Document Type : Original Article
Authors
1
Healthy Ageing Research Centre, Neyshabur University of Medical Sciences, Neyshabur, Iran
2
Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
3
Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
4
School of Medicine, The University of Western Australia, Perth, Australia
5
Department of nursing and midwifery, Neyshabur University of Medical Sciences, Neyshabur, Iran
6
Noncommunicable Diseases Research Center, Neyshabur University of Medical Sciences, Neyshabur, Iran
Abstract
ABSTRACT
Background: Despite controlling for other risk factors of coronary artery disease (CAD), the risk of myocardial infarction (MI) due to vitamin D deficiency is increased. In addition to lipid-lowering effects of statins in CAD prevention and heart failure, these drugs exhibit many pleotropic effects. Part of these beneficial results may be due to the effect of statins on vitamin D levels. The current clinical trial aimed to explore the possible effects of high-intensity statin therapy on the levels of vitamin D metabolites in patients with acute myocardial infarction.
Methods: Patients in the Coronary Care Unit (CCU) with a cardiologist's diagnosis of myocardial infarction for the first time (i.e., typical chest pain greater than 20 min and ST-segment elevation greater than 1 mm in two adjacent leads on ECG) were included in the study. Then patients were divided into two equal groups using a block randomization method, who received atorvastatin 80 mg or rosuvastatin 40 mg as a secondary prevention once daily, plus a routine treatment regimen for 8 weeks. Following an overnight fast of 12 h, a venous blood sample (10 ml) was collected from study subjects within the first 24 h and 8 weeks after the patients were admitted to the hospital. The primary endpoint was the between-group difference in the change of serum vitamin D.
Results: In terms of baseline lipid levels, there was no significant difference between the two groups. In both groups, TC, TG, and LDL-C were decreased and HDL-C levels were increased after 8 weeks of treatment, but no significant difference between two groups was detected (p=0.792, p=0.418, p=0.514, p=0.456 respectively). In the rosuvastatin group, the mean values of hemoglobin A1C (HbA1C) and AST were increased significantly (P<0.05). In both groups, initial vitamin D levels were lower than normal and increased after statin consumption, but it was not statistically significant. The variation of ejection fraction after intervention was more increased after rosuvastatin than atorvastatin treatment (P=0.05).
Conclusion: Atorvastatin and rosuvastatin had no significant effects on 25-hydroxyvitamin D levels. Ejection fraction increased in the rosuvastatin group, but it was not statistically significant (p-value of exactly equal to 0.05). This increase could be due to various factors such as medication use and lifestyle changes.
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