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Coronary Artery Disease: HELP
Articles by Claude Gagne
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Claude Gagné wrote the following 2 articles about Coronary Artery Disease.
 
+ Citations + Abstracts
1 Clinical Trial Apolipoprotein B synthesis inhibition with mipomersen in heterozygous familial hypercholesterolemia: results of a randomized, double-blind, placebo-controlled trial to assess efficacy and safety as add-on therapy in patients with coronary artery disease. 2012

Stein, Evan A / Dufour, Robert / Gagne, Claude / Gaudet, Daniel / East, Cara / Donovan, Joanne M / Chin, Wai / Tribble, Diane L / McGowan, Mary. ·Metabolic and Atherosclerosis Research Center, 5355 Medpace Way, Cincinnati, OH 45227, USA. esteinmrl@aol.com ·Circulation · Pubmed #23060426.

ABSTRACT: BACKGROUND: Heterozygous familial hypercholesterolemia (HeFH) is a common genetic disorder leading to premature coronary artery disease. Despite statins and additional lipid-lowering therapies, many HeFH patients fail to achieve low-density lipoprotein cholesterol (LDL-C) goals. We evaluated mipomersen, an apolipoprotein B synthesis inhibitor, to further lower LDL-C in HeFH patients with coronary artery disease. METHODS AND RESULTS: This double-blind, placebo-controlled, phase 3 trial randomized patients with HeFH and coronary artery disease on maximally tolerated statin and LDL-C ≥2.6 mmol/L (≥100 mg/dL) to weekly subcutaneous mipomersen 200 mg or placebo (2:1) for 26 weeks. The primary end point was percent change in LDL-C from baseline at week 28. Safety assessments included adverse events, laboratory tests, and magnetic resonance imaging assessment of hepatic fat. Of 124 randomized patients (41 placebo, 83 mipomersen), 114 (41 placebo, 73 mipomersen) completed treatment. Mean (95% confidence interval) LDL-C decreased significantly with mipomersen (-28.0% [-34.0% to -22.1%] compared with 5.2% [-0.5% to 10.9%] increase with placebo; P<0.001). Mipomersen significantly reduced apolipoprotein B (-26.3%), total cholesterol (-19.4%), and lipoprotein(a) (-21.1%) compared with placebo (all P<0.001). No significant change occurred in high-density lipoprotein cholesterol. Adverse events included injection site reactions and influenza-like symptoms. Five mipomersen patients (6%) had 2 consecutive alanine aminotransferase values ≥3 times the upper limit of normal at least 7 days apart; none were associated with significant bilirubin increases. Hepatic fat content increased a median of 4.9% with mipomersen versus 0.4% with placebo (P<0.001). CONCLUSIONS: Mipomersen is an effective therapy to further reduce apolipoprotein B-containing lipoproteins, including LDL and lipoprotein(a), in HeFH patients with coronary artery disease on statins and other lipid-lowering therapy. The significance of hepatic fat and transaminase increases remains uncertain at this time. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00706849.

