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Mechanism of Atorvastatin in Improving Cardiac Function in a Rat Model of Myocardial Infarction

In order to explore the mechanism of atorvastatin on cardiac function after myocardial infarction in rats, 40 male Sprague Dawley rats were divided into 4 groups. There were 8 rats in blank group, 8 in control group, 8 in sham operated group and 16 in atorvastatin group. Atorvastatin group is divided into high dose group (30 mg/kg/d) and low dose group (10 mg/kg/d), 8 rats in each group. A rat model of myocardial infarction was established by ligating the left anterior descending artery. The effect of atorvastatin on cardiac function after myocardial infarction was observed. Cardiac function of rats that included the left ventricular ejection fraction, left ventricular end systolic diameter, left ventricular end diastolic diameter and left ventricular fraction shortening were measured and analysed using ultrasound. Blood lipids of rats in each group including total cholesterol, triglycerides, high density lipoprotein and low-density lipoprotein were measured. After 4 w of treatment rats were sacrificed, myocardial tissue was stained with HE and Masson to observe cardiac fibrosis. Results showed that 4 w after ligation, compared to the control group, the levels of left ventricular end systolic and left ventricular end diastolic diameter was decreased significantly in atorvastatin-treated groups A1 and A2, while left ventricular ejection fraction and left ventricular fraction shortening increased significantly. On 4 w after ligation, total cholesterol and lowdensity lipoprotein cholesterol levels in A1 and A2 groups were significantly lower than those in control group. Compared to the control group, the areas of myocardial infarction and cardiac fibrosis in A1 and A2 groups were significantly reduced. It is concluded that atorvastatin could inhibit apoptosis of myocardial cells, reverse ventricular remodeling and improve cardiac function after myocardial infarction, and these findings are of clinical significance.