Association of serum sodium concentration with coronary atherosclerosis in China: follow-up study

Aim: The aim of this study was to test the hypothesis that lower serum sodium may be associated with increased cardiovascular events and all-cause mortality by means of long-term follow-up of subjects with coronary atherosclerosis in a prospective, hospital-based epidemiological study in China. Meth...

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Published inActa pharmacologica Sinica Vol. 30; no. 4; pp. 494 - 500
Main Authors Jia, En-zhi, Xu, Zhen-xia, Yang, Zhi-jian, Zhu, Tie-bing, Wang, Lian-sheng, Chen, Bo, Cao, Ke-jiang, Huang, Jun, Ma, Wen-zhu, Lu, Xiang
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.04.2009
Nature Publishing Group
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Online AccessGet full text
ISSN1671-4083
1745-7254
1745-7254
DOI10.1038/aps.2009.17

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Abstract Aim: The aim of this study was to test the hypothesis that lower serum sodium may be associated with increased cardiovascular events and all-cause mortality by means of long-term follow-up of subjects with coronary atherosclerosis in a prospective, hospital-based epidemiological study in China. Methods: A prospective, hospital-based epidemiological design was used. The study population consisted of 1069 consecutive patients who were scheduled to undergo coronary angiography for suspected or known coronary atherosclerosis. The severity of coronary atherosclerosis was defined using Gensini's score system. Age, sex-adjusted hazard ratios (HR) and 95% confidence intervals (CI) for the quartiles of serum sodium concentration were estimated with Cox proportional hazard models, using quartile 1 as the reference. Cox proportional hazard models were also constructed to estimate the hazard ratios and 95% confidence intervals for all-cause mortality and final end-point events by serum sodium quartile and to adjust for potentially confounding variables. Multivariate models were adjusted for the following variables: age, sex, smoking status, alcohol consumption, body mass index, blood pressure, potassium, chloride, total cholesterol, triglycerides, fasting blood glucose, urea, creatinine, uric acid, and Gensini's score. Results: During the median 2.86 years (3011.66 person-years) of follow-up, 176 final end-point events were documented. These events included 79 deaths and 97 readmissions for coronary heart disease. There was a statistically significant inverse association of serum sodium with all-cause mortality (P〈0.001). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a non-significant inverse association with all-cause mortality, with an adjusted hazard ratio (95% CI) of 0.67 (0.25-1.80). After adjustment for age and increasing quartiles of serum sodium concentration were sex, the hazard ratio and 95% CI for final end-point events across 1.00, 0.85 (0.59-1.22), 0.52 (0.34-0.82), and 0.31 (0.19-0.49). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a statistically significant inverse asso- ciation with final end-point events, with an adjusted hazard ratio (95% CI) of 0.46 (0.26-0.81). Conclusion: The serum sodium concentration showed a statistically significant negative association with coronary events and all-cause mortality in subjects with coronary atherosclerosis; the actual mechanism underlying this association needs further study.
AbstractList Aim: The aim of this study was to test the hypothesis that lower serum sodium may be associated with increased cardiovascular events and all-cause mortality by means of long-term follow-up of subjects with coronary atherosclerosis in a prospective, hospital-based epidemiological study in China. Methods: A prospective, hospital-based epidemiological design was used. The study population consisted of 1069 consecutive patients who were scheduled to undergo coronary angiography for suspected or known coronary atherosclerosis. The severity of coronary atherosclerosis was defined using Gensini's score system. Age, sex-adjusted hazard ratios (HR) and 95% confidence intervals (CI) for the quartiles of serum sodium concentration were estimated with Cox proportional hazard models, using quartile 1 as the reference. Cox proportional hazard models were also constructed to estimate the hazard ratios and 95% confidence intervals for all-cause mortality and final end-point events by serum sodium quartile and to adjust for potentially confounding variables. Multivariate models were adjusted for the following variables: age, sex, smoking status, alcohol consumption, body mass index, blood pressure, potassium, chloride, total cholesterol, triglycerides, fasting blood glucose, urea, creatinine, uric acid, and Gensini's score. Results: During the median 2.86 years (3011.66 person-years) of follow-up, 176 final end-point events were documented. These events included 79 deaths and 97 readmissions for coronary heart disease. There was a statistically significant inverse association of serum sodium with all-cause mortality ( P <0.001). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a non-significant inverse association with all-cause mortality, with an adjusted hazard ratio (95% CI) of 0.67 (0.25–1.80). After adjustment for age and sex, the hazard ratio and 95% CI for final end-point events across increasing quartiles of serum sodium concentration were 1.00, 0.85 (0.59–1.22), 0.52 (0.34–0.82), and 0.31 (0.19–0.49). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a statistically significant inverse association with final end-point events, with an adjusted hazard ratio (95% CI) of 0.46 (0.26–0.81). Conclusion: The serum sodium concentration showed a statistically significant negative association with coronary events and all-cause mortality in subjects with coronary atherosclerosis; the actual mechanism underlying this association needs further study.
