Blerim Mujaj1, Daniel Bos2, Mariana Selwaness3, Maarten J G Leening4, Maryam Kavousi1, Jolanda J Wentzel5, Aad van der Lugt3, Albert Hofman6, Bruno H Stricker7, Meike W Vernooij8, Oscar H Franco1. 1. Department of Epidemiology, Erasmus MC, Rotterdam, The Netherlands. 2. Department of Epidemiology, Erasmus MC, Rotterdam, The Netherlands; Department of Radiology and Nuclear Medicine, Erasmus MC, Rotterdam, The Netherlands; Department of Clinical Epidemiology, Harvard TH Chan School of Public Health, Boston, USA. 3. Department of Radiology and Nuclear Medicine, Erasmus MC, Rotterdam, The Netherlands. 4. Department of Epidemiology, Erasmus MC, Rotterdam, The Netherlands; Department of Cardiology, Erasmus MC, Rotterdam, The Netherlands; Department of Clinical Epidemiology, Harvard TH Chan School of Public Health, Boston, USA. 5. Department of Biomechanics, Erasmus MC, Rotterdam, The Netherlands. 6. Department of Clinical Epidemiology, Harvard TH Chan School of Public Health, Boston, USA. 7. Department of Epidemiology, Erasmus MC, Rotterdam, The Netherlands. Electronic address: b.stricker@erasmusmc.nl. 8. Department of Epidemiology, Erasmus MC, Rotterdam, The Netherlands; Department of Radiology and Nuclear Medicine, Erasmus MC, Rotterdam, The Netherlands.
Abstract
BACKGROUND: Statins represent a key treatment for cardiovascular disease. Nevertheless, the direct effects of statin treatment on the composition of atherosclerotic plaques remain elusive. OBJECTIVES: We aimed to investigate the association of statin treatment with the presence of different plaque components located in the carotid arteries within a population-based setting. METHODS: From the population-based Rotterdam Study, 1740 participants with carotid atherosclerosis (mean age 72.9 years, 46% women) underwent MRI of the carotid arteries to determine the presence of calcification, lipid core, and intraplaque hemorrhage. Information for the duration and dosage of statin use was obtained from pharmacy records for all participants. We used logistic regression models to study the association of statin use with the presence of plaque components. RESULTS: Statin treatment was associated with a higher presence of calcification (OR: 1.73 [95% CI: 1.22-2.44]). Longer duration of use strengthened this association (OR: 1.82 [95% CI: 1.00-3.33] for 10 to 48 months, and OR 1.74 [95% CI: 1.09-2.77] for >48 months, compared to OR: 1.65 [95% CI: 0.94-2.89] for ≤10 months). Current statin treatment was also associated with a lower presence of lipid core (OR: 0.66 [95% CI: 0.42-1.04]), but only when using statins for 10 months or less. Any dosage of statins was associated with a higher presence of calcification, whilst only high dosages (DDD > 1.33) were associated with a lower presence of lipid core. CONCLUSIONS: Active, high-dosage statin use seems to beneficially influence the composition of carotid atherosclerosis by shifting the composition from vulnerable plaque with a lipid core to more stable calcified plaque.
BACKGROUND: Statins represent a key treatment for cardiovascular disease. Nevertheless, the direct effects of statin treatment on the composition of atherosclerotic plaques remain elusive. OBJECTIVES: We aimed to investigate the association of statin treatment with the presence of different plaque components located in the carotid arteries within a population-based setting. METHODS: From the population-based Rotterdam Study, 1740 participants with carotid atherosclerosis (mean age 72.9 years, 46% women) underwent MRI of the carotid arteries to determine the presence of calcification, lipid core, and intraplaque hemorrhage. Information for the duration and dosage of statin use was obtained from pharmacy records for all participants. We used logistic regression models to study the association of statin use with the presence of plaque components. RESULTS: Statin treatment was associated with a higher presence of calcification (OR: 1.73 [95% CI: 1.22-2.44]). Longer duration of use strengthened this association (OR: 1.82 [95% CI: 1.00-3.33] for 10 to 48 months, and OR 1.74 [95% CI: 1.09-2.77] for >48 months, compared to OR: 1.65 [95% CI: 0.94-2.89] for ≤10 months). Current statin treatment was also associated with a lower presence of lipid core (OR: 0.66 [95% CI: 0.42-1.04]), but only when using statins for 10 months or less. Any dosage of statins was associated with a higher presence of calcification, whilst only high dosages (DDD > 1.33) were associated with a lower presence of lipid core. CONCLUSIONS: Active, high-dosage statin use seems to beneficially influence the composition of carotid atherosclerosis by shifting the composition from vulnerable plaque with a lipid core to more stable calcified plaque.
Authors: M Arfan Ikram; Guy Brusselle; Mohsen Ghanbari; André Goedegebure; M Kamran Ikram; Maryam Kavousi; Brenda C T Kieboom; Caroline C W Klaver; Robert J de Knegt; Annemarie I Luik; Tamar E C Nijsten; Robin P Peeters; Frank J A van Rooij; Bruno H Stricker; André G Uitterlinden; Meike W Vernooij; Trudy Voortman Journal: Eur J Epidemiol Date: 2020-05-04 Impact factor: 8.082
Authors: L Saba; W Brinjikji; J D Spence; M Wintermark; M Castillo; G J de Borst; Q Yang; C Yuan; A Buckler; M Edjlali; T Saam; D Saloner; B K Lal; D Capodanno; J Sun; N Balu; R Naylor; A V D Lugt; B A Wasserman; M E Kooi; J Wardlaw; J Gillard; G Lanzino; U Hedin; D Mikulis; A Gupta; J K DeMarco; C Hess; J V Goethem; T Hatsukami; P Rothwell; M M Brown; A R Moody Journal: AJNR Am J Neuroradiol Date: 2021-07-29 Impact factor: 4.966
Authors: Blerim Mujaj; Daniel Bos; Maryam Kavousi; Aad van der Lugt; Jan A Staessen; Oscar H Franco; Meike W Vernooij Journal: Eur J Endocrinol Date: 2020-03 Impact factor: 6.664