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Plasma Lipoprotein(a) Is an Independent Factor Associated With Carotid Wall Thickening in Severely but Not Moderately Hypercholesterolemic Patients

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Background and Purpose To evaluate whether high levels of low-density lipoprotein cholesterol (LDL-C) may promote the atherogenic effect of lipoprotein(a) [Lp(a)], we investigated the association between elevated Lp(a) levels and thickening of intima plus media in the common carotid artery (CC-IMT) in patients with different degrees of hypercholesterolemia. Methods One hundred type II hypercholesterolemic patients and 25 normolipidemic subjects were selected for the study. Plasma lipid and lipoprotein levels were determined enzymatically; Lp(a) levels were determined by enzyme-linked immunosorbent assay. An Lp(a) concentration >30 mg/dL was arbitrarily considered a risk factor. For each patient mean CC-IMT was determined by B-mode ultrasound; in 60 patients and in the 25 control subjects, the maximal IMT in the entire carotid tree was also determined. Results CC-IMT values were higher in hypercholesterolemic patients with plasma Lp(a) levels >30 mg/dL than in those with lower levels ( P <.01). CC-IMT and maximal IMT directly and independently correlated with plasma levels of Lp(a) ( r =.33 and r =.25, respectively; both P <.05). The effect of LDL-C concentrations on the relationship between IMT and Lp(a) was investigated by dividing the patients into quartiles of plasma LDL-C levels. After stratification, CC-IMT significantly correlated with plasma Lp(a) levels in the patients with severe hypercholesterolemia (LDL-C >5.2 mmol/L) but not in patients in the lowest quartile, ie, those with moderate hypercholesterolemia. No correlation between CC-IMT and Lp(a) was found in normolipidemic control subjects. Conclusions Elevated plasma levels of Lp(a) can be considered an additional independent factor associated with thickening of the common carotid arteries in patients with severe hypercholesterolemia but not in those with moderate hypercholesterolemia or in normocholesterolemic subjects.
Title: Plasma Lipoprotein(a) Is an Independent Factor Associated With Carotid Wall Thickening in Severely but Not Moderately Hypercholesterolemic Patients
Description:
Background and Purpose To evaluate whether high levels of low-density lipoprotein cholesterol (LDL-C) may promote the atherogenic effect of lipoprotein(a) [Lp(a)], we investigated the association between elevated Lp(a) levels and thickening of intima plus media in the common carotid artery (CC-IMT) in patients with different degrees of hypercholesterolemia.
Methods One hundred type II hypercholesterolemic patients and 25 normolipidemic subjects were selected for the study.
Plasma lipid and lipoprotein levels were determined enzymatically; Lp(a) levels were determined by enzyme-linked immunosorbent assay.
An Lp(a) concentration >30 mg/dL was arbitrarily considered a risk factor.
For each patient mean CC-IMT was determined by B-mode ultrasound; in 60 patients and in the 25 control subjects, the maximal IMT in the entire carotid tree was also determined.
Results CC-IMT values were higher in hypercholesterolemic patients with plasma Lp(a) levels >30 mg/dL than in those with lower levels ( P <.
01).
CC-IMT and maximal IMT directly and independently correlated with plasma levels of Lp(a) ( r =.
33 and r =.
25, respectively; both P <.
05).
The effect of LDL-C concentrations on the relationship between IMT and Lp(a) was investigated by dividing the patients into quartiles of plasma LDL-C levels.
After stratification, CC-IMT significantly correlated with plasma Lp(a) levels in the patients with severe hypercholesterolemia (LDL-C >5.
2 mmol/L) but not in patients in the lowest quartile, ie, those with moderate hypercholesterolemia.
No correlation between CC-IMT and Lp(a) was found in normolipidemic control subjects.
Conclusions Elevated plasma levels of Lp(a) can be considered an additional independent factor associated with thickening of the common carotid arteries in patients with severe hypercholesterolemia but not in those with moderate hypercholesterolemia or in normocholesterolemic subjects.

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