The aim of this study was to test the hypothesis that lower serum sodium may be associated with increased cardiovascular events and all-cause mortality by means of long-term follow-up of subjects with coronary atherosclerosis in a prospective, hospital-based epidemiological study in China.AIMThe aim of this study was to test the hypothesis that lower serum sodium may be associated with increased cardiovascular events and all-cause mortality by means of long-term follow-up of subjects with coronary atherosclerosis in a prospective, hospital-based epidemiological study in China.A prospective, hospital-based epidemiological design was used. The study population consisted of 1069 consecutive patients who were scheduled to undergo coronary angiography for suspected or known coronary atherosclerosis. The severity of coronary atherosclerosis was defined using Gensini's score system. Age, sex-adjusted hazard ratios (HR) and 95% confidence intervals (CI) for the quartiles of serum sodium concentration were estimated with Cox proportional hazard models, using quartile 1 as the reference. Cox proportional hazard models were also constructed to estimate the hazard ratios and 95% confidence intervals for all-cause mortality and final end-point events by serum sodium quartile and to adjust for potentially confounding variables. Multivariate models were adjusted for the following variables: age, sex, smoking status, alcohol consumption, body mass index, blood pressure, potassium, chloride, total cholesterol, triglycerides, fasting blood glucose, urea, creatinine, uric acid, and Gensini's score.METHODSA prospective, hospital-based epidemiological design was used. The study population consisted of 1069 consecutive patients who were scheduled to undergo coronary angiography for suspected or known coronary atherosclerosis. The severity of coronary atherosclerosis was defined using Gensini's score system. Age, sex-adjusted hazard ratios (HR) and 95% confidence intervals (CI) for the quartiles of serum sodium concentration were estimated with Cox proportional hazard models, using quartile 1 as the reference. Cox proportional hazard models were also constructed to estimate the hazard ratios and 95% confidence intervals for all-cause mortality and final end-point events by serum sodium quartile and to adjust for potentially confounding variables. Multivariate models were adjusted for the following variables: age, sex, smoking status, alcohol consumption, body mass index, blood pressure, potassium, chloride, total cholesterol, triglycerides, fasting blood glucose, urea, creatinine, uric acid, and Gensini's score.During the median 2.86 years (3011.66 person-years) of follow-up, 176 final end-point events were documented. These events included 79 deaths and 97 readmissions for coronary heart disease. There was a statistically significant inverse association of serum sodium with all-cause mortality (P<0.001). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a non-significant inverse association with all-cause mortality, with an adjusted hazard ratio (95% CI) of 0.67 (0.25-1.80). After adjustment for age and sex, the hazard ratio and 95% CI for final end-point events across increasing quartiles of serum sodium concentration were 1.00, 0.85 (0.59-1.22), 0.52 (0.34-0.82), and 0.31 (0.19-0.49). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a statistically significant inverse association with final end-point events, with an adjusted hazard ratio (95% CI) of 0.46 (0.26-0.81).RESULTSDuring the median 2.86 years (3011.66 person-years) of follow-up, 176 final end-point events were documented. These events included 79 deaths and 97 readmissions for coronary heart disease. There was a statistically significant inverse association of serum sodium with all-cause mortality (P<0.001). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a non-significant inverse association with all-cause mortality, with an adjusted hazard ratio (95% CI) of 0.67 (0.25-1.80). After adjustment for age and sex, the hazard ratio and 95% CI for final end-point events across increasing quartiles of serum sodium concentration were 1.00, 0.85 (0.59-1.22), 0.52 (0.34-0.82), and 0.31 (0.19-0.49). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a statistically significant inverse association with final end-point events, with an adjusted hazard ratio (95% CI) of 0.46 (0.26-0.81).The serum sodium concentration showed a statistically significant negative association with coronary events and all-cause mortality in subjects with coronary atherosclerosis; the actual mechanism underlying this association needs further study.CONCLUSIONThe serum sodium concentration showed a statistically significant negative association with coronary events and all-cause mortality in subjects with coronary atherosclerosis; the actual mechanism underlying this association needs further study.
