Abstract
Background
Familial hypercholesterolemia (FH), familial combined hyperlipidemia (FCHL), and elevated
lipoprotein (a) (Lp[a]) increase risk of premature coronary artery disease (CAD).
The objective of this study was to assess the prevalence of FH, FCHL, elevated Lp(a)
and their impact on management in patients with premature CAD.
Methods
We prospectively recruited men ≤ 50 years and women ≤ 55 with obstructive CAD. FH
was defined as Dutch Lipid Clinic Network scores ≥ 6. FCHL was defined as apolipoprotein
B > 1.2 g/L, triglyceride and total cholesterol > 90th population percentile, and
family history of premature cardiovascular disease. Lp(a) ≥ 50 mg/dL was considered
to be elevated.
Results
Among 263 participants, 9.1% met criteria for FH, 12.5% for FCHL, and 19.4% had elevated
Lp(a). Among patients with FH, 37.5% had FH-causing DNA variants. Patients with FH,
but not other dyslipidemias, were more likely than nondyslipidemic patients to have
received lipid-lowering therapy before presenting with CAD (33.3% vs 12.3%, P = 0.04) and combined lipid-lowering therapy after the presentation (41.7% vs 7.7%,
P < 0.001). One year after presentation, 58.3%, 54.5%, and 58.8% of patients with FH,
FCHL, and elevated Lp(a) had low-density lipoprotein cholesterol (LDL-C) < 1.8 mmol/L,
respectively, compared with 68.0 % in reference group. Patients with FCHL were more
likely to have non–high-density lipoprotein (HDL) and apolipoprotein B above recommended
lipid goals (70.0% and 87.9%, respectively).
Conclusions
FH, FCHL, and elevated Lp(a) are common in patients with premature CAD and have differing
impact on treatment and achievement of lipid targets. Assessment for these conditions
in patients with premature CAD provides valuable information for individualized management.
Résumé
Contexte
L’hypercholestérolémie familiale (HF), l’hyperlipidémie combinée familiale (HCF) et
les taux élevés de lipoprotéines (a) [Lp(a)] augmentent le risque de coronaropathie
précoce. L’objectif de cette étude était d’évaluer la prévalence de l’HF, de l’HCF
et des taux élevés de Lp(a) ainsi que leur incidence sur la prise en charge des patients
atteints de coronaropathie précoce.
Méthodologie
Nous avons recruté de façon prospective des hommes ≤ 50 ans et des femmes ≤ 55 ans
atteints de coronaropathie obstructive. L’HF était définie par des scores DLCN (Dutch Lipid Clinic Network) ≥ 6. L’HCF était définie par un taux d’apolipoprotéine B > 1,2 g/l, un taux de triglycérides
et de cholestérol total > 90e percentile de la population, et des antécédents familiaux de maladies cardiovasculaires
précoces. Un taux de Lp(a) ≥ 50 mg/dl était considéré comme élevé.
Résultats
Parmi les 263 participants, 9,1 % répondaient aux critères pour l’HF, 12,5 %, à ceux
pour l’HCF, et 19,4 % présentaient des taux de Lp(a) élevés. Parmi les patients atteints
d’HF, 37,5 % présentaient des variants d'ADN causant l’HF. Les patients atteints d’HF,
mais pas d’autres dyslipidémies étaient plus susceptibles que les patients non dyslipidémiques
d’avoir reçu un traitement hypolipidémiant avant de présenter une coronaropathie (33,3
% vs 12,3 %, p = 0,04) et un traitement hypolipidémiant combiné après sa manifestation (41,7 % vs
7,7 %, p < 0,001). Un an après la manifestation, 58,3 %, 54,5 % et 58,8 % des patients atteints
d’HF ou d’HCF, ou présentant un taux élevé de Lp(a), respectivement, avaient un taux
de cholestérol de lipoprotéines à faible densité (C-LDL) < 1,8 mmol/l, contre 68,0
% dans le groupe de référence. Les patients atteints d’HCF étaient plus susceptibles
de présenter des taux de cholestérol non de lipoprotéines à haute densité (HDL) et
d’apolipoprotéine B supérieurs aux cibles lipidiques recommandées (70,0 % et 87,9
%, respectivement).
Conclusions
L’HF, L’HCF et le taux de Lp(a) élevé sont fréquents chez les patients atteints de
coronaropathie précoce et ont une incidence différente sur le traitement et l’atteinte
des cibles lipidiques. L’évaluation de ces maladies chez les patients atteints de
coronaropathie précoce fournit de précieux renseignements pour une prise en charge
personnalisée.
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Article info
Publication history
Published online: August 26, 2021
Accepted:
August 20,
2021
Received:
May 25,
2021
Footnotes
See page 1741 for disclosure information.
Identification
Copyright
© 2021 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
