Abstract 12726: Sodium Restriction Reveals Early Aortic Impedance and Left Ventricular (LV) Systolic Dysfunction in Overweight/Obese Hypertensives
Introduction: Hypertension is associated with dysregulation of renin-angiotensin system (RAS) activity and increased central aortic pressure (CP), pulse-wave velocity (PWV), characteristic impedance (Zc), LV systolic stiffness and diastolic dysfunction. Progressive damage and failure of volume-sensitive regulation may lead to LV systolic dysfunction. Typical high dietary salt intake leads to fluid retention and RAS suppression that may mask early arterial and systolic changes. We hypothesized that sub-acute intake of very low-sodium diet would result in relative volume depletion/RAS activation and reveal underlying early arterial and systolic dysfunction.
Methods and Results: Thirty-one (age 50±6yr), predominantly white (67%) and male (68%), overweight/obese (BMI 28.3±3.9) subjects participated in a crossover salt protocol. Fifteen hypertensive and 16 age-matched healthy subjects consumed low-sodium (LS 10mmol/d) diet and high-sodium (HS 200mmol/d) diet for 1 week each. A 24hr-urine collection confirmed sodium balance. Hormonal, hemodynamic, and echocardiographic measurements were obtained after overnight fasting and rest in supine posture on a Clinical Research Center. Weight decreased on LS diet in both hypertensive (Δ2.5kg, p=0.001) and healthy (Δ1.5, p=0.001), and PRA increased (LS 2.6±1.8 vs HS 0.3±0.3ng/ml/hr, p=0.002; and LS 1.7±1.3 vs HS 0.3±0.2, p=0.009, respectively). On HS diet, compared with healthy, hypertensives had higher CP, PWV, and lower e`. No difference in Zc, s`, or e`/a` was found. However, on LS diet hypertensives had higher CP, PWV, Zc and lower s` . No difference in e` or e`/a` was observed (Table ).
Conclusion: Sodium restriction reveals early aortic and LV systolic dysfunction in hypertensive overweight/obese individuals not apparent under typical sodium conditions. The interaction of salt intake with vascular and LV function may obscure early pathophysiologic underpinnings of hypertension.
- © 2013 by American Heart Association, Inc.