Aim: The aim of this study was to test the hypothesis that lower serum sodium may be associated with increased cardiovascular events and all-cause mortality by means of long-term follow-up of subjects with coronary atherosclerosis in a prospective, hospital-based epidemiological study in China. Methods: A prospective, hospital-based epidemiological design was used. The study population consisted of 1069 consecutive patients who were scheduled to undergo coronary angiography for suspected or known coronary atherosclerosis. The severity of coronary atherosclerosis was defined using Gensini's score system. Age, sex-adjusted hazard ratios (HR) and 95% confidence intervals (CI) for the quartiles of serum sodium concentration were estimated with Cox proportional hazard models, using quartile 1 as the reference. Cox proportional hazard models were also constructed to estimate the hazard ratios and 95% confidence intervals for all-cause mortality and final end-point events by serum sodium quartile and to adjust for potentially confounding variables. Multivariate models were adjusted for the following variables: age, sex, smoking status, alcohol consumption, body mass index, blood pressure, potassium, chloride, total cholesterol, triglycerides, fasting blood glucose, urea, creatinine, uric acid, and Gensini's score. Results: During the median 2.86 years (3011.66 person-years) of follow-up, 176 final end-point events were documented. These events included 79 deaths and 97 readmissions for coronary heart disease. There was a statistically significant inverse association of serum sodium with all-cause mortality (P〈0.001). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a non-significant inverse association with all-cause mortality, with an adjusted hazard ratio (95% CI) of 0.67 (0.25-1.80). After adjustment for age and increasing quartiles of serum sodium concentration were sex, the hazard ratio and 95% CI for final end-point events across 1.00, 0.85 (0.59-1.22), 0.52 (0.34-0.82), and 0.31 (0.19-0.49). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a statistically significant inverse asso- ciation with final end-point events, with an adjusted hazard ratio (95% CI) of 0.46 (0.26-0.81). Conclusion: The serum sodium concentration showed a statistically significant negative association with coronary events and all-cause mortality in subjects with coronary atherosclerosis; the actual mechanism underlying this association needs further study.
The aim of this study was to test the hypothesis that lower serum sodium may be associated with increased cardiovascular events and all-cause mortality by means of long-term follow-up of subjects with coronary atherosclerosis in a prospective, hospital-based epidemiological study in China. A prospective, hospital-based epidemiological design was used. The study population consisted of 1069 consecutive patients who were scheduled to undergo coronary angiography for suspected or known coronary atherosclerosis. The severity of coronary atherosclerosis was defined using Gensini's score system. Age, sex-adjusted hazard ratios (HR) and 95% confidence intervals (CI) for the quartiles of serum sodium concentration were estimated with Cox proportional hazard models, using quartile 1 as the reference. Cox proportional hazard models were also constructed to estimate the hazard ratios and 95% confidence intervals for all-cause mortality and final end-point events by serum sodium quartile and to adjust for potentially confounding variables. Multivariate models were adjusted for the following variables: age, sex, smoking status, alcohol consumption, body mass index, blood pressure, potassium, chloride, total cholesterol, triglycerides, fasting blood glucose, urea, creatinine, uric acid, and Gensini's score. During the median 2.86 years (3011.66 person-years) of follow-up, 176 final end-point events were documented. These events included 79 deaths and 97 readmissions for coronary heart disease. There was a statistically significant inverse association of serum sodium with all-cause mortality (P<0.001). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a non-significant inverse association with all-cause mortality, with an adjusted hazard ratio (95% CI) of 0.67 (0.25-1.80). After adjustment for age and sex, the hazard ratio and 95% CI for final end-point events across increasing quartiles of serum sodium concentration were 1.00, 0.85 (0.59-1.22), 0.52 (0.34-0.82), and 0.31 (0.19-0.49). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a statistically significant inverse association with final end-point events, with an adjusted hazard ratio (95% CI) of 0.46 (0.26-0.81). The serum sodium concentration showed a statistically significant negative association with coronary events and all-cause mortality in subjects with coronary atherosclerosis; the actual mechanism underlying this association needs further study.
