Esther Mm Ooi1, Katrina L Ellis2, P Hugh R Barrett1, Gerald F Watts3, Joseph Hung4, John P Beilby5, Peter L Thompson6, Paul Stobie7, Brendan M McQuillan8. 1. School of Biomedical Sciences, The University of Western Australia, Perth, Australia. 2. School of Biomedical Sciences, The University of Western Australia, Perth, Australia; Medical School, University of Western Australia, Perth, Australia. 3. Medical School, University of Western Australia, Perth, Australia; Lipid Disorders Clinic, Cardiometabolic Service, Department of Cardiology, Royal Perth Hospital, Perth, Australia. 4. Medical School, University of Western Australia, Perth, Australia; Cardiovascular Medicine, Sir Charles Gairdner Hospital, Perth, Australia. 5. PathWest Laboratory Medicine, Sir Charles Gairdner Hospital, Perth, Australia. 6. Medical School, University of Western Australia, Perth, Australia; Cardiovascular Medicine, Sir Charles Gairdner Hospital, Perth, Australia; Heart Research Institute, QEII Medical Center, Perth, Australia. 7. Cardiovascular Medicine, Sir Charles Gairdner Hospital, Perth, Australia. 8. Medical School, University of Western Australia, Perth, Australia; Cardiovascular Medicine, Sir Charles Gairdner Hospital, Perth, Australia. Electronic address: brendan.mcquillan@uwa.edu.au.
Abstract
BACKGROUND AND AIMS: Lipoprotein(a) [Lp(a)] is an emerging genetic risk factor for cardiovascular disease (CVD). We examined whether plasma Lp(a) concentration and apolipoprotein(a) [apo(a)] isoform size are associated with extent and severity of coronary artery disease (CAD), and the presence of carotid artery plaque. METHODS: We included in our study male participants (n = 263) from a cohort with angiographically defined premature CAD (Carotid Ultrasound in Patients with Ischemic Heart Disease). The angiographic extent and severity of CAD were determined by the modified Gensini and Coronary Artery Stenosis≥20% (CAGE) scores. Carotid artery plaque was assessed by bilateral carotid B-mode ultrasound. Apo(a) isoform size was determined by LPA Kringle IV-2 copy number (KIV-2 CN). RESULTS: Lp(a) concentration, but not KIV-2 CN, was positively associated with the Gensini score. The association remained significant following adjustment for conventional CVD risk factors (all p < 0.05). Lp(a) concentration and elevated Lp(a) [≥50 mg/dL] were positively associated with the CAGE≥20 score, independent of conventional CVD risk factors. KIV-2 C N Q1 (lowest KIV-2 CN quartile) was associated with CAGE≥20 score and KIV-2 CN, with the CAGE≥20 score in those without diabetes. In multivariate models that included phenotypic familial hypercholesterolemia or low-density lipoprotein cholesterol, Lp(a) concentration, but not KIV-2 CN, was independently associated with the Gensini and CAGE≥20 scores. No significant associations between Lp(a) concentration and KIV-2 CN with carotid artery plaque were observed. CONCLUSIONS: Lp(a) concentration, but not apo(a) isoform size, is independently associated with angiographic extent and severity of CAD. Neither Lp(a) nor apo(a) isoform size is associated with carotid artery plaque.
BACKGROUND AND AIMS: Lipoprotein(a) [Lp(a)] is an emerging genetic risk factor for cardiovascular disease (CVD). We examined whether plasma Lp(a) concentration and apolipoprotein(a) [apo(a)] isoform size are associated with extent and severity of coronary artery disease (CAD), and the presence of carotid artery plaque. METHODS: We included in our study male participants (n = 263) from a cohort with angiographically defined premature CAD (Carotid Ultrasound in Patients with Ischemic Heart Disease). The angiographic extent and severity of CAD were determined by the modified Gensini and Coronary Artery Stenosis≥20% (CAGE) scores. Carotid artery plaque was assessed by bilateral carotid B-mode ultrasound. Apo(a) isoform size was determined by LPA Kringle IV-2 copy number (KIV-2 CN). RESULTS:Lp(a) concentration, but not KIV-2 CN, was positively associated with the Gensini score. The association remained significant following adjustment for conventional CVD risk factors (all p < 0.05). Lp(a) concentration and elevated Lp(a) [≥50 mg/dL] were positively associated with the CAGE≥20 score, independent of conventional CVD risk factors. KIV-2 C N Q1 (lowest KIV-2 CN quartile) was associated with CAGE≥20 score and KIV-2 CN, with the CAGE≥20 score in those without diabetes. In multivariate models that included phenotypic familial hypercholesterolemia or low-density lipoprotein cholesterol, Lp(a) concentration, but not KIV-2 CN, was independently associated with the Gensini and CAGE≥20 scores. No significant associations between Lp(a) concentration and KIV-2 CN with carotid artery plaque were observed. CONCLUSIONS:Lp(a) concentration, but not apo(a) isoform size, is independently associated with angiographic extent and severity of CAD. Neither Lp(a) nor apo(a) isoform size is associated with carotid artery plaque.
Authors: Olga I Afanasieva; Marat V Ezhov; Narek A Tmoyan; Oksana A Razova; Marina I Afanasieva; Yuri G Matchin; Sergei N Pokrovsky Journal: Front Cardiovasc Med Date: 2022-03-11
Authors: Jason G van Genderen; Malon Van den Hof; Claudia G de Boer; Hans P G Jansen; Sander J H van Deventer; Sotirios Tsimikas; Joseph L Witztum; John J P Kastelein; Dasja Pajkrt Journal: Viruses Date: 2021-10-14 Impact factor: 5.048