Related Experiment Videos
Lipoprotein (a) concentrations in patients with familial combined hyperlipidemia and hypertension
R T Netea1, M G Netea, S J Bredie
1Department of Medicine, University Hospital Nijmegen, The Netherlands.
Insights
Lipoprotein (a) (Lp(a)) levels are similar in patients with familial combined hyperlipidemia (FCH) and hypertension compared to healthy individuals. However, measuring Lp(a) is still crucial for assessing atherosclerosis risk in these patient groups.
Area of Science:
- Cardiovascular Science
- Clinical Chemistry
- Genetics
Background:
- Lipoprotein (a) (Lp(a)) is an established independent risk factor for coronary heart disease (CHD).
- Elevated Lp(a) significantly increases the risk of premature CHD, especially when combined with hyperlipidemia or hypertension.
Purpose of the Study:
- To assess plasma concentrations of Lp(a) in patients with familial combined hyperlipidemia (FCH) and hypertension.
- To compare Lp(a) levels in these patient groups with those in healthy volunteers.
Main Methods:
- Radioimmunoassay was used to measure Lp(a) plasma concentrations.
- Study included 262 subjects with FCH, 168 patients with hypertension, and 371 healthy volunteers.
Main Results:
- Lp(a) plasma concentrations were similar between FCH patients and controls (P > 0.05).
- Lp(a) levels in hypertensive patients did not differ significantly from controls (P > 0.05).
- No significant difference in Lp(a) was observed in patients with essential hypertension (EH), regardless of lipid levels, or in those with renal artery stenosis (RAS).
Conclusions:
- Plasma Lp(a) concentrations are comparable across FCH, EH (normo- or hyperlipidemic), and RAS patient groups versus healthy controls.
- Despite similar levels, measuring Lp(a) in patients with hyperlipidemia or hypertension is vital for evaluating severe atherosclerosis risk.
Background:
Lipoprotein (a) (Lp(a)) is an independent risk factor for coronary heart disease (CHD), and its association with hyperlipidemia and/or hypertension greatly increases the risk of premature CHD.
Methods:
The present study assessed plasma concentrations of Lp(a) in hyperlipidemic subjects from families with well-defined familial combined hyperlipidemia (FCH) (n = 262) and from patients with hypertension (n = 168), and to compare it with Lp(a) plasma levels in healthy volunteers (n = 371). Lp(a) concentrations were measured using a specific radioimmunoassay.
Results:
The Lp(a) plasma concentrations were similar in FCH patients (median 204 mg/l, range 16-2163 mg/l) and in the control group (155, 16-1846 mg/l; P > 0.05). The Lp(a) levels in patients with hypertension (157, 10-1985 mg/l) did not differ from those of controls (P > 0.05). The Lp(a) concentrations were similar in patients with essential hypertension (EH) and normal lipid levels, and in hyperlipidemic EH patients. A tendency towards higher levels of Lp(a) was observed in patients with secondary hypertension due to renal artery stenosis (RAS) (n = 26, Lp(a) 232, 16-1110 mg/l), but this was not statistically significant.
Conclusions:
Plasma concentrations of Lp(a) are similar in patients with FCH, with EH, either normo- or hyperlipidemic, and with RAS, when compared with healthy controls. However, measuring the Lp(a) levels in patients with either hyperlipidemia or hypertension remains important for assessing the risk potential for severe atherosclerosis in these patients.