Subclinical coronary atherosclerosis and cardiovascular risk stratification in heterozygous familial hypercholesterolemia patients undergoing statin treatment
Carregando...
Citações na Scopus
11
Tipo de produção
article
Data de publicação
2019
Título da Revista
ISSN da Revista
Título do Volume
Editora
LIPPINCOTT WILLIAMS & WILKINS
Autores
Citação
CURRENT OPINION IN LIPIDOLOGY, v.30, n.2, p.82-87, 2019
Resumo
Purpose of review To discuss the heterogeneity of atherosclerotic cardiovascular disease (ASCVD) risk in heterozygous familial hypercholesterolemia and evidence and limitations of clinical risk scores and subclinical coronary atherosclerosis (SCA) imaging to evaluate risk. Recent findings Risk evaluation in contemporary familial hypercholesterolemia cohorts needs to consider the cause of the familial hypercholesterolemia phenotype, for example the presence of autosomal molecular defects that impart a greater ASCVD risk than in polygenic hypercholesterolemia, prospective follow-up and the impact of statin treatment. As atherosclerosis is multifactorial, clinical scores like the Montreal familial hypercholesterolemia score and SAFEHEART risk equation have been proposed to stratify ASCVD in statintreated, molecularly defined familial hypercholesterolemia individuals. However, these scores need further validation. SCA distribution in familial hypercholesterolemia individuals undergoing conventional lipidlowering treatment is heterogeneous, with 45-50% of individuals not presenting any coronary artery calcification (CAC). One study suggests that the absence of CAC associates with no ASCVD events in asymptomatic familial hypercholesterolemia individuals undergoing statin therapy despite elevated residual LDL-cholesterol levels. In contrast, the presence of CAC was independently associated with ASCVD events. Summary ASCVD risk is heterogeneous in statin-treated familial hypercholesterolemia individuals. Further studies are necessary to determine how risk stratification, especially with SCA detection, impacts on prescription of proprotein convertase subtilisin kexin type 9 inhibitors within a cost-constrained environment.
Palavras-chave
coronary artery calcification, familial hypercholesterolemia, proprotein convertase subtilisin kexin type 9, risk stratification, statins, subclinical atherosclerosis
Referências
- Alonso R, 2008, ATHEROSCLEROSIS, V200, P315, DOI 10.1016/j.atherosclerosis.2007.12.024
- Besseling J, 2016, J AM COLL CARDIOL, V68, P252, DOI 10.1016/j.jacc.2016.04.054
- Besseling J, 2014, ATHEROSCLEROSIS, V233, P219, DOI 10.1016/j.atherosclerosis.2013.12.020
- Gidding SS, 2015, CIRCULATION, V132, P2167, DOI 10.1161/CIR.0000000000000297
- Grundy Scott M, 2018, J Am Coll Cardiol, DOI 10.1016/j.jacc.2018.11.003
- Harada PH, 2018, ATHEROSCLEROSIS, V277, P273, DOI 10.1016/j.atherosclerosis.2018.08.021
- Hlatky MA, 2017, J AM COLL CARDIOL, V70, P2677, DOI 10.1016/j.jacc.2017.10.001
- Humphries SE, 2018, ATHEROSCLEROSIS, V274, P41, DOI 10.1016/j.atherosclerosis.2018.04.040
- Jansen ACM, 2004, J INTERN MED, V256, P482, DOI 10.1111/j.1365-2796.2004.01405.x
- Khera AV, 2016, J AM COLL CARDIOL, V67, P2578, DOI 10.1016/j.jacc.2016.03.520
- Kramer CK, 2013, BMJ-BRIT MED J, V346, DOI 10.1136/bmj.f1654
- Martinez LRC, 2008, ATHEROSCLEROSIS, V200, P83, DOI 10.1016/j.atherosclerosis.2007.12.014
- Miname Marcio H, 2018, JACC Cardiovasc Imaging, DOI 10.1016/j.jcmg.2018.09.019
- Miname MH, 2010, ATHEROSCLEROSIS, V213, P486, DOI 10.1016/j.atherosclerosis.2010.10.001
- Mundal LJ, 2018, HEART, V104, P1600, DOI 10.1136/heartjnl-2017-312706
- Neefjes LA, 2011, ATHEROSCLEROSIS, V219, P721, DOI 10.1016/j.atherosclerosis.2011.09.052
- Nicholls SJ, 2018, J AM COLL CARDIOL, V72, P2012, DOI 10.1016/j.jacc.2018.06.078
- Paquette M, 2017, J CLIN LIPIDOL, V11, P1161, DOI 10.1016/j.jacl.2017.07.008
- Paquette M, 2017, J CLIN LIPIDOL, V11, P80, DOI 10.1016/j.jacl.2016.10.004
- de Isla LP, 2017, CIRCULATION, V135, P2133, DOI 10.1161/CIRCULATIONAHA.116.024541
- Polonsky TS, 2010, JAMA-J AM MED ASSOC, V303, P1610, DOI 10.1001/jama.2010.461
- Ridker PM, 2018, J CLIN LIPIDOL, V12, P958, DOI 10.1016/j.jacl.2018.03.088
- Santos RD, 2016, LANCET DIABETES ENDO, V4, P850, DOI 10.1016/S2213-8587(16)30041-9
- Sharifi M, 2017, ATHEROSCLEROSIS, V263, P405, DOI 10.1016/j.atherosclerosis.2017.05.015
- Silva PRS, 2016, ATHEROSCLEROSIS, V250, P144, DOI 10.1016/j.atherosclerosis.2016.05.023
- Vallejo-Vaz AJ, 2018, ATHEROSCLEROSIS, V277, P234, DOI 10.1016/j.atherosclerosis.2018.08.051
- Versmissen J, 2008, BMJ-BRIT MED J, V337, DOI 10.1136/bmj.a2423
- Ye ZX, 2007, AM J CARDIOL, V100, P1119, DOI 10.1016/j.amjcard.2007.05.034
- 2018, J CLIN LIPIDOL, V12, P948, DOI 10.1016/J.JACL.2018.04.003