Monensin (MN) has affinity for monovalent cations such as Na and disruption of Na dynamics in tissues could affect the permeability of cardiac muscle cells. High or continued doses of MN have been suggested to result in cardiac myopathy, blood stasis and interstitial pulmonary edema. The objective of this study was to evaluate cardiac damage, not clinically detected, using a Creatine-Kinase Myocardic (CK-MB) commercial kit. Thirty Angus × Hereford steers, (BW = 205 ± 12 kg) were used to evaluate the effect of 2 doses of dietary MN during finishing in feedlot. Steers were randomly allotted into 3 groups of 10 each for a feedlot period of 168 d. Group 1: un-supplemented MN (G1: Control, CO), group 2: supplemented with 1 mg of MN/kg of body weight (BW) (G2: 1 mg/kg) and group 3, supplemented with MN 1.5 mg of MN/kg of BW (G3: 1.5 mg/kg). Steers were weighed on d 0, 63, 98, 126 and 168, with blood sampling at each time. Steers that received MN were 25 and 30 kg heavier (P < 0.05) than the controls (G2 and G3, respectively). Concentration of CK-MB increased linearly (P < 0.05) for the 3 groups (Table 1). Treatment effects were not that evident. Concentration of CK-MB was greater for G3 than G1 and G2 on sampling at d 63 and 168 (P < 0.05). No macroscopic lesions either on lungs or cardiac muscle were observed at harvest. Table 1. Concentration means and standard deviations for CK-MB throughout the trial

Group	Day 1	Day 63	Day 98	Day 126	Day 168
G1: Control	25.1 ± 10.0A	40.4 ± 22.4A	68.2 ± 9.0B	89.6 ± 18.3B	72.9 ± 20.3A
G2: 1 mg/kg BW	32.1 ± 6.3A	40.4 ± 14.7A	49.0 ± 13.7A	62.1 ± 22.5A	61.2 ± 23.9A
G3: 1.5 mg/kg BW	26.8 ± 13.1A	61.7 ± 21.4B	57.0 ± 11.3A	76.4 ± 25.0A	92.6 ± 18.4B

^A,B Treatment means followed by different letters denote statistical differences at P ≤ 0.05.