Abstract
Objective: To evaluate the left ventricular mass (LVM) reduction induced by dietary sodium restriction. Patients and Methods: A simple sodium-restricted diet was advised in 138 treated hypertensives. They had to avoid common salt loads, such as cheese and salt-preserved meat, and were switched from regular to salt-free bread. Blood pressure (BP), 24-h urinary sodium (UNaV) and LVM were recorded at baseline, after 2 months. and after 2years. Results: In 76 patients UNaV decreased in the recommended range after 2 months and remained low at 2 years. In 62 patients UNaV levels decreased after 2 months and then increased back to baseline at 2 years. Initially the two groups did not differ in terms of BP (134.3 ± 16.10/80.84 ± 12.23 vs. 134.2 ± 16.67/81.55 ± 11.18 mmHg, mean ± SD), body weight (72.64 ± 15.17 vs. 73.79 ± 12.69 kg), UNaV (161.0 ± 42.22 vs. 158.2 ± 48.66 mEq/24 h), and LVM index (LVMI; 97.09 ± 20.42 vs. 97.31 ± 18.91 g/m2). After 2years. they did not differ in terms of BP (125.3 ± 10.69/74.97 ± 7.67 vs. 124.5 ± 9.95/75.21 ± 7.64 mmHg) and body weight (71.14 ± 14.29 vs. 71.50 ± 11.87 kg). Significant differences were seen for UNaV (97.3 ± 23.01 vs. 152.6 ± 49.96 mEq/24 h) and LVMI (86.38 ± 18.17 vs. 103.1 ± 21.06 g/m2). Multiple regression analysis: UNaV directly and independently predicted LVMI variations, either as absolute values (R2 = 0.369; β = 0.611; p < 0.001), or changes from baseline to +2years. (R2 = 0.454; β = 0.677; p < 0.001). Systolic BP was a weaker predictor of LVMI (R2 = 0.369; β = 0.168; p = 0.027; R2 = 0.454; β = 0.012; p = 0.890), whereas diastolic BP was not correlated with LVMI. The prevalence of left ventricular hypertrophy decreased (29/76 to 15/76) in the first group while it increased in the less compliant patients (25/62 to 36/62; Chi2 p = 0.002). Conclusion: LVM seems linked to sodium consumption in patients already under proper BP control by medications.
Highlights
Hypertension is the primary modifiable cardiovascular risk factor [1,2]
Cardiovascular complications in hypertension can be predicted by an increased left ventricular mass (LVM), the regression of Left ventricular hypertrophy (LVH) during blood pressure (BP) lowering treatment is associated with a reduction of cardiovascular events [4]
During the eighties, the potential contribution of dietary sodium on LVM hypertrophy has been pointed out and it was found to be independent of BP values [11]
Summary
Hypertension is the primary modifiable cardiovascular risk factor [1,2]. Left ventricular hypertrophy (LVH) is both a common complication of hypertension and a crucial risk factor for cardiovascular morbidity and mortality [3]. In spite of the well-recognized role of the low-sodium diet in the primary approach in the management of hypertension [1,2], how low should the sodium be in a patient’s diet remains a matter of hard debate [12], since some dissenting scientists have claimed unfavorable effects of the (recommended) low-sodium approach [13] In this context, the recommended intake of sodium (2.3 g a day, as suggested by the international Guidelines [1,2]) has been questioned on the basis of very large studies [13]. Dissenting researchers claimed a sort of J-shaped relationship between sodium intake and cardiovascular events, showing how the Guidelines’ recommended limit would be harmful for patients and suggesting that actual sodium consumption around the world represents the “optimal”
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