Statins
Elevated Lp(a) does not predict restenosis or cardiac events after coronary angioplasty, a FLARE trial analysis of 823 patients (Atherosclerosis 2001)
Original title: The influence of plasma lipoprotein (a) on angiographic restenosis and coronary events in patients undergoing planned coronary balloon angioplasty. Ancillary analysis of the Fluvastatin Angioplasty Restenosis (FLARE) trial
This ancillary analysis of the FLARE trial (Fluvastatin Angioplasty Restenosis), a multicenter randomised study of 834 patients undergoing elective balloon angioplasty, examined whether baseline Lp(a) predicts angiographic restenosis or clinical events in 823 patients with successful angioplasty and baseline Lp(a) measurements (891 lesions analysed). No association was found between Lp(a) and quantitative or binary restenosis measures; late loss was 0.27 in the lowest Lp(a) quintile versus 0.23 in the highest (P>0.05). Elevated Lp(a) was not associated with increased risk of major coronary events over 40 weeks, with a major adverse cardiac event occurring in 24% of the lowest quintile and 26% of the highest (P>0.05). Fluvastatin did not affect Lp(a) levels. The findings show elevated Lp(a) is not associated with restenosis or clinical events after elective coronary balloon angioplasty and should not be considered a risk factor for post-angioplasty restenosis.
Original abstract
Elevated Lipoprotein (a) [Lp (a)] has been reported frequently, but not consistently, to be associated with restenosis following percutaneous transluminal coronary angioplasty (PTCA). The purpose of this study was to examine the association between Lp (a) and restenosis and clinical events in the context of a multi-centre randomised restenosis [Fluvastatin Angioplasty Restenosis (FLARE)] study of patients undergoing elective PTCA with full angiographic follow up. In the FLARE trial 40 mg fluvastatin twice daily did not influence restenosis, compared with placebo, after successful balloon angioplasty, measured as late loss in 834 patients, but did reduce the risk of death or myocardial infarction. Lp (a) was not effected by fluvastatin. Lp (a) and other biochemical details were established prior to planned PTCA. Among those undergoing successful PTCA, follow up angiography was performed at 26+/-2 weeks. Clinical follow up was complete to week 40. Included in this analysis are the 823 patients who underwent successful angioplasty and had a baseline Lp (a) performed yielding 891 lesions for quantitative coronary angiography (QCA). No association was observed between Lp (a) and either quantitative markers of restenosis or binary restenosis rates. Late loss was 0.27 (SD 0.51) in the lowest quintile (Lp (a) 0-4 g/dl) compared with 0.23 (SD 0.49) (P>0.05). Elevated Lp (a) was not associated with an increased risk of individual or combined major coronary events over 40 weeks. A major adverse cardiac event (MACE) occurred in 41 (24%) of the lowest quintile and 42 (26%) of the highest (P>0.05). In conclusion, elevated Lp (a) was not associated with restenosis or clinical events following elective coronary balloon angioplasty in this randomised clinical trial and should not be considered a risk factor for post angioplasty restenosis.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.