Background: Dietary sodium restriction and upholding adequate potassium intake is an important lifestyle modification strategy advocated in guidelines for management of hypertension and for lowering cardiovascular risk in the general population. Interestingly, and topic of controversy, the relation with development of clinical manifest vascular disease (CVD) is likely to be U- or J-shaped for urinary sodium excretion (24hUNa) and sodium-to-potassium ratio (24hUNa/K). Benefit of optimal Na/K ratio intake seems greatest in patients already diagnosed with hypertension and in preventing stroke. However, for both 24hUNa and 24hUNa/K ratio, evidence for subsequent major cardiovascular events (MACE) in patients who already have CVD is sparse.
Purpose: To assess the relation between estimated 24hUNa and 24hUNa/K ratio and risk of MACE. To evaluate estimated 24hUNa and 24hUNa/K ratio between 1996–2015, in patients with CVD.
Methods: Data of 7,561 patients enrolled in the Second Manifestations of ARTerial disease (SMART) study was used. At inclusion each participant is asked to provide a morning fasting urine sample. To estimate 24hUNa and 24hUNa/K ratio, Kawasaki, INTERSALT and Tanaka formulas were used. We also calculated Na/K ratio for a single morning fasting urine sample (mfuNa/K). Cox proportional hazards regression analyses were used to evaluate the relation between quintiles (Q) of 24hUNa, 24hUNa/K ratio, mfuNa/K ratio and risk of MACE. MACE was defined as composite of stroke, myocardial infarction, retinal infarction, terminal heart failure and vascular mortality. The analyses were adjusted for age, gender, kidney function, history of diabetes, non-hdl and smoking status. Restricted cubic splines were used to investigate nonlinear relations. We performed trend in time analyses for 24hUNa and 24hUNa/K ratio from 1996 until 2015.
Results: The median follow up was 7.2 years (IQR 3.5–10.5) and total follow up was 54,909 years. The total number of MACE was 1,332. For mfuNa/K ratio and Kawasaki 24hUNa/K ratio there was a nonlinear J-shaped relation with MACE (Fig. 1). For mfuNa/K ratio, Q1 vs Q4 (reference) HR 1.21 (95% CI 1.02–1.43). Kawasaki 24hUNa/K ratio Q1 vs Q4 (reference) HR 1.20 (95% CI 1.01–1.42). Tanaka 24hUNa/K ratio Q1 vs Q4 (reference) HR 1.16 (95% CI 0.98–1.37). For 24hUNa there was no relation with recurrent MACE during follow up: Kawasaki 24UNa Q1 vs Q4 (reference) HR 0.99 (95% CI 0.83–1.19), Q5 vs Q4 HR 1.09 (95% CI 0.92–1.31). In the period 1996–2015 there were no changes in mean estimated 24hUNa and 24hUNa/K ratio.
Conclusion: In patients with CVD there is a J-shaped relation between estimated dietary sodium-to-potassium ratio and risk of MACE. Lowest dietary sodium-to-potassium ratio is associated with increased risk for MACE. Sodium dietary intake is not associated with increased risk of MACE. In the period 1996–2015 there is no change in estimated dietary intake of sodium and sodium-to-potassium ratio in patients with CVD.