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Elevated lipoprotein(a) level predicts repeated peripheral revascularization
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Abstract
Background
Despite high-intensity lipid-lowering therapy, there is a residual risk of cardiovascular events that could be associated with lipoprotein(a) [Lp(a)]. Data about the role of Lp(a) in the development of significant stenosis after carotid and lower extremity artery revascularization are lacking.
Purpose
To evaluate the relationship of Lp(a) level with repeated revascularization due to restenosis or de novo stenosis after endovascular or surgery repair of carotid and lower limb arteries.
Methods
The study included 258 patients (209 men and 49 women, mean age 67 years) who underwent revascularization of carotid and/or arteries of lower extremities for symptomatic stenotic atherosclerosis. Restenosis or de novo stenosis has been assessed by ultrasonography or angiography. History and physical examination have been performed to identify atherosclerosis risk factors. Lipids, C-reactive protein, Lp(a) concentrations were measured in blood serum.
Results
During 3 years follow-up, repeated revascularization due to restenosis or de novo stenosis was registered in 111 patients. Hyperlipoproteinemia(a) [Lp(a) ≥30 mg/dL] was associated with an increased risk of repeated revascularization with hazard ratio 2.9; 95% confidence interval 2.0–4.2, p<0.01 (figure). C-reactive protein and other clinical and laboratory variables did not differ in patients with and without repeated peripheral revascularization. According to Cox regression analysis adjusted for all risk factors, hyperlipoproteinemia(a) remained an independent predictor of severe restenosis or de novo stenosis of carotid and lower extremity arteries and was associated with a threefold increased risk of repeated revascularization.
Conclusions
In a three-year prospective study of patients after peripheral revascularization, Lp(a) level ≥30 mg/dL was shown as an independent risk factor for repeated revascularization.
Funding Acknowledgement
Type of funding sources: None. Survival analysis
Oxford University Press (OUP)
Title: Elevated lipoprotein(a) level predicts repeated peripheral revascularization
Description:
Abstract
Background
Despite high-intensity lipid-lowering therapy, there is a residual risk of cardiovascular events that could be associated with lipoprotein(a) [Lp(a)].
Data about the role of Lp(a) in the development of significant stenosis after carotid and lower extremity artery revascularization are lacking.
Purpose
To evaluate the relationship of Lp(a) level with repeated revascularization due to restenosis or de novo stenosis after endovascular or surgery repair of carotid and lower limb arteries.
Methods
The study included 258 patients (209 men and 49 women, mean age 67 years) who underwent revascularization of carotid and/or arteries of lower extremities for symptomatic stenotic atherosclerosis.
Restenosis or de novo stenosis has been assessed by ultrasonography or angiography.
History and physical examination have been performed to identify atherosclerosis risk factors.
Lipids, C-reactive protein, Lp(a) concentrations were measured in blood serum.
Results
During 3 years follow-up, repeated revascularization due to restenosis or de novo stenosis was registered in 111 patients.
Hyperlipoproteinemia(a) [Lp(a) ≥30 mg/dL] was associated with an increased risk of repeated revascularization with hazard ratio 2.
9; 95% confidence interval 2.
0–4.
2, p<0.
01 (figure).
C-reactive protein and other clinical and laboratory variables did not differ in patients with and without repeated peripheral revascularization.
According to Cox regression analysis adjusted for all risk factors, hyperlipoproteinemia(a) remained an independent predictor of severe restenosis or de novo stenosis of carotid and lower extremity arteries and was associated with a threefold increased risk of repeated revascularization.
Conclusions
In a three-year prospective study of patients after peripheral revascularization, Lp(a) level ≥30 mg/dL was shown as an independent risk factor for repeated revascularization.
Funding Acknowledgement
Type of funding sources: None.
Survival analysis.
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