scholarly journals Cataract Surgery in Elderly Subjects with Heterozygous Familial Hypercholesterolemia in Prolonged Treatment with Statins

2021 ◽  
Vol 10 (16) ◽  
pp. 3494
Author(s):  
Victoria Marco-Benedí ◽  
Martín Laclaustra ◽  
Rosa M. Sánchez-Hernández ◽  
Emilio Ortega-Martínez de Victoria ◽  
Juan Pedro-Botet ◽  
...  
Keyword(s):  
Cataract Surgery ◽  
Familial Hypercholesterolemia ◽  
Linear Models ◽  
Pathogenic Mutation ◽  
Statin Treatment ◽  
Lipid Lowering ◽  
Prolonged Treatment ◽  
Elderly Subjects ◽  
Heterozygous Familial Hypercholesterolemia ◽  
Surgery In Elderly

Background: Cataracts are the main cause of blindness and represent one fifth of visual problems worldwide. It is still unknown whether prolonged statin treatment favors the development of cataracts. We aimed to ascertain the prevalence of cataract surgery in elderly subjects with genetically diagnosed heterozygous familial hypercholesterolemia (HeFH) receiving statin treatment for ≥5 years, and compare this with controls. Methods: This is an observational, multicenter, case–control study from five lipid clinics in Spain. We collected data with the following inclusion criteria: age ≥65 years, LDL cholesterol levels ≥220 mg/dL without lipid-lowering drugs, a pathogenic mutation in a candidate gene for HeFH (LDLR, APOB, or PCSK9) and statin treatment for ≥5 years. Controls were selected from relatives of HeFH patients without hypercholesterolemia. Linear and logistic regressions based on generalized linear models and generalized estimating equations (GEE) were used. Cataract surgery was used as a proxy for cataract development. Results: We analyzed 205 subjects, 112 HeFH, and 93 controls, with a mean age of 71.8 (6.5) and 70.0 (7.3) years, respectively. HeFH subjects presented no difference in clinical characteristics, including smoking, hypertension, and type 2 diabetes mellitus, compared with controls. The mean duration of lipid-lowering treatment in HeFH was 22.5 (8.7) years. Cataract surgery prevalence was not significantly different between cases and controls. The presence of cataracts was associated neither with LDLc nor with the length of the statin therapy. Conclusion: In the present study, HeFH was not a risk factor for cataract surgery and prolonged statin treatment did not favor it either. These findings suggest that statin treatment is not related with cataracts.

scholarly journals Aortic Valvular Disease in Elderly Subjects with Heterozygous Familial Hypercholesterolemia: Impact of Lipid-Lowering Therapy

2019 ◽  
Vol 8 (12) ◽  
pp. 2209 ◽  
Author(s):  
Victoria Marco-Benedí ◽  
Martin Laclaustra ◽  
Juan M. Casado-Dominguez ◽  
Rosa Villa-Pobo ◽  
Rocío Mateo-Gallego ◽  
...  
Keyword(s):  
Risk Factors ◽  
Aortic Valve ◽  
Familial Hypercholesterolemia ◽  
Genetic Diagnosis ◽  
Statin Treatment ◽  
Valvular Disease ◽  
Lipid Lowering ◽  
Elderly Subjects ◽  
Lipid Lowering Therapy ◽  
Aortic Sclerosis

Hypercholesterolemia and statins are risk factors for aortic stenosis (AS) and vascular calcification, respectively. Whether heterozygous subjects with familial hypercholesterolemia (HeFH) treated with statins are at risk of AS is unknown. We study the prevalence of AS, aortic valve calcification (AoVC), and aortic sclerosis (ASc) in elderly subjects with HeFH in a prolonged statin treatment. Case-control study, cases were adults ≥65 years of age with a genetic diagnosis of HeFH, LDLc >220 mg/dl, and statin treatment ≥5 years. Controls were relatives of HeFH patients, with LDLc <190 mg/dl. Participants underwent a cardiac ultrasound for aortic valve analysis. We studied 205 subjects, 112 HeFH and 93 controls, with mean age 71.8(6.5) years and 70.0(7.3) years, respectively. HeHF, with respect to controls, presented greater gradients of aortic transvalvular pressure, 7.4(7.3) mmHg versus 5.0(2.8) mmHg, and maximum aortic velocity, 1.7(0.7) m/s versus 1.5(0.4) m/s, and lower aortic valve opening area, 2.0(0.7) cm2 versus 2.4(0.6) cm2 (all p < 0.05). AoVC and ASc were also more prevalent in HeFH (p < 0.05 between groups). Moderate/severe AS prevalence was higher among HeFH: 7.1% versus 1.1% (age- and sex-adjusted odds ratio (OR) 8.33, p = 0.03). Independent risk factors for aortic valve disease in HeFH were age and LDLc before treatment. The number of years under statin treatment was not associated with any aortic valve measurement. Subjects ≥65 years with HeFH in prolonged statin treatment show more aortic valvular disease and higher frequency of AS than controls. Life-long elevated LDLc exposure, rather than time of exposure to statins, explains this higher risk.

