Martin P Bogsrud1, Asgeir Græsdal2, Dan Johansen3, Gisle Langslet4, Anders Hovland5, Kjell-Erik Arnesen6, Liv J Mundal6, Kjetil Retterstøl7, Cecilie Wium6, Kirsten B Holven8. 1. Norwegian National Advisory Unit on Familial Hypercholesterolemia, Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway; The Lipid Clinic, Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway; Unit for Cardiac and Cardiovascular Genetics, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway. Electronic address: mabogs@ous-hf.no. 2. Vestfold Medical Center, Sandefjord, Norway. 3. Norwegian National Advisory Unit on Familial Hypercholesterolemia, Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway. 4. Norwegian National Advisory Unit on Familial Hypercholesterolemia, Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway; The Lipid Clinic, Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway. 5. Division of Internal Medicine, Nordland Hospital Bodø, Bodø, Norway; Department of Clinical Medicine, University of Tromsø, Tromsø, Norway. 6. The Lipid Clinic, Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway. 7. The Lipid Clinic, Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway; Faculty of Medicine, Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway. 8. Norwegian National Advisory Unit on Familial Hypercholesterolemia, Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway; Faculty of Medicine, Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Abstract
BACKGROUND: Current treatment goals for familial hypercholesterolemia (FH) recommended by the European Atherosclerosis Society (EAS) are LDL-C ≤2.5 mmol/L (∼100 mg/dL) or ≤1.8 mmol/L (∼70 mg/dL) in very high-risk subjects. OBJECTIVE: The objective of the present study was to investigate characteristics and treatment status in subjects with genetically verified FH followed at specialized lipid clinics in Norway. METHODS: Data from treatment registries of 714 adult (>18 years) subjects with FH. RESULTS: Fifty-seven percent were female. Mean age (SD) at last visit was 44 (16.3) years, and the subjects had been followed at a lipid clinic for 11.1 (7.9) years. Two hundred forty-five (34%) were classified as very-high-risk, and 44% of these had established coronary heart disease. Very-high-risk FH subjects more often received maximal statin dose (54% vs 33%, P < .001), ezetimibe (76% vs 48%, P < .001) or resins (23% vs 9%, P < .001), and achieved LDL-C was lower (3.2 vs 3.5 mmol/L [124 vs 135 mg/dL], P = .003) than normal-risk FH. LDL-C treatment goal was achieved in 25% and 8% of subjects with normal-risk and very-high-risk FH, respectively. Lp(a) levels were available in 599 subjects, and they were divided into 2 groups: ≥90 mg/dL (n = 96) and <90 mg/dL (n = 503). Despite similar lipid levels, body mass index, smoking status, presence of diabetes, and blood pressure, prevalence of coronary heart disease was doubled in the high- compared to low-Lp(a) group (30% vs 14%, P < .001). CONCLUSION: Very few FH subjects achieve their LDL-C treatment goal. New treatment modalities are needed. Independent of LDL-C and other risk factors, high Lp(a) seem to be an important additional risk factor in genetically verified FH.
BACKGROUND: Current treatment goals for familial hypercholesterolemia (FH) recommended by the European Atherosclerosis Society (EAS) are LDL-C ≤2.5 mmol/L (∼100 mg/dL) or ≤1.8 mmol/L (∼70 mg/dL) in very high-risk subjects. OBJECTIVE: The objective of the present study was to investigate characteristics and treatment status in subjects with genetically verified FH followed at specialized lipid clinics in Norway. METHODS: Data from treatment registries of 714 adult (>18 years) subjects with FH. RESULTS: Fifty-seven percent were female. Mean age (SD) at last visit was 44 (16.3) years, and the subjects had been followed at a lipid clinic for 11.1 (7.9) years. Two hundred forty-five (34%) were classified as very-high-risk, and 44% of these had established coronary heart disease. Very-high-risk FH subjects more often received maximal statin dose (54% vs 33%, P < .001), ezetimibe (76% vs 48%, P < .001) or resins (23% vs 9%, P < .001), and achieved LDL-C was lower (3.2 vs 3.5 mmol/L [124 vs 135 mg/dL], P = .003) than normal-risk FH. LDL-C treatment goal was achieved in 25% and 8% of subjects with normal-risk and very-high-risk FH, respectively. Lp(a) levels were available in 599 subjects, and they were divided into 2 groups: ≥90 mg/dL (n = 96) and <90 mg/dL (n = 503). Despite similar lipid levels, body mass index, smoking status, presence of diabetes, and blood pressure, prevalence of coronary heart disease was doubled in the high- compared to low-Lp(a) group (30% vs 14%, P < .001). CONCLUSION: Very few FH subjects achieve their LDL-C treatment goal. New treatment modalities are needed. Independent of LDL-C and other risk factors, high Lp(a) seem to be an important additional risk factor in genetically verified FH.
Authors: Liv J Mundal; Anders Hovland; Jannicke Igland; Marit B Veierød; Kirsten B Holven; Martin Prøven Bogsrud; Grethe S Tell; Trond P Leren; Kjetil Retterstøl Journal: JAMA Cardiol Date: 2019-11-01 Impact factor: 14.676
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