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Should we Consider Lipoprotein (a) in Cardiovascular Disease Risk Assessment in Patients with Familial
Panagiotis Anagnostis1,2, Pavlos Siolos2, Dimitrios Krikidis3
1Unit of Reproductive Endocrinology, 1st Department of Obstetrics and Gynaecology, Medical School, Aristotle University of Thessaloniki, Greece.
Insights
Familial hypercholesterolaemia (FH) patients have elevated Lipoprotein (a) [Lp(a)] levels, a key factor in cardiovascular disease (CVD) risk. Understanding Lp(a) is crucial for managing FH and preventing CVD.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Lipidology
Background:
- Familial hypercholesterolaemia (FH) is a genetic lipid disorder affecting 1 in 200-500 people.
- FH significantly increases Cardiovascular Disease (CVD) risk but is often underdiagnosed and undertreated.
- Lipoprotein (a) [Lp(a)] is an LDL-like molecule with an additional apolipoprotein (a).
Purpose of the Study:
- To review and discuss existing data on Lp(a) in FH patients.
- To evaluate the role of Lp(a) in augmenting CVD risk within the FH population.
Main Methods:
- A comprehensive literature search was conducted.
- Studies focused on evaluating the cardiovascular effects of Lp(a) in FH patients.
Main Results:
- Lp(a) is an established independent risk factor for CVD, particularly coronary artery disease (CAD).
- Elevated Lp(a) concentrations are observed in most adults and children with FH.
- An independent association exists between Lp(a) and CVD (primarily CAD) risk in FH patients.
Conclusions:
- Therapeutic agents like niacin, oestrogens, tibolone, and PCSK9 inhibitors can reduce Lp(a) by 25-30%.
- The clinical benefit of Lp(a) reduction with these therapies requires further establishment.
Background:
Familial hypercholesterolaemia (FH) is a genetically determined lipid disorder, affecting 1 per 200-500 individuals in the general population. It is significantly and independently associated with an increased risk of Cardiovascular Disease (CVD), although it remains still an underrecognized and undertreated disease. Lipoprotein (a) [Lp(a)] is a low-density-lipoprotein (LDL)-like molecule, containing an additional protein, apolipoprotein (a).
Objective:
This review aims to present and discuss available data on the role of Lp(a) in patients with FH, in terms of its potential augmentation of CVD risk.
Methods:
A comprehensive search of the literature was performed to identify studies evaluating the CV effects of Lp(a) in patients with FH.
Results:
Lp(a) has been recognised as an independent risk factor for CVD, mainly coronary artery disease (CAD). Most, but not all, studies show increased Lp(a) concentrations in adults and children with FH. There is also evidence of an independent association between Lp(a) and CVD (mainly CAD) risk in these patients.
Conclusion:
Some therapeutic modalities, such as niacin, oestrogens, tibolone and proprotein convertase subtilisin/ kexin type 9 (PCSK9) inhibitors may effectively reduce Lp(a) concentrations by 25-30%, although their clinical benefit of this effect remains to be established.
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