title: Left ventricular geometry and endogenous ouabain in a Flemish population.
abstract: BACKGROUND
  Endogenous ouabain, an endogenous digitalis-like steroid, is synthesized in the adrenal glands and possibly in the hypothalamus. In vitro and in vivo, endogenous ouabain triggers growth and proliferation of cardiomyocytes.
  
  
  OBJECTIVE
  We therefore investigated the association between left ventricular structure and function and plasma endogenous ouabain in a general population.
  
  
  METHODS
  We randomly recruited 536 individuals from a general population (50.7% women, mean age 53.1 years). Measurements included echocardiographic left ventricular structure and function, blood pressure, plasma endogenous ouabain, and the 24-h urinary excretion of sodium.
  
  
  RESULTS
  The geometric mean plasma endogenous ouabain was 95.5 pmol/l (interquartile range 79.4-120.2 pmol/l). We expressed effect sizes for a 1-SD increase in plasma endogenous ouabain (0.21 on the logarithmic scale), while accounting for important covariables. For a 1-SD increment in plasma endogenous ouabain, SBP, left ventricular posterior wall, the interventricular septum, and relative wall thickness increased by 1.59 mmHg (P = 0.009), 0.138 mm (P = 0.003), 0.152 mm (P = 0.013), and 0.71 x 10 (P = 0.008), respectively. In a sensitivity analysis, involving 431 individuals aged 29-71 years (10-90th percentile interval), a 1-SD increase in plasma endogenous ouabain was associated with opposite trends in ejection fraction (+0.90%, P = 0.005) and left ventricular systolic longitudinal strain (-0.48%, P = 0.011). Moreover, in individuals whose sodium excretion was above median (160 mmol/24 h), the aforementioned associations reached a higher level of statistical significance.
  
  
  CONCLUSIONS
  Our population-based study suggested that endogenous ouabain might have a trophic effect on the myocardium, independent of blood pressure and other covariables. The clinical implication of these findings remains to be elucidated.
authors.affiliation: Studies Coordinating Centre, Department of Cardiovascular Diseases, University of Leuven, Belgium.
authors.forename: Tatiana
authors.initials: T
authors.lastname: Kuznetsova
authors.forename: Paolo
authors.initials: P
authors.lastname: Manunta
authors.forename: Nunnzia
authors.initials: N
authors.lastname: Casamassima
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Messaggio
authors.forename: Yu
authors.initials: Y
authors.lastname: Jin
authors.forename: Lutgarde
authors.initials: L
authors.lastname: Thijs
authors.forename: Tom
authors.initials: T
authors.lastname: Richart
authors.forename: Robert H
authors.initials: RH
authors.lastname: Fagard
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Bianchi
authors.forename: Jan A
authors.initials: JA
authors.lastname: Staessen
mesh_terms: D000328:Adult; D000368:Aged; D001530:Belgium; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010042:Ouabain / Q000097:blood*; D010641:Phenotype; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D010042:Ouabain