Homoarginine and cardiovascular outcome in the population-based Dallas Heart Study
Standard
Homoarginine and cardiovascular outcome in the population-based Dallas Heart Study. / Atzler, Dorothee; Gore, M Odette; Ayers, Colby R; Choe, Chi-un; Böger, Rainer H; de Lemos, James A; McGuire, Darren K; Schwedhelm, Edzard.
in: ARTERIOSCL THROM VAS, Jahrgang 34, Nr. 11, 01.11.2014, S. 2501-7.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - Homoarginine and cardiovascular outcome in the population-based Dallas Heart Study
AU - Atzler, Dorothee
AU - Gore, M Odette
AU - Ayers, Colby R
AU - Choe, Chi-un
AU - Böger, Rainer H
AU - de Lemos, James A
AU - McGuire, Darren K
AU - Schwedhelm, Edzard
N1 - © 2014 American Heart Association, Inc.
PY - 2014/11/1
Y1 - 2014/11/1
N2 - OBJECTIVE: The nonproteinogenic amino acid homoarginine has been postulated to have antiatherosclerotic effects as a weak substrate of nitric oxide synthase. This investigation in the population-based Dallas Heart Study (DHS) aimed to evaluate the association of homoarginine with clinical and subclinical cardiovascular outcomes.APPROACH AND RESULTS: Plasma homoarginine was measured in 3514 participants of the DHS using liquid chromatography-tandem mass spectrometry. Associations between homoarginine and major adverse cardiovascular events and all-cause mortality were analyzed using Cox proportional hazard models adjusting for cardiovascular risk factors. Linear regression was used to assess cross-sectional associations between homoarginine and subclinical cardiovascular disease, including coronary artery calcium measured by electron beam-computed tomography, and aortic plaque burden and aortic wall thickness by MRI. Median age was 43 (interquartile range, 36-52) years, with 56% women and 52% black participants. Median follow-up was 9.4 (9.0-9.8) years. Median plasma homoarginine was 2.80 (2.14-3.54) μmol/L. In multivariable models, higher homoarginine was associated with lower rate of major adverse cardiovascular events (hazard ratio, 0.86; 95% confidence interval, 0.75-0.98) and lower all-cause mortality (hazard ratio, 0.82; 0.73-0.92; per 1 log SD increase in homoarginine). Homoarginine was inversely and independently associated with aortic wall thickness (β-estimate, -0.04; P<0.01) but not with aortic plaque burden and coronary artery calcium.CONCLUSIONS: Homoarginine is inversely associated with subclinical vascular disease and with risk for cardiovascular disease events. Additional studies are needed to evaluate whether the regulation of plasma homoarginine could emerge as a novel therapeutic option to improve outcomes in cardiovascular disease.
AB - OBJECTIVE: The nonproteinogenic amino acid homoarginine has been postulated to have antiatherosclerotic effects as a weak substrate of nitric oxide synthase. This investigation in the population-based Dallas Heart Study (DHS) aimed to evaluate the association of homoarginine with clinical and subclinical cardiovascular outcomes.APPROACH AND RESULTS: Plasma homoarginine was measured in 3514 participants of the DHS using liquid chromatography-tandem mass spectrometry. Associations between homoarginine and major adverse cardiovascular events and all-cause mortality were analyzed using Cox proportional hazard models adjusting for cardiovascular risk factors. Linear regression was used to assess cross-sectional associations between homoarginine and subclinical cardiovascular disease, including coronary artery calcium measured by electron beam-computed tomography, and aortic plaque burden and aortic wall thickness by MRI. Median age was 43 (interquartile range, 36-52) years, with 56% women and 52% black participants. Median follow-up was 9.4 (9.0-9.8) years. Median plasma homoarginine was 2.80 (2.14-3.54) μmol/L. In multivariable models, higher homoarginine was associated with lower rate of major adverse cardiovascular events (hazard ratio, 0.86; 95% confidence interval, 0.75-0.98) and lower all-cause mortality (hazard ratio, 0.82; 0.73-0.92; per 1 log SD increase in homoarginine). Homoarginine was inversely and independently associated with aortic wall thickness (β-estimate, -0.04; P<0.01) but not with aortic plaque burden and coronary artery calcium.CONCLUSIONS: Homoarginine is inversely associated with subclinical vascular disease and with risk for cardiovascular disease events. Additional studies are needed to evaluate whether the regulation of plasma homoarginine could emerge as a novel therapeutic option to improve outcomes in cardiovascular disease.
KW - Adult
KW - Aorta
KW - Biological Markers
KW - Cardiovascular Diseases
KW - Cross-Sectional Studies
KW - Female
KW - Follow-Up Studies
KW - Homoarginine
KW - Humans
KW - Incidence
KW - Male
KW - Middle Aged
KW - Proportional Hazards Models
KW - Risk Factors
KW - Texas
U2 - 10.1161/ATVBAHA.114.304398
DO - 10.1161/ATVBAHA.114.304398
M3 - SCORING: Journal article
C2 - 25189571
VL - 34
SP - 2501
EP - 2507
JO - ARTERIOSCL THROM VAS
JF - ARTERIOSCL THROM VAS
SN - 1079-5642
IS - 11
ER -