Acute arrhythmogenesis after myocardial infarction in normotensive rats: Influence of high salt intake

A high salt diet is a known risk factor for cardiovascular diseases that leads to cardiac hypertrophy and creates a substrate for arrhythmias and sudden death. However, acute arrhythmogenesis after infarction has not been studied. Male Wistar rats (21 days) received drinking water (MI) or 1% NaCl solution (MI-Salt-C) for 4 weeks. Water was given to another group for 4 weeks, and on the day before surgery, animals received a 1% NaCl solution (MI-Salt-A). Non-invasive systolic blood pressure (SBP) was obtained before surgery. Myocardial infarction (MI) was produced by permanent occlusion of the left coronary artery. Electrocardiogram was monitored during the first 30 min post-occlusion to evaluate arrhythmias. Although SBP was not altered by salt intake (SHAM: 114 ± 2, MI: 112 ± 2, MI-Salt-C: 115 ± 2, MI-Salt-A: 116 ± 4 mm Hg), ventricular hypertrophy was observed in the animals receiving chronic salt diet (SHAM: 0.22 ± 0.008, MI: 0.23 ± 0.007, MI-Salt-C: 0.28 ± 0.01; MI-Salt-A: 0.23 ± 0.01 g/cm; P < 0.05). Ventricular premature beats increased in both salt-loaded groups compared to MI group (MI: 805 ± 81, MI-Salt-C: 1145 ± 98; MI-Salt-A: 1023 ± 77; P < 0.05). Atrioventricular blockade was only observed in animals subjected to high salt intake (MI-Salt-C: 38.9%; MI-Salt-A: 42.1%). High salt intake was associated with increased post-infarct arrhythmias; however, this effect was unrelated to ventricular hypertrophy.