Effect of Statin Therapy on Lipoprotein (A) evels in Patients Post Percutaneous Coronary Intervention- Prospective Study
DOI:
https://doi.org/10.64252/y6msv622Keywords:
Statin therapy, Lipoprotein(a), Percutaneous coronary intervention, Dyslipidaemia, LDL-C, Residual cardiovascular riskAbstract
Introduction: Cardiovascular diseases are a leading cause of death worldwide, with coronary artery disease (CAD) accounting for a major proportion of deaths. Dyslipidaemia contributes significantly to CAD progression, and lipoprotein(a) [Lp(a)] has emerged as an independent risk factor for adverse cardiovascular outcomes. Percutaneous coronary intervention (PCI) is widely performed for CAD; however, residual risk persists due to lipid abnormalities. Statins are the cornerstone of lipid-lowering therapy post-PCI; their effect on Lp(a) remains uncertain. This study evaluated the impact of statin therapy on lipid parameters, including Lp(a) levels, in post-PCI patients.
Aim: To assess the effect of statin therapy on total cholesterol, LDL-C, HDL-C, triglycerides, and Lp(a) levels in patients following PCI.
Materials and Methods: This prospective study included 57 patients with dyslipidaemia aged 18–65 years who underwent PCI. The participants received atorvastatin (20 mg) or rosuvastatin (10 mg) for 90 days. Fasting lipid profiles and Lp(a) levels were measured at baseline and after therapy, with statistical significance set at p<0.05.
Results: Most patients were between 51 and 60 years (43.9%), and males constituted 56.1% of the study population. Coexisting diabetes and hypertension were present in 70.2% of the cases, reflecting a high-risk group. After 90 days of statin therapy, the mean total cholesterol significantly decreased from 190.16 ± 65.11 to 163.77 ± 60.91 mg/dL (p<0.0001), while LDL-C reduced from 131.37 ± 46.21 to 107.82 ± 46.30 mg/dL (p<0.0001). Triglyceride levels also showed a significant decrease from 145.00 mg/dL to 119.00 mg/dL (p<0.0001). In contrast, HDL-C levels remained largely unchanged, showing no significant variation. Importantly, Lp(a) levels rose significantly from 23.07 ± 5.56 to 31.86 ± 13.56 mg/dL (p<0.0001), indicating that although statins effectively control conventional lipids, they may worsen residual risk by elevating Lp(a) levels.
Conclusion: Statin therapy after PCI markedly improved total cholesterol, LDL-C, and triglyceride levels, confirming its central role in the secondary prevention of CAD. However, unchanged HDL-C levels and a significant increase in Lp(a) highlight an important therapeutic limitation.
