title: Correlation between increased urinary sodium excretion and decreased left ventricular diastolic function in patients with type 2 diabetes mellitus.
abstract: BACKGROUND
  Increased salt intake may induce hypertension, lead to cardiac hypertrophy, and exacerbate heart failure. When elderly patients develop heart failure, diastolic dysfunction is often observed, although the ejection fraction has decreased. Diabetes mellitus (DM) is an established risk factor for heart failure. However, little is known about the relationship between cardiac function and urinary sodium excretion (U-Na) in patients with DM.
  
  
  METHODS
  We measured 24-hour U-Na; cardiac function was evaluated directly during coronary catheterization in type 2 DM (n = 46) or non-DM (n = 55) patients with preserved cardiac systolic function (ejection fraction > or = 60%). Cardiac diastolic and systolic function was evaluated as - dp/dt and + dp/dt, respectively.
  
  
  RESULTS
  The average of U-Na was 166.6 +/- 61.2 mEq/24 hour (mean +/- SD). In all patients, stepwise multivariate regression analysis revealed that - dp/dt had a negative correlation with serum B-type natriuretic peptide (BNP; beta = - 0.23, P = .021) and U-Na (beta = - 0.24, P = .013). On the other hand, + dp/dt negatively correlated with BNP (beta = - 0.30, P < .001), but did not relate to U-Na. In the DM-patients, stepwise multivariate regression analysis showed that - dp/dt still had a negative correlation with U-Na (beta = - 0.33, P = .025).
  
  
  CONCLUSIONS
  The results indicated that increased urinary sodium excretion is associated with an impairment of cardiac diastolic function, especially in patients with DM, suggesting that a reduction of salt intake may improve cardiac diastolic function.
authors.affiliation: Division of General Internal Medicine, Department of Health Promotion, Science of Health Improvement, Kyushu Dental College, Kitakyushu, Japan. kagishu@hotmail.com
authors.forename: Shuntaro
authors.initials: S
authors.lastname: Kagiyama
authors.forename: Tokushi
authors.initials: T
authors.lastname: Koga
authors.forename: Shigeru
authors.initials: S
authors.lastname: Kaseda
authors.forename: Shiro
authors.initials: S
authors.lastname: Ishihara
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Kawazoe
authors.forename: Seizo
authors.initials: S
authors.lastname: Sadoshima
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Matsumura
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Takata
authors.forename: Takuya
authors.initials: T
authors.lastname: Tsuchihashi
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Iida
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D006328:Cardiac Catheterization; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000178:diet therapy / Q000503:physiopathology / Q000652:urine; D003971:Diastole; D004039:Diet, Sodium-Restricted; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009318:Natriuresis; D020097:Natriuretic Peptide, Brain / Q000097:blood; D012044:Regression Analysis; D018570:Risk Assessment; D012307:Risk Factors; D012964:Sodium / Q000652:urine*; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000178:diet therapy / Q000209:etiology* / Q000503:physiopathology / Q000652:urine; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: D015415:Biomarkers; D017673:Sodium Chloride, Dietary; D020097:Natriuretic Peptide, Brain; D012964:Sodium