Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Coronary Artery Disease: HELP
Articles by Robert Dufour
Based on 5 articles published since 2010
(Why 5 articles?)
||||

Between 2010 and 2020, Robert Dufour wrote the following 5 articles about Coronary Artery Disease.
 
+ Citations + Abstracts
1 Guideline Screening for the presence of coronary artery disease. 2013

Anonymous5130770 / Poirier, Paul / Dufour, Robert / Carpentier, André / Larose, Éric. · ·Can J Diabetes · Pubmed #24070928.

ABSTRACT: -- No abstract --

2 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.

3 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.

4 Article PHACTR1 genotype predicts coronary artery disease in patients with familial hypercholesterolemia. 2018

Paquette, Martine / Dufour, Robert / Baass, Alexis. ·Nutrition, Metabolism and Atherosclerosis Clinic, Institut de recherches cliniques de Montréal, Québec, Canada. · Nutrition, Metabolism and Atherosclerosis Clinic, Institut de recherches cliniques de Montréal, Québec, Canada; Department of Nutrition, Université de Montréal, Québec, Canada. · Nutrition, Metabolism and Atherosclerosis Clinic, Institut de recherches cliniques de Montréal, Québec, Canada; Division of Experimental Medicine, Department of Medicine, McGill University, Québec, Canada; Division of Medical Biochemistry, Department of Medicine, McGill University, Québec, Canada. Electronic address: alexis.baass@ircm.qc.ca. ·J Clin Lipidol · Pubmed #29784573.

ABSTRACT: BACKGROUND: Familial hypercholesterolemia (FH) is the most frequent autosomal codominant disease worldwide and is characterized by elevated low-density lipoprotein cholesterol and premature coronary artery disease (CAD). Polymorphisms in phosphatase and actin regulator 1 (PHACTR1) have been shown to be associated with cardiovascular risk in large genome-wide association studies studies. OBJECTIVE: The aim of the present study is to evaluate the association between the rs12526453 polymorphism in the PHACTR1 gene and the prevalence of CAD in FH patients. METHODS: A cohort of 668 adult genetically confirmed heterozygous FH subjects were included in the present study. Logistic regression models were used to evaluate the strength of the association between rs12526453 genotype and CAD prevalence. RESULTS: Noncarriers (CC) of the rs12526453 represented 41% of the cohort, whereas heterozygous (CG) and homozygous (GG) carriers represented 44% and 15%, respectively. The prevalence of CAD was significantly higher in non-carriers of the rs12526453 polymorphism compared to heterozygous and homozygous carriers (38.0%, 25.8%, 24.5%, respectively, P = .001). When a dominant logistic regression model was studied, the association between this single-nucleotide polymorphism and CAD prevalence was significant even after correction for all classical cardiovascular risk factors (odds ratio 0.48, 95% confidence intervals 0.31-0.74, P = .001). CONCLUSION: In the present study, we have shown that the rs12526453 single-nucleotide polymorphism of the PHACTR1 gene is significantly associated with a 50% reduction in the odds of CAD events in FH subjects. Because the protective G allele is frequent in the Caucasian population (allelic frequency of 0.26), screening for this polymorphism in Caucasian FH subjects could further help to stratify risk of CAD in this population.

5 Article Scavenger Receptor LOX1 Genotype Predicts Coronary Artery Disease in Patients With Familial Hypercholesterolemia. 2017

Paquette, Martine / Dufour, Robert / Baass, Alexis. ·Nutrition, Metabolism, and Atherosclerosis Clinic, Institut de recherches cliniques de Montréal, Montréal, Québec, Canada. · Nutrition, Metabolism, and Atherosclerosis Clinic, Institut de recherches cliniques de Montréal, Montréal, Québec, Canada; Department of Nutrition, Université de Montréal, Montréal, Québec, Canada. · Nutrition, Metabolism, and Atherosclerosis Clinic, Institut de recherches cliniques de Montréal, Montréal, Québec, Canada; Division of Experimental Medicine, Department of Medicine, McGill University, Montréal, Québec, Canada; Division of Medical Biochemistry, Department of Medicine, McGill University, Montréal, Québec, Canada. Electronic address: alexis.baass@ircm.qc.ca. ·Can J Cardiol · Pubmed #28941610.

ABSTRACT: BACKGROUND: Familial hypercholesterolemia (FH) is a monogenic disease associated with elevated low-density lipoprotein (LDL) cholesterol and oxidized LDL (oxLDL) leading to premature cardiovascular disease. Lectin-like oxLDL receptor-1 (LOX1) is one of the major contributors of oxLDL uptake and degradation in macrophages, which leads to foam cell formation and the development of atherosclerosis. This study investigated the effect of the rs11053646 genotype of the oxidized low-density lipoprotein receptor 1 (OLR1) gene on coronary artery disease (CAD) risk in a cohort of FH patients. METHODS: A total of 665 genetically confirmed heterozygous adult patients with FH were included in the analysis. We evaluated the association between the rs11053646 genotype (GG vs GC) and CAD. RESULTS: The GC genotype (K167N carriers) represented 12.9% of the study cohort (n = 86), whereas 87.1% of the participants were noncarriers (GG genotype) (n = 579). A significantly higher proportion of GC carriers experienced a CAD event (40.7%) than did GG carriers (29.0%; P = 0.03). The presence of a C allele remained significantly associated with an increased CAD risk, even when the regression model was corrected for all traditional CAD risk factors (odds ratio, 3.05; 95% confidence interval, 1.63-5.70; P = 0.0005). The negative impact of carrying the C allele on CAD risk was similar in both sexes but was significantly more important in smokers as well as in younger patients with FH. CONCLUSIONS: Carrying the C allele of the rs11053646 variant of the OLR1 gene was associated with an increased risk of CAD in heterozygous adult patients with FH, and this risk could be even greater in smokers as well as in younger patients.