Microbiota‐Dependent Metabolite Trimethylamine N‐Oxide and Coronary Artery Calcium in the Coronary Artery Risk Development in Young Adults Study (CARDIA)

Autor: J. Jeffrey Carr, Donald M. Lloyd-Jones, Penny Gordon-Larsen, Brian J. Bennett, David R. Jacobs, Myron D. Gross, Katie A. Meyer, Steven H. Zeisel, Thomas Z. Benton
Jazyk: angličtina
Rok vydání: 2016
Předmět:
0301 basic medicine
Male
Pathology
Epidemiology
Trimethylamine N-oxide
Coronary Artery Disease
030204 cardiovascular system & hematology
Rate ratio
Carotid Intima-Media Thickness
chemistry.chemical_compound
0302 clinical medicine
Interquartile range
Risk Factors
Longitudinal Studies
Prospective Studies
Original Research
education.field_of_study
Incidence (epidemiology)
Incidence
follow‐up study
Middle Aged
3. Good health
risk factor
Cohort
Cardiology
cardiovascular system
Disease Progression
Biomarker (medicine)
biomarker
Female
Cardiology and Cardiovascular Medicine
Adult
medicine.medical_specialty
Population
White People
03 medical and health sciences
Methylamines
Internal medicine
medicine
Humans
cardiovascular diseases
Risk factor
education
Vascular Calcification
business.industry
Computerized Tomography (CT)
Atherosclerosis
United States
Gastrointestinal Microbiome
Black or African American
030104 developmental biology
chemistry
business
Tomography
X-Ray Computed
Biomarkers
Zdroj: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
ISSN: 2047-9980
Popis: Background Clinical studies implicate trimethylamine N‐oxide ( TMAO ; a gut microbiota‐dependent nutrient metabolite) in cardiovascular disease risk. There is a lack of population‐based data on the role of TMAO in advancing early atherosclerotic disease. We tested the prospective associations between TMAO and coronary artery calcium ( CAC ) and carotid intima‐media thickness ( cIMT ). Methods and Results Data were from the Coronary Artery Risk Development in Young Adults Study ( CARDIA ), a biracial cohort of US adults recruited in 1985–1986 (n=5115). We randomly sampled 817 participants (aged 33–55 years) who attended examinations in 2000–2001, 2005–2006, and 2010–2011, at which CAC was measured by computed tomography and cIMT (2005–2006) by ultrasound. TMAO was quantified using liquid chromotography mass spectrometry on plasma collected in 2000–2001. Outcomes were incident CAC , defined as Agatston units=0 in 2000–2001 and >0 over 10‐year follow‐up, CAC progression (any increase over 10‐year follow‐up), and continuous cIMT . Over the study period, 25% (n=184) of those free of CAC in 2000–2001 (n=746) developed detectable CAC . In 2000–2001, median (interquartile range) TMAO was 2.6 (1.8–4.2) μmol/L. In multivariable‐adjusted models, TMAO was not associated with 10‐year CAC incidence (rate ratio=1.03; 95% CI : 0.71–1.52) or CAC progression (0.97; 0.68–1.38) in Poisson regression, or cIMT (beta coefficient: −0.009; −0.03 to 0.01) in linear regression, comparing the fourth to the first quartiles of TMAO. Conclusions In this population‐based study, TMAO was not associated with measures of atherosclerosis: CAC incidence, CAC progression, or cIMT . These data indicate that TMAO may not contribute significantly to advancing early atherosclerotic disease risk among healthy early‐middle‐aged adults.
Databáze: OpenAIRE
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