Lipoprotein(a) and family history for cardiovascular disease in paediatric patients: A new frontier in cardiovascular risk stratification. Data from the LIPIGEN paediatric group

被引:11
|
作者
Pederiva, Cristina [1 ]
Capra, Maria Elena [2 ]
Biasucci, Giacomo [2 ]
Banderali, Giuseppe [1 ]
Fabrizi, Enrico [3 ]
Gazzotti, Marta [4 ]
Casula, Manuela [5 ,6 ]
Catapano, Alberico L. [5 ,6 ]
机构
[1] ASST Santi Paolo & Carlo, Paediat Unit, Study & Prevent Atherosclerosis Childhood, Clin Serv Dyslipidaemias, I-20142 Milan, Italy
[2] Guglielmo da Saliceto Hosp, Ctr Paediat Dyslipidaemias, Paediat & Neonatol Unit, I-29121 Piacenza, Italy
[3] Univ Cattolica S Cuore, DISES & DSS, Via Emilia Parmense 84, I-29122 Piacenza, Italy
[4] Fdn SISA Societ Italiana Studio Aterosclerosi, Via Giuseppe Balzaretti 7, I-20133 Milan, Italy
[5] Univ Milan, Dept Pharmacol & Biomol Sci, Epidemiol & Prevent Pharmacol Serv SEFAP, Milan, Italy
[6] IRCCS Multimed, Sesto San Giovanni, MI, Italy
关键词
Lp(a); Children/adolescents; Premature CVD; Family history; High cardiovascular risk; Paediatric FH; ELEVATED LIPOPROTEIN(A); MYOCARDIAL-INFARCTION; HEART-DISEASE; CHILDREN; HYPERCHOLESTEROLEMIA; ATHEROSCLEROSIS; APOLIPOPROTEIN(A); METAANALYSIS; GENETICS; EVENTS;
D O I
10.1016/j.atherosclerosis.2022.04.021
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background and aims: Little is known about the role of Lp(a) in the assessment of cardiovascular risk in the paediatric population. Trying to clarify the clinical relevance of Lp(a) in risk stratification, the aim of the study is to evaluate the association between Lp(a) plasma levels in children with familial hypercholesterolaemia (FH) and positive family history for premature cardiovascular disease (pCVD) in first-and second-degree relatives. Methods: 653 Caucasian children and adolescents (334 females and 319 males), aged 2-17 years, with diagnosis of FH from a paediatric cohort included in the LIPIGEN Network, were selected. We compared family history of pCVD, lipid and genetic profile in two groups based on Lp(a) levels below or above 30 mg/dL. To determine the independent predictors of pCVD, a multivariate logistic regression was used, with all clinical characteristics and blood measurements as predictors. Results: Subjects with Lp(a) > 30 mg/dl more frequently reported positive family history of pCVD compared to subjects with Lp(a)<= 30 mg/dl (69.90% vs 36.66%, p < 0.0001), while did not show differences in terms of median [interquartile range] LDL-cholesterol level (153.00 [88.00 vs 164.50 [90.25] mg/dL, p = 0.3105). In the regression analysis, Lp(a) > 30 mg/dl was an independent predictor of family history of pCVD. Comparing subjects with or without family history of pCVD, we reported significant differences for Lp(a) > 30 mg/dl (46.25% vs 17.65%, p < 0.0001), FH genetic mutation (50.48% vs 40.75%, p = 0,0157), as well as for LDLcholesterol (p = 0.0013) and total cholesterol (p = 0.0101). Conclusions: Children/adolescents with FH and Lp(a) > 30 mg/dl where more likely to have a positive family history of pCVD. Lp(a) screening in children and adolescents with FH may enhance risk assessment and help identify those subjects, children and relatives, at increased pCVD risk.
引用
收藏
页码:233 / 239
页数:7
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