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

• Infarcted rats were treated with low- or high-sodium diet for 60 days.
• High salt intake increases mortality after myocardial infarction.
• Low salt diet did not change the post-infarction ventricular remodeling.

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 ± 41μ2; MI, 712 ± 53 μm2) 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.