. Faculty of Health Sciences, Simon Fraser University, BC, Canada; Division of Cardiology, Providence Health Care, BC, Canada. 6. Department of Laboratory Medicine, McMaster University, Hamilton, ON, Canada. 7. Estudios Clínicos Latinoamérica, Rosario, Argentina. 8. Dante Pazzanese Institute of Cardiology, Sao Paulo, SP, Brazil. 9. Fundacion Oftalmologica de Santander-FOSCAL, Medical School, Universidad de Santander Floridablanca-Santander, Colombia. 10. Universidad de La Frontera, Temuco, Chile. 11. National Centre for Cardiovascular Diseases, Cardiovascular Institute and Fuwai Hospital, Chinese Academy of Medical Sciences, Beijing, China. 12. Medical Research & Biometrics Center, National Center for Cardiovascular Diseases, FuWai Hospital, Beijing, China. 13. Center for Disease Control & Prevention Nanchang County, Nanchang City, Jiangxi Province, China. 14. Departments of Community Health Sciences and Medicine, Aga Khan University, Karachi, Pakistan. 15. Community Health & Epidemiology, St John's Research Institute, Bangalore, India. 16. The School of Life Sciences and The Centre for Health, Population, and Development, Independent University, Bangladesh. 17. Faculty of Medicine, Universiti Teknologi MARA, Sungai Buloh, Selangor, Malaysia. 18. Division of Angiology, Wroclaw Medical University, Wrocław, Poland; Department of Internal Medicine, 4th Military Hospital in Wroclaw, Poland. 19. Istanbul Medeniyet University, Faculty of Medicine, Department of Internal Medicine, Istanbul, Turkey. 20. Sahlgrenska Academy University of Gothenburg, Gothenburg, Sweden. 21. Hypertension Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran. 22. Hatta Hospital, Dubai Health Authority, Dubai, UAE. 23. MRC Unit for Hypertension and CVD/Hypertension in Africa Research Team, North-West University, Potchefstroom, North West Province, South Africa. 24. University of Zimbabwe, College of Health Sciences, Physiology Department, Harare, Zimbabwe. 25. Population Health Research Institute, Hamilton Health Sciences, Hamilton, ON, Canada; Department of Nephrology, University of Erlangen-Nurnberg and Munich General Hospitals, Munich, Germany. 26. Population Health Research Institute, Hamilton Health Sciences, Hamilton, ON, Canada; Department of Clinical Epidemiology and Biostatistics, Hamilton, ON, Canada; Department of Medicine, Hamilton, ON, Canada.
Abstract
BACKGROUND: Several studies reported a U-shaped association between urinary sodium excretion and cardiovascular disease events and mortality. Whether these associations vary between those individuals with and without hypertension is uncertain. We aimed to explore whether the association between sodium intake and cardiovascular disease events and all-cause mortality is modified by hypertension status. METHODS: In this pooled analysis, we studied 133,118 individuals (63,559 with hypertension and 69,559 without hypertension), median age of 55 years (IQR 45-63), from 49 countries in four large prospective studies and estimated 24-h urinary sodium excretion (as group-level measure of intake). We related this to the composite outcome of death and major cardiovascular disease events over a median of 4.2 years (IQR 3.0-5.0) and blood pressure. FINDINGS: Increased sodium intake was associated with greater increases in systolic blood pressure in individuals with hypertension (2.08 mm Hg change per g sodium increase) compared with individuals without hypertension (1.22 mm Hg change per g; pinteraction<0.0001). In those individuals with hypertension (6835 events), sodium excretion of 7 g/day or more (7060 [11%] of population with hypertension: hazard ratio [HR] 1.23 [95% CI 1.11-1.37]; p<0.0001) and less than 3 g/day (7006 [11%] of population with hypertension: 1.34 [1.23-1.47]; p<0.0001) were both associated with increased risk compared with sodium excretion of 4-5 g/day (reference 25% of the population with hypertension). In those individuals without hypertension (3021 events), compared with 4-5 g/day (18,508 [27%] of the population without hypertension), higher sodium excretion was not associated with risk of the primary composite outcome (≥ 7 g/day in 6271 [9%] of the population without hypertension; HR 0.90 [95% CI 0.76-1.08]; p=0.2547), whereas an excretion of less than 3 g/day was associated with a significantly increased risk (7547 [11%] of the population without hypertension; HR 1.26 [95% CI 1.10-1.45]; p=0.0009). INTERPRETATION: Compared with moderate sodium intake, high sodium intake is associated with an increased risk of cardiovascular events and death in hypertensive populations (no association in normotensive population), while the association of low sodium intake with increased risk of cardiovascular events and death is observed in those with or without hypertension. These data suggest that lowering sodium intake is best targeted at populations with hypertension who consume high sodium diets. FUNDING: Full funding sources listed at end of paper (see Acknowledgments).
