Laura Pletsch-Borba1, Mariana Selwaness2, Aad van der Lugt3, Albert Hofman4, Oscar H Franco5, Meike W Vernooij6. 1. Department of Epidemiology, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands; Department of Radiology, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands; The Netherlands Institute of Health Sciences, Erasmus Medical Center University Medical Center, Rotterdam, the Netherlands. 2. Department of Epidemiology, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands; Department of Radiology, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands. 3. Department of Radiology, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands. 4. Department of Epidemiology, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands; Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, Massachusetts. 5. Department of Epidemiology, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands. 6. Department of Epidemiology, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands; Department of Radiology, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands. Electronic address: m.vernooij@erasmusmc.nl.
Abstract
OBJECTIVES: The goal of this study was to determine how carotid plaque components (e.g., intraplaque hemorrhage [IPH], calcification, lipid core) change over time and which cardiovascular risk factors are associated with the development of each component. BACKGROUND: Carotid atherosclerotic plaque components are important markers of plaque vulnerability. How these components change and which factors lead to the development and changes in the components remain unclear. METHODS: A total of 198 participants (mean age 67.5 ± 10.6 years) from the population-based Rotterdam Study, all with carotid wall thickening on ultrasound, underwent 2 magnetic resonance imaging scans for carotid plaque characterization (mean interscan interval 4.1 ± 0.2 years). Presence of IPH, calcification, and lipid-rich necrotic core was assessed on both sides on the baseline and follow-up scans. The association between cardiovascular risk factors and incident carotid plaque components was assessed. RESULTS: In the 396 arteries, all plaque components significantly changed over time. Incidence of IPH, calcification, and lipid core was, respectively, 18.5%, 59.2%, and 39.6%. The factor most strongly associated with the incidence of IPH was use of antihypertensive drugs (multivariate adjusted odds ratio [OR]: 3.87; 95% confidence interval [CI]: 1.90 to 7.90) and severe hypertension (multivariate adjusted OR: 4.70; 95% CI: 1.50 to 14.80). The incidence of calcification was associated with hypertension (OR: 2.20; 95% CI: 1.07 to 4.40). Higher cholesterol levels were associated with incidence of lipid cores (multivariate adjusted OR per unit increase in cholesterol: 1.40; 95% CI: 1.10 to 1.70). CONCLUSIONS: In these community-dwelling subjects, characteristics of plaque composition changed dramatically within a few years, and cardiovascular risk factors played a major role in these changes. Hypertension and its treatment and serum cholesterol levels were the main risk factors for the development of atherosclerotic plaque components over time.
OBJECTIVES: The goal of this study was to determine how carotid plaque components (e.g., intraplaque hemorrhage [IPH], calcification, lipid core) change over time and which cardiovascular risk factors are associated with the development of each component. BACKGROUND: Carotid atherosclerotic plaque components are important markers of plaque vulnerability. How these components change and which factors lead to the development and changes in the components remain unclear. METHODS: A total of 198 participants (mean age 67.5 ± 10.6 years) from the population-based Rotterdam Study, all with carotid wall thickening on ultrasound, underwent 2 magnetic resonance imaging scans for carotid plaque characterization (mean interscan interval 4.1 ± 0.2 years). Presence of IPH, calcification, and lipid-rich necrotic core was assessed on both sides on the baseline and follow-up scans. The association between cardiovascular risk factors and incident carotid plaque components was assessed. RESULTS: In the 396 arteries, all plaque components significantly changed over time. Incidence of IPH, calcification, and lipid core was, respectively, 18.5%, 59.2%, and 39.6%. The factor most strongly associated with the incidence of IPH was use of antihypertensive drugs (multivariate adjusted odds ratio [OR]: 3.87; 95% confidence interval [CI]: 1.90 to 7.90) and severe hypertension (multivariate adjusted OR: 4.70; 95% CI: 1.50 to 14.80). The incidence of calcification was associated with hypertension (OR: 2.20; 95% CI: 1.07 to 4.40). Higher cholesterol levels were associated with incidence of lipid cores (multivariate adjusted OR per unit increase in cholesterol: 1.40; 95% CI: 1.10 to 1.70). CONCLUSIONS: In these community-dwelling subjects, characteristics of plaque composition changed dramatically within a few years, and cardiovascular risk factors played a major role in these changes. Hypertension and its treatment and serum cholesterol levels were the main risk factors for the development of atherosclerotic plaque components over time.
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