Familial hypercholesterolaemia: beware of lipoprotein(a)

2016 ◽  
Vol 4 (7) ◽  
pp. 553-555 ◽  
Author(s):  
Raul D Santos
2016 ◽  
Vol 4 (9) ◽  
pp. 730 ◽  
Author(s):  
Leopoldo Pérez de Isla ◽  
Adriana Saltijeral Cerezo ◽  
Rodrigo Alonso ◽  
Pedro Mata

2006 ◽  
Vol 260 (2) ◽  
pp. 183-185
Author(s):  
J. S. Rana ◽  
A. C. Jansen ◽  
A. H. Zwinderman ◽  
E. S. van Aalst-Cohen ◽  
J. W. Jukema ◽  
...  

The Lancet ◽  
1988 ◽  
Vol 332 (8622) ◽  
pp. 1262-1263 ◽  
Author(s):  
K. Widhalm ◽  
Dieter Genser ◽  
Tissa Vitarana ◽  
Gaya Colombage ◽  
Vasanthi Bandaranayake ◽  
...  

2012 ◽  
Vol 1 (3) ◽  
pp. 1-9 ◽  
Author(s):  
Mary Seed ◽  
D John Betteridge ◽  
Jackie Cooper ◽  
Muriel Caslake ◽  
Paul N Durrington ◽  
...  

Objective To assess the relationship of levels of inflammatory risk markers to presence of clinical coronary artery disease (CAD) in patients with treated heterozygous familial hypercholesterolaemia. Design A cross-sectional study of patients on the Simon Broome Familial Hyperlipidaemia Register. Setting Six hospital outpatient clinics in the UK. Participants A total of 211 men and 199 women with heterozygous familial hypercholesterolaemia. Main outcome measures Analysis of conventional risk factors and concentrations of high-sensitivity C-reactive protein (hsCRP), lipoprotein (a), serum intercellular adhesion molecule (sICAM), interIeukin-6 (IL-6) and lipoprotein-associated phospholipase A2 (LpPLA2) mass. Results CAD was present in 104 men and in 55 women; the mean ages of onset were 43.1 and 46.5 years, respectively. On univariate analysis there was a positive relationship of CAD with age, male sex, smoking, IL-6 and sICAM, and an inverse relationship with low-density lipoprotein (LDL) and LpPLA2. On multivariate analysis, age, smoking, low LDL and low LpPLA2 were associated with CAD. When LpPLA2 values were adjusted for apoB and aspirin usage, there was no significant difference between those with and without CAD. Only age and smoking were independently associated with CAD in men, and IL-6 and lipoprotein(a) in women. Conclusions Although on univariate analysis inflammatory marker levels were associated with CAD in these patients, the majority of the associations, including that for hsCRP, disappeared when corrected for smoking and apoB. This may be because atherosclerotic plaques in these statin-treated patients were quiescent or an effect of aspirin usage. In this observational study newer risk markers were not usefully associated with the presence or absence of symptomatic CAD.


2019 ◽  
Vol 24 (31) ◽  
pp. 3665-3671 ◽  
Author(s):  
Panagiotis Anagnostis ◽  
Pavlos Siolos ◽  
Dimitrios Krikidis ◽  
Dimitrios G. Goulis ◽  
John C. Stevenson

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.


2019 ◽  
Vol 122 (07) ◽  
pp. 790-799
Author(s):  
Ingunn Narverud ◽  
Martin P. Bogsrud ◽  
Linn K. L. Øyri ◽  
Stine M. Ulven ◽  
Kjetil Retterstøl ◽  
...  

AbstractElevated lipoprotein(a) (Lp(a)) is associated with CVD and is mainly genetically determined. Studies suggest a role of dietary fatty acids (FA) in the regulation of Lp(a); however, no studies have investigated the association between plasma Lp(a) concentration and n-6 FA. We aimed to investigate whether plasma Lp(a) concentration was associated with dietary n-6 FA intake and plasma levels of arachidonic acid (AA) in subjects with familial hypercholesterolaemia (FH). We included FH subjects with (n 68) and without (n 77) elevated Lp(a) defined as ≥75 nmol/l and healthy subjects (n 14). Total FA profile was analysed by GC–flame ionisation detector analysis, and the daily intake of macronutrients (including the sum of n-6 FA: 18 : 2n-6, 20 : 2n-6, 20 : 3n-6 and 20 : 4n-6) were computed from completed FFQ. FH subjects with elevated Lp(a) had higher plasma levels of AA compared with FH subjects without elevated Lp(a) (P = 0·03). Furthermore, both FH subjects with and without elevated Lp(a) had higher plasma levels of AA compared with controls (P < 0·001). The multivariable analyses showed associations between dietary n-6 FA intake and plasma levels of AA (P = 0·02) and between plasma levels of Lp(a) and AA (P = 0·006). Our data suggest a novel link between plasma Lp(a) concentration, dietary n-6 FA and plasma AA concentration, which may explain the small diet-induced increase in Lp(a) levels associated with lifestyle changes. Although the increase may not be clinically relevant, this association may be mechanistically interesting in understanding more of the role and regulation of Lp(a).


Sign in / Sign up

Export Citation Format

Share Document