Long term statin treatment reduces lipoprotein(a) concentrations in heterozygous familial hypercholesterolaemia

S van Wissen1, T J Smilde, M D Trip

  • 1Department of Vascular Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, Netherlands. s.vanwissen@amc.uva.nl

Insights

Long-term statin therapy significantly reduces lipoprotein(a) (Lp(a)) levels in patients with familial hypercholesterolaemia (FH). However, these reductions did not correlate with changes in atherosclerosis progression, questioning Lp(a)

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Genetics

Background:

  • Elevated plasma lipoprotein(a) (Lp(a)) is a known risk factor for cardiovascular disease.
  • The role of Lp(a) as an independent risk factor in familial hypercholesterolaemia (FH) and the long-term effects of statins on Lp(a) remain unclear.

Purpose of the Study:

  • To investigate Lp(a) concentrations in FH patients undergoing statin treatment.
  • To assess the relationship between statin therapy, Lp(a) levels, and atherosclerosis progression over two years.

Main Methods:

  • A two-year, randomized, double-blind trial (ASAP trial) involving 325 heterozygous FH patients.
  • Patients received either 80 mg atorvastatin or 40 mg simvastatin daily.
  • Changes in Lp(a) concentrations and carotid artery intima-media thickness were measured at one and two years.

Main Results:

  • Both atorvastatin and simvastatin significantly reduced Lp(a) concentrations in FH patients over two years.
  • Atorvastatin showed a greater initial reduction in Lp(a) compared to simvastatin at one year, but this difference was not sustained at two years.
  • No correlation was found between baseline Lp(a) levels and cardiovascular events, LDL cholesterol, or intima-media thickness. Changes in Lp(a) did not correlate with changes in intima-media thickness.

Conclusions:

  • Long-term statin treatment effectively lowers Lp(a) levels in FH patients.
  • The observed reduction in Lp(a) did not correlate with a decrease in intima-media thickness, suggesting Lp(a) may not be a significant driver of atherosclerosis progression in this population.
Abstract

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