2 Article Simplified Canadian Definition for Familial Hypercholesterolemia. 2018

Ruel, Isabelle / Brisson, Diane / Aljenedil, Sumayah / Awan, Zuhier / Baass, Alexis / Bélanger, Alexandre / Bergeron, Jean / Bewick, David / Brophy, James M / Brunham, Liam R / Couture, Patrick / Dufour, Robert / Francis, Gordon A / Frohlich, Jiri / Gagné, Claude / Gaudet, Daniel / Grégoire, Jean C / Gupta, Milan / Hegele, Robert A / Mancini, G B John / McCrindle, Brian W / Pang, Jing / Raggi, Paolo / Tu, Jack V / Watts, Gerald F / Genest, Jacques. ·Research Institute of the McGill University Health Centre, Royal Victoria Hospital, Montreal, Quebec, Canada. Electronic address: isabelle.ruel@mail.mcgill.ca. · Lipidology Unit, Community Genomic Medicine Centre and ECOGENE-21, Department of Medicine, Université de Montréal, Saguenay, Quebec, Canada. · Research Institute of the McGill University Health Centre, Royal Victoria Hospital, Montreal, Quebec, Canada. · Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia. · Division of Experimental Medicine and Medical Biochemistry, Department of Medicine, McGill University, Quebec, Canada; Nutrition, Metabolism and Atherosclerosis Clinic, Institut de recherches cliniques de Montréal, Quebec, Canada. · Lipid Research Centre, CHU de Québec-Université Laval, Québec City, Quebec, Canada. · Division of Cardiology, Department of Medicine, Dalhousie University, St John, New Brunswick, Canada. · Research Institute of the McGill University Health Centre, Royal Victoria Hospital, Montreal, Quebec, Canada; Department of Medicine, McGill University, Royal Victoria Hospital, Montreal, Quebec, Canada. · Healthy Heart Program Prevention Clinic, St Paul's Hospital, Vancouver, British Columbia, Canada, Department of Medicine, University of British Columbia, Vancouver, British Columbia, and Centre for Heart Lung Innovation, Providence Health Care Research Institute, University of British Columbia, Vancouver, British Columbia, Canada. · Nutrition, Metabolism and Atherosclerosis Clinic, Institut de recherches cliniques de Montréal, Quebec, Canada, Department of Nutrition, Université de Montréal, Quebec, Canada. · Healthy Heart Program Prevention Clinic, St Paul's Hospital, Vancouver, British Columbia, Canada, Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada. · Montreal Heart Institute, Montreal, Quebec, Canada. · McMaster University, Hamilton, Ontario, Canada, Canadian Collaborative Research Network, Brampton, Ontario, Canada. · Departments of Medicine and Biochemistry, Schulich School of Medicine and Robarts Research Institute, Western University, London, Ontario, Canada. · Department of Medicine, Division of Cardiology, University of British Columbia, Vancouver, British Columbia, Canada. · Division of Cardiology, The Labatt Family Heart Centre, The Hospital for Sick Children, University of Toronto, Ontario, Canada. · School of Medicine, Faculty of Health and Medical Sciences, University of Western Australia, Perth, Australia. · Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada. · Faculty of Medicine, University of Toronto, Institute for Clinical Evaluative Sciences, Schulich Heart Centre, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada. · School of Medicine, Faculty of Health and Medical Sciences, University of Western Australia, Perth, Australia; Lipid Disorders Clinic, Department of Cardiology, Royal Perth Hospital, Perth, Australia. ·Can J Cardiol · Pubmed #30093300.

ABSTRACT: Familial hypercholesterolemia (FH) is an autosomal codominant lipoprotein disorder characterized by elevated low-density lipoprotein cholesterol (LDL-C) and high risk of premature atherosclerotic cardiovascular disease. Definitions for FH rely on complex algorithms that are on the basis of levels of total or LDL-C, clinical features, family history, and DNA analysis that are often difficult to obtain. We propose a novel simplified definition for FH. Definite FH includes: (1) elevated LDL-C (≥ 8.50 mmol/L); or (2) LDL-C ≥ 5.0 mmol/L (for age 40 years or older; ≥ 4.0 mmol/L if age younger than 18 years; and ≥ 4.5 mmol/L if age is between 18 and 39 years) when associated with at least 1 of: (1) tendon xanthomas; or (2) causal DNA mutation in the LDLR, APOB, or PCSK9 genes in the proband or first-degree relative. Probable FH is defined as subjects with an elevated LDL-C (≥ 5.0 mmol/L) and the presence of premature atherosclerotic cardiovascular disease in the patient or a first-degree relative or an elevated LDL-C in a first-degree relative. LDL-C cut points were determined from a large database comprising > 3.3 million subjects. To compare the proposed definition with currently used algorithms (ie, the Simon Broome Register and Dutch Lipid Clinic Network), we performed concordance analyses in 5987 individuals from Canada. The new FH definition showed very good agreement compared with the Simon Broome Register and Dutch Lipid Clinic Network criteria (κ = 0.969 and 0.966, respectively). In conclusion, the proposed FH definition has diagnostic performance comparable to existing criteria, but adapted to the Canadian population, and will facilitate the diagnosis of FH patients.