The aim of this study was to test the hypothesis that lower serum sodium may be associated with increased cardiovascular events and all-cause mortality by means of long-term follow-up of subjects with coronary atherosclerosis in a prospective, hospital-based epidemiological study in China. A prospective, hospital-based epidemiological design was used. The study population consisted of 1069 consecutive patients who were scheduled to undergo coronary angiography for suspected or known coronary atherosclerosis. The severity of coronary atherosclerosis was defined using Gensini's score system. Age, sex-adjusted hazard ratios (HR) and 95% confidence intervals (CI) for the quartiles of serum sodium concentration were estimated with Cox proportional hazard models, using quartile 1 as the reference. Cox proportional hazard models were also constructed to estimate the hazard ratios and 95% confidence intervals for all-cause mortality and final end-point events by serum sodium quartile and to adjust for potentially confounding variables. Multivariate models were adjusted for the following variables: age, sex, smoking status, alcohol consumption, body mass index, blood pressure, potassium, chloride, total cholesterol, triglycerides, fasting blood glucose, urea, creatinine, uric acid, and Gensini's score. During the median 2.86 years (3011.66 person-years) of follow-up, 176 final end-point events were documented. These events included 79 deaths and 97 readmissions for coronary heart disease. There was a statistically significant inverse association of serum sodium with all-cause mortality (P<0.001). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a non-significant inverse association with all-cause mortality, with an adjusted hazard ratio (95% CI) of 0.67 (0.25-1.80). After adjustment for age and sex, the hazard ratio and 95% CI for final end-point events across increasing quartiles of serum sodium concentration were 1.00, 0.85 (0.59-1.22), 0.52 (0.34-0.82), and 0.31 (0.19-0.49). After full adjustment comparing the highest serum sodium quartile to the lowest, there was a statistically significant inverse association with final end-point events, with an adjusted hazard ratio (95% CI) of 0.46 (0.26-0.81). The serum sodium concentration showed a statistically significant negative association with coronary events and all-cause mortality in subjects with coronary atherosclerosis; the actual mechanism underlying this association needs further study.
Author En-zhi JIA Zhen-xia XU Zhi-jian YANG Tie-bing ZHU Lian-sheng WANG Bo CHEN Ke-jiang CAO JunHUANG Wen-zhu MA Xiang LU
AuthorAffiliation Department of Cardiovascular Medicine, the first Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China Department of cardiovascular medicine, the second affiliated hospital of Nanjing Medical University, Nanjing 210011, China
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DocumentTitleAlternate Association of serum sodium concentration with coronary atherosclerosis in China: follow-up study
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Issue 4
Keywords sodium
follow-up
coronary atherosclerosis
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Notes sodium
follow-up
coronary atherosclerosis
R541.4
sodium; coronary atherosclerosis; follow-up
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PublicationTitle Acta pharmacologica Sinica
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References GroteKDrexlerHSchiefferBRenin-angiotensin system and atherosclerosisNephrol Dial Transplant20041977031:CAS:528:DC%2BD2cXitl2ksr0%3D10.1093/ndt/gfh030
GrassiGDell'OroRSeravalleGFogliaGTrevanoFQManciaGShort- and long-term neuroadrenergic effects of moderate dietary sodium restriction in essential hypertensionCirculation20021061957611:CAS:528:DC%2BD38XnsVartro%3D10.1161/01.CIR.0000033519.45615.C7
HeFJMacGregorGAHow far should salt intake be reduced?Hypertension200342109391:CAS:528:DC%2BD3sXpsVGis7g%3D10.1161/01.HYP.0000102864.05174.E8
JudkinsMPA percutaneous transfemoral techniqueRadiology196789815211:STN:280:DyaF1c%2FgtVOrtg%3D%3D10.1148/89.5.815
DzauVJTissue angiotensin and pathobiology of vascular disease-A unifying hypothesisHypertension2001371047521:CAS:528:DC%2BD3MXjtFejt70%3D10.1161/01.HYP.37.4.1047
PetrieJRMorrisADMinamisawaKHilditchTEElliottHLSmallMDietary sodium restriction impairs insulin sensitivity in noninsulin-dependent diabetes mellitusJ Clin Endocrinol Metab199883155271:CAS:528:DyaK1cXjtF2hurs%3D9589654
GraudalNAGallieAMGaredPEffects of sodium restriction on blood pressure, rennin, aldosterone, catecholamines, cholesterols, and triglyceride — a meta analysisJAMA19982791383911:CAS:528:DyaK1cXjtlSiu7Y%3D10.1001/jama.279.17.1383
Joint National Committee for the Prevention, Detection, Evaluation, and treatment of High Blood PressureThe Seventh Report of the Joint National Committee for the Prevention, Detection, Evaluation, and treatment of High Blood Pressure (JNC VII)JAMA200328925607210.1001/jama.289.19.2560
CohenHWHailpernSMAldermanMHSodium intake and mortality follow-up in the Third National Health and Nutrition Examination Survey (NHANES III)J Gen Intern Med200823129730210.1007/s11606-008-0645-6
SasakiSZhangXHKestelootHDietary sodium, potassium, saturated fat, alcohol and stroke mortalityStroke19952678391:STN:280:DyaK2M3lvFWjtg%3D%3D10.1161/01.STR.26.5.783
AldermanMHCohenHMadhavanSDietary sodium intake and mortality: National Health and Nutrition Examination Survey (NHANES I)Lancet199835178151:STN:280:DyaK1c7nvVOksw%3D%3D10.1016/S0140-6736(97)09092-2
GensiniGGA more meaningful scoring system for determinating the severity of coronary heart diseaseAm J Cardiol1983516061:STN:280:DyaL3s7itlyitw%3D%3D10.1016/S0002-9149(83)80105-2
HeJOgdenLGVupputuriSBazzanoLALoriaCWheltonPKDietary sodium intake and subsequent risk of cardiovascular disease in overweight adultsJAMA19992822027341:STN:280:DC%2BD3c%2FlslensA%3D%3D10.1001/jama.282.21.2027
American Heart Association. Heart disease and stroke statistics: 2005 Update. Dallas, Tex: American Heart Association; 2004.
