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(Hypertension. 2009;54:489.)
© 2009 American Heart Association, Inc.

Original Articles

Independent Relations of Left Ventricular Structure With the 24-Hour Urinary Excretion of Sodium and Aldosterone

Yu Jin; Tatiana Kuznetsova; Marc Maillard; Tom Richart; Lutgarde Thijs; Murielle Bochud; Marie-Christine Herregods; Michel Burnier; Robert Fagard; Jan A. Staessen

From the Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Diseases (Y.J., T.K., T.R., L.T., R.F., J.A.S.), and the Division of Cardiology, Department of Cardiovascular Diseases (M.C.H.), University of Leuven, Belgium; the Department of Epidemiology (T.R., J.A.S.), Maastricht University, the Netherlands; and the Division of Nephrology and Hypertension (M.M., M. Bochud, M. Burnier), University of Lausanne, Switzerland.

Correspondence to Jan A. Staessen, MD, PhD, FAHA, FESC, Studies Coordinating Centre, Laboratory of Hypertension, Campus Sint Rafaël, Kapucijnenvoer 35 block d level 00, B-3000 Leuven, Belgium. E-mail jan.staessen{at}med.kuleuven.be

Previous studies reported on the association of left ventricular mass index (LVMI) with urinary sodium or with circulating or urinary aldosterone. We investigated the independent associations of LVMI with the urinary excretion of both sodium and aldosterone. We randomly recruited 317 untreated subjects from a white population (45.1% women; mean age 48.2 years). Measurements included echocardiographic left ventricular (LV) properties, the 24-hour urinary excretion of sodium and aldosterone, plasma renin activity (PRA), and proximal (RNa_prox) and distal (RNa_dist) renal sodium reabsorption, assessed from the endogenous lithium clearance. In multivariable-adjusted models, we expressed changes in LVMI per 1-SD increase in the explanatory variables, while accounting for sex, age, systolic blood pressure, and the waist-to-hip ratio. LVMI increased independently with the urinary excretion of both sodium (+2.48 g/m²; P=0.005) and aldosterone (+2.63 g/m²; P=0.004). Higher sodium excretion was associated with increased mean wall thickness (MWT: +0.126 mm, P=0.054), but with no change in LV end-diastolic diameter (LVID: +0.12 mm, P=0.64). In contrast, higher aldosterone excretion was associated with higher LVID (+0.54 mm; P=0.017), but with no change in MWT (+0.070 mm; P=0.28). Higher RNa_dist was associated with lower relative wall thickness (–0.81x10^–2, P=0.017), because of opposite trends in LVID (+0.33 mm; P=0.13) and MWT (–0.130 mm; P=0.040). LVMI was not associated with PRA or RNa_prox. In conclusion, LVMI independently increased with both urinary sodium and aldosterone excretion. Increased MWT explained the association of LVMI with urinary sodium and increased LVID the association of LVMI with urinary aldosterone.

Key Words: aldosterone • left ventricle • plasma renin activity • population science • renal sodium handling

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