Risk of cataract surgery in subjects with heterozygous familial hypercholesterolemia in prolonged treatment with statins

2020 ◽  
Vol 315 ◽  
pp. e81
Author(s):  
V. Marco Benedí ◽  
M. Laclaustra ◽  
J.M. Casado-Dominguez ◽  
R. Villa Pobo ◽  
R. Mateo-Gallego ◽  
...  
Keyword(s):  
Cataract Surgery ◽  
Familial Hypercholesterolemia ◽  
Prolonged Treatment ◽  
Heterozygous Familial Hypercholesterolemia

scholarly journals 2214Prevalence and severity of coronary disease in patients with familial hypercholesterolemia hospitalized for an acute myocardial infarction: data from the RICO survey

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Farnier ◽  
B Mouhat ◽  
T Pommier ◽  
H Yao ◽  
M Maza ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Familial Hypercholesterolemia ◽  
Statin Treatment ◽  
University Hospital ◽  
Lipid Lowering ◽  
Syntax Score ◽  
World Population ◽  
Lipid Lowering Therapy ◽  
History Of ◽  
Acute Mi

Abstract Aim Individuals with heterozygous familial hypercholesterolemia (FH) are at high risk of early myocardial infarction (MI). However, coronary artery disease (CAD) burden of FH remains not well described. From a large database of a regional registry of acute MI, we aimed to address prevalence of FH and severity of CAD. Methods Consecutive patients hospitalized with MI in a multicentre database from 2001–2017 were considered. An algorithm, adapted from Dutch Lipid Clinic Network criteria, was built upon 4 variables (LDL-cholesterol (LDL-C) and lipid lowering agents, premature and family history of CAD) to identify FH probabilities. Results Among the 11624 patients included in the survey, 249 (2.1%) had probable/definite FH (score ≥6), and 2405 (20.7%) had possible FH (score 3–5). When compared with patients without FH (score 0–2), FH patients (score ≥6) were 20y younger (51 (46–57) vs 71 (61–80) y, p<0.001), with a lower rate of hypertension (47 vs 59%, p<0.001), diabetes (17 vs 25%, p<0.001) and prior stroke (4 vs 8%, p=0.016), but a higher prevalence of smokers (56 vs 23%, p<0.001), personal (20 vs 15%, p=0.02) or familial history of CAD (78 vs 18%, p<0.001). Chronic statin treatment was only used in 48% of FH patients and ezetimibe in 8%. After adjustment for age, sex and diabetes, FH patients were characterized by increased extent of CAD (syntax score 11 (4–19) vs 7 (1–13), p<0.001) and multivessel disease (55 vs 40%, p<0.001). Conclusion In this large real world population of acute MI, a high prevalence of FH was found. FH patients were characterized by their young age associated with the severity of CAD burden and limited use of preventive lipid lowering therapy. Acknowledgement/Funding University Hospital Center Dijon Bourgogne, Agence Régionale de Santé Bourgogne Franche Comté, France

scholarly journals Impact of Statin Treatment on the Clinical Fate of Heterozygous Familial Hypercholesterolemia

2010 ◽  
Vol 17 (7) ◽  
pp. 667-674 ◽  
Author(s):  
Mariko Harada-Shiba ◽  
Takako Sugisawa ◽  
Hisashi Makino ◽  
Mitsuru Abe ◽  
Motoo Tsushima ◽  
...  
Keyword(s):  
Familial Hypercholesterolemia ◽  
Statin Treatment ◽  
Heterozygous Familial Hypercholesterolemia

scholarly journals Lp (a) >50 mg/dl predicts atherosclerotic cardiovascular events in patients with heterozygous familial hypercholesterolemia who achieved LDL-C <2.6 mmol/l

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Funabashi ◽  
Y Kataoka ◽  
M Hori ◽  
M Ogura ◽  
K Matsuki ◽  
...  
Keyword(s):  
Familial Hypercholesterolemia ◽  
Coronary Revascularization ◽  
Statistical Significance ◽  
Lipid Lowering ◽  
Current Guideline ◽  
Potential Therapeutic Target ◽  
Heterozygous Familial Hypercholesterolemia ◽  
Significant Difference ◽  
History Of ◽  
Atherosclerotic Cardiovascular Diseases