CohenHWHailpernSMFangJAldermanMHSodium intake and mortality in the NHANES II follow-up studyAm J Med2006119275e71410.1016/j.amjmed.2005.10.042
JiaEZYangZJZhuTBWangLSChenBCaoKJSerum sodium concentration is significantly associated with the angiographic characteristics of coronary atherosclerosisActa Pharmacol Sin2007281136421:CAS:528:DC%2BD2sXptFKhsbs%3D10.1111/j.1745-7254.2007.00597.x
NagataCTakatsukaNShimizuNShimizuHSodium intake and risk of death from stroke in Japanese men and womenStroke2004351543710.1161/01.STR.0000130425.50441.b0
TuomilehtoJJousilahtiPRastenyteDMoltchanovVTanskanenAPietinenPUrinary sodium excretion and cardiovascular mortality in Finland: a prospective studyLancet2001357848511:CAS:528:DC%2BD3MXitVOitLg%3D10.1016/S0140-6736(00)04199-4
PearsonTABlairSNDanielsSREckelRHFairJMFortmannSPAHA guidelines for primary prevention of cardiovascular disease and stroke: 2002 Update: consensus panel guide to comprehensive risk reduction for adult patients without coronary or other atherosclerotic vascular diseases. American Heart Association Science Advisory and Coordinating CommitteeCirculation20021063889110.1161/01.CIR.0000020190.45892.75
AldermanMHMadhavanSOoiWLCohenHSealeyJELaraghJHAssociation of the rennin-sodium profile with the risk of myocardial infarction in patients with hypertensionN Engl J Med199132410981041:STN:280:DyaK3M7nvFClsw%3D%3D10.1056/NEJM199104183241605
MurrayCJLLopezADAlternative projections of mortality and disability by cause 1990–2020: Global Burden of Disease StudyLancet199734914985041:STN:280:DyaK2szhtVaqsw%3D%3D10.1016/S0140-6736(96)07492-2
S Sasaki (BFaps200917_CR15) 1995; 26
C Nagata (BFaps200917_CR18) 2004; 35
K Grote (BFaps200917_CR19) 2004; 19
HW Cohen (BFaps200917_CR6) 2006; 119
HW Cohen (BFaps200917_CR7) 2008; 23
G Grassi (BFaps200917_CR10) 2002; 106
Joint National Committee for the Prevention, Detection, Evaluation, and treatment of High Blood Pressure (BFaps200917_CR3) 2003; 289
JR Petrie (BFaps200917_CR11) 1998; 83
J Tuomilehto (BFaps200917_CR17) 2001; 357
MH Alderman (BFaps200917_CR5) 1998; 351
CJL Murray (BFaps200917_CR2) 1997; 349
FJ He (BFaps200917_CR14) 2003; 42
TA Pearson (BFaps200917_CR4) 2002; 106
J He (BFaps200917_CR16) 1999; 282
BFaps200917_CR1
GG Gensini (BFaps200917_CR13) 1983; 51
EZ Jia (BFaps200917_CR8) 2007; 28
MP Judkins (BFaps200917_CR12) 1967; 89
NA Graudal (BFaps200917_CR20) 1998; 279
MH Alderman (BFaps200917_CR9) 1991; 324
VJ Dzau (BFaps200917_CR21) 2001; 37
9519949 - Lancet. 1998 Mar 14;351(9105):781-5
7740567 - Stroke. 1995 May;26(5):783-9
9167458 - Lancet. 1997 May 24;349(9064):1498-504
11304501 - Hypertension. 2001 Apr;37(4):1047-52
12119259 - Circulation. 2002 Jul 16;106(3):388-91
11265954 - Lancet. 2001 Mar 17;357(9259):848-51
12370219 - Circulation. 2002 Oct 8;106(15):1957-61
1759997 - N Engl J Med. 1991 Apr 18;324(16):1098-104
15031327 - Nephrol Dial Transplant. 2004 Apr;19(4):770-3
15143292 - Stroke. 2004 Jul;35(7):1543-7
14610100 - Hypertension. 2003 Dec;42(6):1093-9
6823874 - Am J Cardiol. 1983 Feb;51(3):606
18465175 - J Gen Intern Med. 2008 Sep;23(9):1297-302
16490476 - Am J Med. 2006 Mar;119(3):275.e7-14
10591385 - JAMA. 1999 Dec 1;282(21):2027-34
6048074 - Radiology. 1967 Nov;89(5):815-24
9582047 - JAMA. 1998 May 6;279(17):1383-91
