Effects of High-Dose Rosuvastatin on Ventricular Remodelling and Cardiac Function in ST-Segment Elevation Myocardial Infarction

Abstract

Objective

To investigate the effects of high-dose rosuvastatin on ventricular remodelling and cardiac function in ST-segment elevation myocardial infarction (STEMI).

Materials and Methods

From January 2017 to March 2019, the clinical data of 93 patients with STEMI were collected and analysed, with 46 cases in the conventional-dose group (rosuvastatin, 10 mg/d) and 47 cases in the high-dose group (rosuvastatin, 20 mg/d). Blood lipid (TC, TG, LDL-C and HDL-C), serum inflammatory markers (hs-CRP, IL-6, TNF-α and ICAM-1), ventricular remodelling markers (NT-pro BNP, MMP-9, TIMP-4 and Gal-3) and indicators of cardiac function (LVESD, LVESD, LVESV, LVEDV, IVST and LVEF) were collected from all patients at the time of admission and 8 weeks after rosuvastatin treatment.

Results

After treatment with rosuvastatin for 8 weeks, compared with those in conventional-dose group, the levels of TC, TG, LDL-C, hs-CRP, IL-6, TNF-α, ICAM-1, NT-pro BNP, MMP-9 and Gal-3 in the high-dose group decreased significantly (P<0.05), while the increase of HDL-C and TIMP-4 levels was more obvious (P<0.05) than that in the conventional-dose group. Moreover, LVEF was significantly higher (P<0.05) and LVESD, LVESD, LVESV, LVEDV and IVST were significantly lower (P< 0.05) after treatment than before treatment in both groups. The improvement of cardiac ultrasound results in the high-dose group was more significant than that in the conventional-dose group (P< 0.05).

Conclusion

This study suggests that high-dose rosuvastatin was better than conventional-dose rosuvastatin for improving blood lipid metabolism, reducing the inflammatory response, and preventing and treating ventricular remodelling and myocardial fibrosis, indicating that high-dose rosuvastatin had stronger therapeutic effect on STEMI than conventional-dose rosuvastatin.

Keywords:

• rosuvastatin
• ST elevation myocardial infarction
• blood lipids
• inflammatory factor
• ventricular remodelling
• myocardial fibrosis

Acknowledgments

This study was supported by Zhongshan Hospital of Fudan University.

Disclosure

The authors declare no conflict of interest for this work.