Background: Clinical significance of statin-induced high-density lipoprotein cholesterol (HDL-C) changes is not well known. We investigated the factors affecting rosuvastatin-induced HDL-C changes and their correlation with 12-month major adverse cardiovascular events (MACE) in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) and percutaneous coronary intervention (PCI). Materials and methods: We analyzed 556 consecutive NSTE-ACS patients who underwent PCI and received rosuvastatin 10. mg before discharge. We measured serum lipids, including total cholesterol, triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), and HDL-C at baseline and at 4 weeks. The relationship between on-treatment lipid levels, baseline lipid levels, and 12-month MACE was assessed. Results: Rosuvastatin treatment increased the mean HDL-C concentration by 1.1 ± 9.8. mg/dl (4.3 ± 23.0%). HDL-C was increased in 312 patients (56.1%), but decreased in 244 patients (43.9%) after statin treatment. Changes in HDL-C during first month were inversely correlated with baseline HDL-C levels (r=-0.379, p<0.001). The patients with increased HDL-C showed higher baseline TG levels but lower on-treatment TG levels. Changes in TG were correlated with changes in HDL-C (r=-0.212, p<0.001). The incidence of 12-month MACE according to changes in HDL-C was similar between the two groups (11.9% vs. 12.3%, p=0.875). Multivariate analysis revealed that baseline HDL-C level was the only significant predictor of rosuvastatin-induced HDL-C changes. Conclusion: Baseline HDL-C concentration was an independent predictor of rosuvastatin-induced HDL-C changes. Statin-induced HDL-C changes did not predict 12-month MACE in patients with NSTE-ACS. © 2012 Japanese College of Cardiology.
Yun, K. H., Shin, S. N., Ko, J. S., Rhee, S. J., Kim, N. H., Oh, S. K., & Jeong, J. W. (2012). Rosuvastatin-induced high-density lipoprotein changes in patients who underwent percutaneous coronary intervention for non-ST-segment elevation acute coronary syndrome. Journal of Cardiology, 60(5), 383–388. https://doi.org/10.1016/j.jjcc.2012.07.008