17640474 - Acta Pharmacol Sin. 2007 Aug;28(8):1136-42
12748199 - JAMA. 2003 May 21;289(19):2560-72
9589654 - J Clin Endocrinol Metab. 1998 May;83(5):1552-7
References_xml – reference: AldermanMHCohenHMadhavanSDietary sodium intake and mortality: National Health and Nutrition Examination Survey (NHANES I)Lancet199835178151:STN:280:DyaK1c7nvVOksw%3D%3D10.1016/S0140-6736(97)09092-2
– reference: JudkinsMPA percutaneous transfemoral techniqueRadiology196789815211:STN:280:DyaF1c%2FgtVOrtg%3D%3D10.1148/89.5.815
– reference: Joint National Committee for the Prevention, Detection, Evaluation, and treatment of High Blood PressureThe Seventh Report of the Joint National Committee for the Prevention, Detection, Evaluation, and treatment of High Blood Pressure (JNC VII)JAMA200328925607210.1001/jama.289.19.2560
– reference: GroteKDrexlerHSchiefferBRenin-angiotensin system and atherosclerosisNephrol Dial Transplant20041977031:CAS:528:DC%2BD2cXitl2ksr0%3D10.1093/ndt/gfh030
– reference: GrassiGDell'OroRSeravalleGFogliaGTrevanoFQManciaGShort- and long-term neuroadrenergic effects of moderate dietary sodium restriction in essential hypertensionCirculation20021061957611:CAS:528:DC%2BD38XnsVartro%3D10.1161/01.CIR.0000033519.45615.C7
– reference: American Heart Association. Heart disease and stroke statistics: 2005 Update. Dallas, Tex: American Heart Association; 2004.
– reference: TuomilehtoJJousilahtiPRastenyteDMoltchanovVTanskanenAPietinenPUrinary sodium excretion and cardiovascular mortality in Finland: a prospective studyLancet2001357848511:CAS:528:DC%2BD3MXitVOitLg%3D10.1016/S0140-6736(00)04199-4
– reference: NagataCTakatsukaNShimizuNShimizuHSodium intake and risk of death from stroke in Japanese men and womenStroke2004351543710.1161/01.STR.0000130425.50441.b0
– reference: HeJOgdenLGVupputuriSBazzanoLALoriaCWheltonPKDietary sodium intake and subsequent risk of cardiovascular disease in overweight adultsJAMA19992822027341:STN:280:DC%2BD3c%2FlslensA%3D%3D10.1001/jama.282.21.2027
– reference: CohenHWHailpernSMFangJAldermanMHSodium intake and mortality in the NHANES II follow-up studyAm J Med2006119275e71410.1016/j.amjmed.2005.10.042
– reference: JiaEZYangZJZhuTBWangLSChenBCaoKJSerum sodium concentration is significantly associated with the angiographic characteristics of coronary atherosclerosisActa Pharmacol Sin2007281136421:CAS:528:DC%2BD2sXptFKhsbs%3D10.1111/j.1745-7254.2007.00597.x
– reference: PetrieJRMorrisADMinamisawaKHilditchTEElliottHLSmallMDietary sodium restriction impairs insulin sensitivity in noninsulin-dependent diabetes mellitusJ Clin Endocrinol Metab199883155271:CAS:528:DyaK1cXjtF2hurs%3D9589654
– reference: DzauVJTissue angiotensin and pathobiology of vascular disease-A unifying hypothesisHypertension2001371047521:CAS:528:DC%2BD3MXjtFejt70%3D10.1161/01.HYP.37.4.1047
– reference: MurrayCJLLopezADAlternative projections of mortality and disability by cause 1990–2020: Global Burden of Disease StudyLancet199734914985041:STN:280:DyaK2szhtVaqsw%3D%3D10.1016/S0140-6736(96)07492-2
– reference: HeFJMacGregorGAHow far should salt intake be reduced?Hypertension200342109391:CAS:528:DC%2BD3sXpsVGis7g%3D10.1161/01.HYP.0000102864.05174.E8
– reference: SasakiSZhangXHKestelootHDietary sodium, potassium, saturated fat, alcohol and stroke mortalityStroke19952678391:STN:280:DyaK2M3lvFWjtg%3D%3D10.1161/01.STR.26.5.783