Abstract Introduction Lipoprotein (a) [Lp (a)] is a plasma lipoprotein which exhibits atherogenic properties. Lp(a) ≥50 mg/dl has been recently shown to associate with a risk of atherosclerotic cardiovascular diseases (ASCVD) in patients with heterozygous familial hypercholesterolemia (HeFH). While current guideline recommends lowering LDL-C as a first-line therapeutic approach in HeFH subjects, it remains to be fully determined whether an elevated level of Lp(a) confers additional ASCVD risks in HeFH patients who achieved a lower LDL-C level. Purpose To investigate cardiovascular outcomes in HeFH subjects with a lower LDL-C but an elevated Lp(a) levels. Methods 182 HeFH patients with on-treatment LDL-C &lt;2.6 mmol/l under lipid-lowering therapies were analyzed. Clinical characteristics and MACE (= a composite of all-cause death, ACS, stroke, PAD and coronary revascularization) were compared in HeFH subjects with Lp(a) ≥ vs. &lt;50 mg/dl. Results The averaged LDL-C and Lp (a) levels were 1.9 mmol/l and 26.8 mg/dl, respectively. 19.2% of study subjects exhibited Lp(a)≥50 mg/dl. HeFH patients with Lp(a) ≥50 mg/dl were more likely to be older and have a history of hypertension, but these comparisons did not meet statistical significance. There was no significant difference in on-treatment LDL-C, HDL-C and Triglyceride level (Table). However, during the observational period (median=4.7 years), there was a 2.7-fold (95% CI, 1.41–5.02; p=0.004) greater likelihood of experiencing MACE in subjects with Lp(a) ≥50 mg/dl (picture). Even after adjusting clinical demographics, Lp(a) ≥50 mg/dl remained an independent predictor for the occurrence of MACE (hazard ratio=2.53, 95% CI: 1.29–4.82, p&lt;0.001). Conclusions Despite achieving on-treatment LDL-C &lt;2.6 mmol/l, an elevated risk of MACE was observed in HeFH patients with Lp(a) ≥50 mg/dl. Our findings suggest an increased level of Lp(a) as a risk stratification marker and a potential therapeutic target in patients with HeFH. Clinical outcome Funding Acknowledgement Type of funding source: None

Lipoprotein Apheresis and Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors in Patients With Heterozygous Familial Hypercholesterolemia: A One Center Study

2020 ◽  
Vol 26 (1) ◽  
pp. 51-58
Author(s):  
Vana Kolovou ◽  
Niki Katsiki ◽  
Stamatis Makrygiannis ◽  
Sophie Mavrogieni ◽  
Nikoletta Karampetsou ◽  
...  
Keyword(s):  
Familial Hypercholesterolemia ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Lipid Lowering ◽  
Proprotein Convertase ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein Apheresis ◽  
Heterozygous Familial Hypercholesterolemia ◽  
Previously Treated

Aim: We evaluated the lipid-lowering (LL) effect of proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) in patients with heterozygous familial hypercholesterolemia (HeFH) treated with LL-drugs and lipoprotein apheresis (LA). Patients and Methods: The PCSK9i treatment (evolocumab 420 mg/4 weeks, alirocumab 150 mg/2 weeks, or alirocumab 75 mg/2 weeks: 9, 6, and 2 patients, respectively) was initiated in patients with HeFH (n = 17; aged 35-69 years, 10 men, previously treated with statins + ezetimibe ± colesevelam and LA sessions for 2-12 years). A lipid profile was obtained before and immediately after the LA session and before, 1 and 2 months after switching to PCSK9i treatment. The duration of PCSK9i therapy ranged from 3 to 18 months. Results: Median total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) levels before LA were 268, 198, 46, and 126 mg/dL, respectively, and decreased (at the end of the LA session) to 117, 50, 40, and 51 mg/dL, respectively ( P < .001 for TC and P = .001 for all other comparisons). The median time-averaged LDL-C levels following LA were 155 (121, 176; median [25th, 75th percentile]) mg/dL. Median TC, LDL-C, and TG levels before PCSK9i therapy were 269, 190, and 127 mg/dL and decreased to 152, 100, and 95 mg/dL, respectively ( P = .002, P < .002, and P < .03, respectively). Steady LDL-C levels with PCSK9i treatment were significantly lower compared with time-averaged LDL-C levels following LA (median value: 100 vs 155 mg/dL; P = .008). With PCSK9i, from 13 patients with CHD, 6 (46.1%) patients achieved LDL-C <70 mg/dL, and 2 patients (15.4%) achieved LDL-C <100 mg/dL. Lipoprotein apheresis was discontinued in all patients except for 2 who continued once monthly. Conclusions: PCSK9i can reduce LDL-C more consistently over time compared with a transient decrease following LA in HeFH patients. PCSK9i therapy may reduce the frequency of LA. Larger trials are required to establish the clinical implications of PCSK9i in patients previously on LA.

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