Restenosis after intracoronary stent placement: can apolipoprotein(a) polymorphism play a role?

Background: The relationship between lipoprotein(a) and restenosis after intracoronary stent implantation has been analysed by two specific studies, but the role of apoliprotein(a) polymorphism was not considered. The aim of the present prospective study was to evaluate whether lipoprotein(a) levels and apolipoprotein(a) phenotypes are predictors of restenosis after elective stent implantation in patients with de novo lesions of coronary arteries. Methods: We recruited 182 patients with a new lesion successfully treated with elective placement of one or two Palmaz–Schatz stents. Follow-up angiography was scheduled at 6 months or earlier if clinically indicated. Nine patients were lost to the follow up. Among 173 patients enrolled, restenosis was present in 52 (30.0%) and absent in 121 (70.0%). Results: Lipoprotein(a) levels were higher in the restenosis than in the nonrestenosis group (29.5±17.2 versus 27.4±20.2 mg/dl), even if the difference did not attain statistical significance (P=0.067). The restenosis group had a percentage of subjects with at least one apolipoprotein(a) isoform of low molecular weight significantly greater than the nonrestenosis group (82.7 versus 66.9%; P=0.035). A multiple logistic regression analysis showed that multiple stenting (RR: 4.01; CI 95%: 1.65–13.91; P=0.004), presence of diabetes (RR: 3.96; CI 95%: 1.67–9.37; P=0.002) and presence of multivessel disease (RR: 2.71; CI 95%: 1.19–6.16; P=0.017) were predictors of restenosis after stent placement. Lipoprotein(a) and apolipoprotein(a) polymorphism did not enter the model as predictive variables. Conclusions: Our study confirms that multiple stenting, diabetes and multivessel disease are powerful predictors of restenosis after intracoronary stent implantation. On the contrary, lipoprotein(a) and apolipoprotein(a) polymorphism do not appear to be reliable markers of restenosis in patients with stent implantation.