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Impact of statin therapy on LDL and non-HDL cholesterol levels in subjects with heterozygous familial hypercholesterolaemia.

Endocrinology and Nutrition Department. Hospital Del Mar; Paseo Marítimo, 25-29; E-08003, Barcelona, Spain; Department of Medicine, Universitat Autònoma de Barcelona. Campus Universitari Mar; Dr. Aiguader, 80; E-08003, Barcelona, Spain. Lipid Unit, Hospital Universitario Miguel Servet, IIS Aragón, CIBERCV, Universidad de Zaragoza, Zaragoza, Spain. Endocrinology and Nutrition Department. Hospital Del Mar; Paseo Marítimo, 25-29; E-08003, Barcelona, Spain; Department of Medicine, Universitat Autònoma de Barcelona. Campus Universitari Mar; Dr. Aiguader, 80; E-08003, Barcelona, Spain; Institut Hospital Del Mar D'Investigacions Mèdiques (IMIM), Dr. Aiguader, 80; E-08003, Barcelona, Spain. Lipid and Vascular Risk Unit, Department of Internal Medicine, Hospital de Bellvitge, CIBEROBN, Hospitalet de Llobregat, Barcelona, Spain. Lipid and Vascular Risk Unit, Hospital San Rafael, A Coruña, Spain. Unitat de Medicina Vascular i Metabolisme, Hospital Universitari Sant Joan. IISPV, CIBERDEM, Universitat Rovira i Virgili, Reus, Spain. Lipid Clinic, Hospital Clinic, CIBEROBN, 08036, Barcelona, Spain. Lipid Unit, Department of Internal Medicine, Hospital San Pedro, Logroño, Spain. Lipid Unit, Department of Internal Medicine, Hospital de Figueres, Figueres, Girona, Spain. Endocrinology and Nutrition Department. Hospital Del Mar; Paseo Marítimo, 25-29; E-08003, Barcelona, Spain; Department of Medicine, Universitat Autònoma de Barcelona. Campus Universitari Mar; Dr. Aiguader, 80; E-08003, Barcelona, Spain; Institut Hospital Del Mar D'Investigacions Mèdiques (IMIM), Dr. Aiguader, 80; E-08003, Barcelona, Spain. Electronic address: 86620@parcdesalutmar.cat.

Nutrition, metabolism, and cardiovascular diseases : NMCD. 2021;(5):1594-1603
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Abstract

BACKGROUND AND AIMS Cardiovascular risk in heterozygous familial hypercholesterolaemia (HeFH) is driven by LDL cholesterol levels. Since lipid response to statin therapy presents individual variation, this study aimed to compare mean LDL and non-HDL cholesterol reductions and their variability achieved with different types and doses of the most frequently prescribed statins. METHODS AND RESULTS Among primary hypercholesterolaemia cases on the Spanish Arteriosclerosis Society registry, 2894 with probable/definite HeFH and complete information on drug therapy and lipid profile were included. LDL cholesterol reduction ranged from 30.2 ± 17.0% with simvastatin 10 mg to 48.2 ± 14.7% with rosuvastatin 40 mg. After the addition of ezetimibe, an additional 26, 24, 21 and 24% reduction in LDL cholesterol levels was obtained for rosuvastatin, 5, 10, 20 and 40 mg, respectively. Subjects with definite HeFH and a confirmed genetic mutation had a more discrete LDL cholesterol reduction compared to definite HeFH subjects with no genetic mutation. A suboptimal response (<15% or <30% reduction in LDL cholesterol levels, respectively with low-/moderate-intensity and high-intensity statin therapy) was observed in 13.5% and, respectively, 20.3% of the subjects. CONCLUSION According to the LDL cholesterol reduction in HeFH patients, the ranking for more to less potent statins was rosuvastatin, atorvastatin and simvastatin; however, at maximum dosage, atorvastatin and rosuvastatin were nearly equivalent. HeFH subjects with positive genetic diagnosis had a lower lipid-lowering response. Approximately 1 in 5 patients on high-intensity statin therapy presented a suboptimal response.

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Publication Type : Comparative Study ; Observational Study

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