– reference: GensiniGGA more meaningful scoring system for determinating the severity of coronary heart diseaseAm J Cardiol1983516061:STN:280:DyaL3s7itlyitw%3D%3D10.1016/S0002-9149(83)80105-2
– reference: CohenHWHailpernSMAldermanMHSodium intake and mortality follow-up in the Third National Health and Nutrition Examination Survey (NHANES III)J Gen Intern Med200823129730210.1007/s11606-008-0645-6
– reference: AldermanMHMadhavanSOoiWLCohenHSealeyJELaraghJHAssociation of the rennin-sodium profile with the risk of myocardial infarction in patients with hypertensionN Engl J Med199132410981041:STN:280:DyaK3M7nvFClsw%3D%3D10.1056/NEJM199104183241605
– reference: PearsonTABlairSNDanielsSREckelRHFairJMFortmannSPAHA guidelines for primary prevention of cardiovascular disease and stroke: 2002 Update: consensus panel guide to comprehensive risk reduction for adult patients without coronary or other atherosclerotic vascular diseases. American Heart Association Science Advisory and Coordinating CommitteeCirculation20021063889110.1161/01.CIR.0000020190.45892.75
– reference: GraudalNAGallieAMGaredPEffects of sodium restriction on blood pressure, rennin, aldosterone, catecholamines, cholesterols, and triglyceride — a meta analysisJAMA19982791383911:CAS:528:DyaK1cXjtlSiu7Y%3D10.1001/jama.279.17.1383
– volume: 35
  start-page: 1543
  year: 2004
  ident: BFaps200917_CR18
  publication-title: Stroke
  doi: 10.1161/01.STR.0000130425.50441.b0
– volume: 279
  start-page: 1383
  year: 1998
  ident: BFaps200917_CR20
  publication-title: JAMA
  doi: 10.1001/jama.279.17.1383
– volume: 324
  start-page: 1098
  year: 1991
  ident: BFaps200917_CR9
  publication-title: N Engl J Med
  doi: 10.1056/NEJM199104183241605
– volume: 106
  start-page: 388
  year: 2002
  ident: BFaps200917_CR4
  publication-title: Circulation
  doi: 10.1161/01.CIR.0000020190.45892.75
– volume: 106
  start-page: 1957
  year: 2002
  ident: BFaps200917_CR10
  publication-title: Circulation
  doi: 10.1161/01.CIR.0000033519.45615.C7
– volume: 26
  start-page: 783
  year: 1995
  ident: BFaps200917_CR15
  publication-title: Stroke
  doi: 10.1161/01.STR.26.5.783
– volume: 351
  start-page: 781
  year: 1998
  ident: BFaps200917_CR5
  publication-title: Lancet
  doi: 10.1016/S0140-6736(97)09092-2
– volume: 19
  start-page: 770
  year: 2004
  ident: BFaps200917_CR19
  publication-title: Nephrol Dial Transplant
  doi: 10.1093/ndt/gfh030
– volume: 83
  start-page: 1552
  year: 1998
  ident: BFaps200917_CR11
  publication-title: J Clin Endocrinol Metab
– volume: 289
  start-page: 2560
  year: 2003
  ident: BFaps200917_CR3
  publication-title: JAMA
  doi: 10.1001/jama.289.19.2560
– volume: 42
  start-page: 1093
  year: 2003
  ident: BFaps200917_CR14
  publication-title: Hypertension
  doi: 10.1161/01.HYP.0000102864.05174.E8
– volume: 37
  start-page: 1047
  year: 2001
  ident: BFaps200917_CR21
  publication-title: Hypertension
  doi: 10.1161/01.HYP.37.4.1047
– volume: 349
  start-page: 1498
  year: 1997
  ident: BFaps200917_CR2
  publication-title: Lancet
  doi: 10.1016/S0140-6736(96)07492-2
– volume: 357
  start-page: 848
  year: 2001
  ident: BFaps200917_CR17
  publication-title: Lancet
  doi: 10.1016/S0140-6736(00)04199-4