BACKGROUND: Several studies reported a U-shaped association between urinary sodium excretion and cardiovascular disease events and mortality. Whether these associations vary between those individuals with and without hypertension is uncertain. We aimed to explore whether the association between sodium intake and cardiovascular disease events and all-cause mortality is modified by hypertension status. METHODS: In this pooled analysis, we studied 133,118 individuals (63,559 with hypertension and 69,559 without hypertension), median age of 55 years (IQR 45-63), from 49 countries in four large prospective studies and estimated 24-h urinary sodium excretion (as group-level measure of intake). We related this to the composite outcome of death and major cardiovascular disease events over a median of 4.2 years (IQR 3.0-5.0) and blood pressure. FINDINGS: Increased sodium intake was associated with greater increases in systolic blood pressure in individuals with hypertension (2.08 mm Hg change per g sodium increase) compared with individuals without hypertension (1.22 mm Hg change per g; pinteraction<0.0001). In those individuals with hypertension (6835 events), sodium excretion of 7 g/day or more (7060 [11%] of population with hypertension: hazard ratio [HR] 1.23 [95% CI 1.11-1.37]; p<0.0001) and less than 3 g/day (7006 [11%] of population with hypertension: 1.34 [1.23-1.47]; p<0.0001) were both associated with increased risk compared with sodium excretion of 4-5 g/day (reference 25% of the population with hypertension). In those individuals without hypertension (3021 events), compared with 4-5 g/day (18,508 [27%] of the population without hypertension), higher sodium excretion was not associated with risk of the primary composite outcome (≥ 7 g/day in 6271 [9%] of the population without hypertension; HR 0.90 [95% CI 0.76-1.08]; p=0.2547), whereas an excretion of less than 3 g/day was associated with a significantly increased risk (7547 [11%] of the population without hypertension; HR 1.26 [95% CI 1.10-1.45]; p=0.0009). INTERPRETATION: Compared with moderate sodium intake, high sodium intake is associated with an increased risk of cardiovascular events and death in hypertensive populations (no association in normotensive population), while the association of low sodium intake with increased risk of cardiovascular events and death is observed in those with or without hypertension. These data suggest that lowering sodium intake is best targeted at populations with hypertension who consume high sodium diets. FUNDING: Full funding sources listed at end of paper (see Acknowledgments).
Authors: Feng J He; Norm R C Campbell; Yuan Ma; Graham A MacGregor; Mary E Cogswell; Nancy R Cook Journal: Int J Epidemiol Date: 2018-12-01 Impact factor: 7.196
Authors: Qi Sun; Kimberly A Bertrand; Adrian A Franke; Bernard Rosner; Gary C Curhan; Walter C Willett Journal: Am J Clin Nutr Date: 2016-11-09 Impact factor: 7.045
Authors: Robert M Carey; David A Calhoun; George L Bakris; Robert D Brook; Stacie L Daugherty; Cheryl R Dennison-Himmelfarb; Brent M Egan; John M Flack; Samuel S Gidding; Eric Judd; Daniel T Lackland; Cheryl L Laffer; Christopher Newton-Cheh; Steven M Smith; Sandra J Taler; Stephen C Textor; Tanya N Turan; William B White Journal: Hypertension Date: 2018-11 Impact factor: 10.190