Objective:To study the changes of myocardial viscoelasticity and its pathological mechanism after acute myocardial infarction（AMI）in mongrels with AMI. Methods:IUIS was used to detect creep tests in six healthy mongrels before myocardial infarction（NAMI group）

at 1 hour after AMI（AMI-1 group）

and 3 hour after AMI（AMI-3 group）in diastole in vivo. Viscoelastic parameters were extracted through the three-parameter Viscoelastic model. Immunohistochemistry of microtubulin and desmin were carried out with myocardium samples. Correlation analyses were carried out in the detection results. Results:The parameters of E∞increased obviously after AMI than before AMI（P

<

0.05）

they were as follows:（5.30±0.48）k Pa

（5.73±0.32）k Pa vs.（4.31±0.40）k Pa

also the parameters of E1

they were as follows:（6.78±0.41）k Pa

（11.67±0.39）k Pa vs.（5.05±0.29）k Pa. The parameters of E

2

both decreased obviously after AMI than before AMI（P

<

0.05）

they were as follows:（23.07±0.28）k Pa

（10.94±0.64）k Pa vs.（29.67±0.63）k Pa

also the parameters of η

they were as follows:（0.60±0.04）Pa·s

（0.65±0.05）Pa·s vs.（0.74±0.07）Pa·s. The parameters of τ in AMI-3 group increased obviously（P

<

0.05）

they were as follows:（58.91±4.52）ms vs.（23.34±0.43）ms. Desmin and microtubulin decreased obviously after AMI for 3 hours（P

<

0.05）. The decrease of intracellular microtubule related with E

2

、τ at 3 hours after AMI. Conclusion:Elastic hardness increases

viscous component reduces

but rely on longer relaxation and the ability of myocardial relaxation decreases in 3 hours after AMI. The decrease of diastolic capacity partly is attributed to decrease of myocardium intracellular microtubule.