– volume: 51
  start-page: 606
  year: 1983
  ident: BFaps200917_CR13
  publication-title: Am J Cardiol
  doi: 10.1016/S0002-9149(83)80105-2
– volume: 23
  start-page: 1297
  year: 2008
  ident: BFaps200917_CR7
  publication-title: J Gen Intern Med
  doi: 10.1007/s11606-008-0645-6
– volume: 119
  start-page: 275e7
  year: 2006
  ident: BFaps200917_CR6
  publication-title: Am J Med
  doi: 10.1016/j.amjmed.2005.10.042
– volume: 28
  start-page: 1136
  year: 2007
  ident: BFaps200917_CR8
  publication-title: Acta Pharmacol Sin
  doi: 10.1111/j.1745-7254.2007.00597.x
– volume: 89
  start-page: 815
  year: 1967
  ident: BFaps200917_CR12
  publication-title: Radiology
  doi: 10.1148/89.5.815
– volume: 282
  start-page: 2027
  year: 1999
  ident: BFaps200917_CR16
  publication-title: JAMA
  doi: 10.1001/jama.282.21.2027
– ident: BFaps200917_CR1
– reference: 16490476 - Am J Med. 2006 Mar;119(3):275.e7-14
– reference: 12748199 - JAMA. 2003 May 21;289(19):2560-72
– reference: 15031327 - Nephrol Dial Transplant. 2004 Apr;19(4):770-3
– reference: 6048074 - Radiology. 1967 Nov;89(5):815-24
– reference: 10591385 - JAMA. 1999 Dec 1;282(21):2027-34
– reference: 6823874 - Am J Cardiol. 1983 Feb;51(3):606
– reference: 18465175 - J Gen Intern Med. 2008 Sep;23(9):1297-302
– reference: 9589654 - J Clin Endocrinol Metab. 1998 May;83(5):1552-7
– reference: 7740567 - Stroke. 1995 May;26(5):783-9
– reference: 9582047 - JAMA. 1998 May 6;279(17):1383-91
– reference: 9167458 - Lancet. 1997 May 24;349(9064):1498-504
– reference: 17640474 - Acta Pharmacol Sin. 2007 Aug;28(8):1136-42
– reference: 15143292 - Stroke. 2004 Jul;35(7):1543-7
– reference: 12370219 - Circulation. 2002 Oct 8;106(15):1957-61
– reference: 14610100 - Hypertension. 2003 Dec;42(6):1093-9
– reference: 1759997 - N Engl J Med. 1991 Apr 18;324(16):1098-104
– reference: 9519949 - Lancet. 1998 Mar 14;351(9105):781-5
– reference: 12119259 - Circulation. 2002 Jul 16;106(3):388-91
– reference: 11304501 - Hypertension. 2001 Apr;37(4):1047-52
– reference: 11265954 - Lancet. 2001 Mar 17;357(9259):848-51
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Snippet Aim: The aim of this study was to test the hypothesis that lower serum sodium may be associated with increased cardiovascular events and all-cause mortality...
Aim: The aim of this study was to test the hypothesis that lower serum sodium may be associated with increased cardiovascular events and all-cause mortality by...
The aim of this study was to test the hypothesis that lower serum sodium may be associated with increased cardiovascular events and all-cause mortality by...
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StartPage 494
SubjectTerms Aged
Biomedical and Life Sciences
Biomedicine
China
Coronary Artery Disease - blood
Coronary Artery Disease - etiology
Coronary Artery Disease - mortality
Cox比例风险模型
Female
Follow-Up Studies
Humans
Immunology
Internal Medicine
Male
Medical Microbiology
Middle Aged
Original
original-article
Pharmacology/Toxicology
Prospective Studies
Sodium - blood
Vaccine
冠心病事件
冠状动脉粥样硬化
终点事件
血清钠浓度
随访研究
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Title Association of serum sodium concentration with coronary atherosclerosis in China: follow-up study
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