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Urinary Sodium Excretion and Cardiovascular Disease Mortality

Urinary Sodium Excretion and Cardiovascular Disease Mortality To the Editor: The study by Dr Stolarz-Skrzypek and colleagues1 showed that systolic blood pressure changes over time were associated with changes in sodium excretion but not with a higher risk of hypertension or CVD complications. Lower sodium excretion was associated with higher CVD mortality. In our view, the study has some limitations. First, patients with established CVD at baseline were excluded. However, the authors did not report whether patients with other risk factors, such as family history of CVD,2 high levels of low-density lipoprotein cholesterol, abdominal obesity, or inflammatory markers,3 were also excluded. Second, no food frequency questionnaire was administered to participants even though other dietary factors beyond sodium and potassium can play an important role in prevention of hypertension and high blood pressure.4 Third, no information about physical activity or use of statins, protective factors for CVD and mortality, was provided nor were they included as potential confounders in the multivariable analyses. Fourth, the study population was relatively young and predominantly white and lacked information about sodium sensitivity, although it is known that among normotensive young adults with a family history of hypertension, higher sodium intake might contribute to the increased risk for hypertension.5 Back to top Article Information Conflict of Interest Disclosures: Both authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported. References 1. Stolarz-Skrzypek K, Kuznetsova T, Thijs L, et al; European Project on Genes in Hypertension (EPOGH) Investigators. Fatal and nonfatal outcomes, incidence of hypertension, and blood pressure changes in relation to urinary sodium excretion. JAMA. 2011;305(17):1777-178521540421PubMedGoogle ScholarCrossref 2. Lloyd-Jones DM, Nam BH, D’Agostino RB Sr, et al. Parental cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults: a prospective study of parents and offspring. JAMA. 2004;291(18):2204-221115138242PubMedGoogle ScholarCrossref 3. Pai JK, Pischon T, Ma J, et al. Inflammatory markers and the risk of coronary heart disease in men and women. N Engl J Med. 2004;351(25):2599-261015602020PubMedGoogle ScholarCrossref 4. Appel LJ, Moore TJ, Obarzanek E, et al; DASH Collaborative Research Group. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med. 1997;336(16):1117-11249099655PubMedGoogle ScholarCrossref 5. Schlaich MP, Klingbeil AU, Jacobi J, et al. Altered aldosterone response to salt intake and angiotensin II infusion in young normotensive men with parental history of arterial hypertension. J Hypertens. 2002;20(1):117-12411791034PubMedGoogle ScholarCrossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA American Medical Association

Urinary Sodium Excretion and Cardiovascular Disease Mortality

JAMA , Volume 306 (10) – Sep 14, 2011

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Publisher
American Medical Association
Copyright
Copyright © 2011 American Medical Association. All Rights Reserved.
ISSN
0098-7484
eISSN
1538-3598
DOI
10.1001/jama.2011.1296
Publisher site
See Article on Publisher Site

Abstract

To the Editor: The study by Dr Stolarz-Skrzypek and colleagues1 showed that systolic blood pressure changes over time were associated with changes in sodium excretion but not with a higher risk of hypertension or CVD complications. Lower sodium excretion was associated with higher CVD mortality. In our view, the study has some limitations. First, patients with established CVD at baseline were excluded. However, the authors did not report whether patients with other risk factors, such as family history of CVD,2 high levels of low-density lipoprotein cholesterol, abdominal obesity, or inflammatory markers,3 were also excluded. Second, no food frequency questionnaire was administered to participants even though other dietary factors beyond sodium and potassium can play an important role in prevention of hypertension and high blood pressure.4 Third, no information about physical activity or use of statins, protective factors for CVD and mortality, was provided nor were they included as potential confounders in the multivariable analyses. Fourth, the study population was relatively young and predominantly white and lacked information about sodium sensitivity, although it is known that among normotensive young adults with a family history of hypertension, higher sodium intake might contribute to the increased risk for hypertension.5 Back to top Article Information Conflict of Interest Disclosures: Both authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported. References 1. Stolarz-Skrzypek K, Kuznetsova T, Thijs L, et al; European Project on Genes in Hypertension (EPOGH) Investigators. Fatal and nonfatal outcomes, incidence of hypertension, and blood pressure changes in relation to urinary sodium excretion. JAMA. 2011;305(17):1777-178521540421PubMedGoogle ScholarCrossref 2. Lloyd-Jones DM, Nam BH, D’Agostino RB Sr, et al. Parental cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults: a prospective study of parents and offspring. JAMA. 2004;291(18):2204-221115138242PubMedGoogle ScholarCrossref 3. Pai JK, Pischon T, Ma J, et al. Inflammatory markers and the risk of coronary heart disease in men and women. N Engl J Med. 2004;351(25):2599-261015602020PubMedGoogle ScholarCrossref 4. Appel LJ, Moore TJ, Obarzanek E, et al; DASH Collaborative Research Group. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med. 1997;336(16):1117-11249099655PubMedGoogle ScholarCrossref 5. Schlaich MP, Klingbeil AU, Jacobi J, et al. Altered aldosterone response to salt intake and angiotensin II infusion in young normotensive men with parental history of arterial hypertension. J Hypertens. 2002;20(1):117-12411791034PubMedGoogle ScholarCrossref

Journal

JAMAAmerican Medical Association

Published: Sep 14, 2011

References