Effects of high and low salt intake on left ventricular remodeling after myocardial infarction in normotensive rats

The dietary-sodium restriction is a standard approach following an acute myocardial infarction (MI). We examined the hypothesis in which the use of a high or low-sodium diet would worsen post-infarction left ventricular remodeling in rats and facilitate the development of heart failure. Left coronary artery ligation or sham-operated (SO) was produced in male Wistar rats (250-290 g). After surgery, animals were assigned to one of the three diets: standard amount of sodium (0.3% NaCl, SO and MI groups), a high-sodium diet (0.6% NaCl, SO-High and MI-High groups), or a low-sodium diet (0.03% NaCl, SO-Low and MI-Low groups). Diets were provided for 8 weeks post-surgery. Mortality rate was elevated in high-salt group (MI-Low, 21.4%; MI, 35.3%; MI-High, 47.6%). Contractility parameter was seen to be impaired in MI-Low animals (3195 ± 211 mm Hg/s) compared with MI (3751 ± 200 mm Hg/s). Low-salt diet did not prevent myocardial collagen deposition (MI-Low, 5.2 ± 0.5%; MI, 5.0 ± 0.4%) nor myocyte hypertrophy (MI-Low, 608 ± 41μ(2); MI, 712 ± 53 μm(2)) in left ventricle after MI. High-salt intake increases collagen volume fraction (SO, 3.3 ± 0.4%; SO-High, 4.7 ± 0.4%) in animals sham, but no major changes after MI. Our results show that ventricular remodeling was not altered by immediate introduction of low sodium after MI, and it may be a safe strategy as a therapeutic intervention to avoid volume retention. However, high sodium can be harmful, accelerating the post-infaction ventricular remodeling.