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 in | Acta pharmacologica Sinica Vol. 30; no. 4; pp. 494 - 500 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.04.2009
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1671-4083 1745-7254 1745-7254 |
| DOI | 10.1038/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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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19305419$$D View this record in MEDLINE/PubMed |
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| PublicationPlace_xml | – name: London – name: United States – name: Shanghai |
| PublicationTitle | Acta pharmacologica Sinica |
| PublicationTitleAbbrev | Acta Pharmacol Sin |
| PublicationTitleAlternate | Acta Pharmacologica Sinica |
| PublicationYear | 2009 |
| Publisher | Nature Publishing Group UK Nature Publishing Group |
| Publisher_xml | – name: Nature Publishing Group UK – name: Nature Publishing Group |
| 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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| 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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