Effects of statins (atorvastatin) on serum lipoprotein levels in patients with primary hyperlipidemia and coronary heart disease.

UNLABELLED

The aim of our study was to investigate the effects of atorvastatin on serum levels of total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), apolipoprotein A1 (apoA1), apolipoprotein B (apoB) and lipoprotein (a) in patients with primary hyperlipidemia and established coronary heart disease.

MATERIAL AND METHODS

A group of 96 patients (pts), of both sexes, aged 34-59, with primary hyperlipidemia and coronary heart disease were monitored at baseline and 12 times within 12 months by the measurement of total cholesterol (TC), low-density lipoprotein (LDL) and high-density lipoprotein (HDL). Apolipoprotein A1 (apoA1), apolipoprotein B (apoB), and lipoprotein (a) were monitored at baseline, after 6 months and after 12 months of atorvastatin therapy. The analyses were performed in the laboratory of the Clinical Biochemistry Institute of the Clinical Centre in Skopje. Serum levels of TC were evaluated using the calorimetric method, LDL was calculated according to Friedewald's formula, and HDL was determined with a precipitation test. Serum levels of apoA1, apoB and lipoprotein (a) were measured by the immunoturbidimetric method. The therapeutic doses of atorvastatin used were 40 mg. Liver enzymes, alanine aminotransferase (AST), aspartate aminotransferase (ALT) and creatine kinase (CPK) level were also monitored in our patients.

RESULTS

According to our results, total cholesterol (TC), low-density lipoprotein (LDL) and apolipoprotein B (apoB) levels decreased after treatment by 43.58%, by 41.46%, and by 6,8%; high-density lipoprotein (HDL) increased insignificantly by 4%, apolipoprotein A1 (apoA1) and lipoprotein (a) remained unchanged.

CONCLUSION

The significant reduction of total serum cholesterol, LDL, and apoprotein B levels achieved represents the good result of the atorvastatin therapy, as opposed to the effects on HDL values, which showed no significant increase. Serum apolipoprotein A1 levels and serum lipoprotein (a) levels remainned unchanged at baseline and after 12 months of atorvastatin therapy, and they remained stable over time. This probably means that atorvastatin has no therapeutic effect on the two parameters investigated. Elevation in alanine aminotransferase and aspartate aminotransferase levels greater than twice the upper limit of normal were seen in only one patient, after 12 months of atorvastatin therapy. Creatine kinase levels remained stable over time.