Intake of Vitamin K Antagonists and Worsening of Cardiac and Vascular Disease: Results From the Population‐Based Gutenberg Health Study

Medientyp: E-Artikel
Titel: Intake of Vitamin K Antagonists and Worsening of Cardiac and Vascular Disease: Results From the Population‐Based Gutenberg Health Study
Beteiligte: Eggebrecht, Lisa; Prochaska, Jürgen H.; Schulz, Andreas; Arnold, Natalie; Jünger, Claus; Göbel, Sebastian; Laubert‐Reh, Dagmar; Binder, Harald; Beutel, Manfred E.; Pfeiffer, Nobert; Blankenberg, Stefan; Lackner, Karl J.; Spronk, Henri M.; ten Cate, Hugo; Münzel, Thomas; Wild, Philipp S.
Erschienen: Ovid Technologies (Wolters Kluwer Health), 2018
Erschienen in: Journal of the American Heart Association
Sprache: Englisch
DOI: 10.1161/jaha.118.008650
ISSN: 2047-9980
Schlagwörter: Cardiology and Cardiovascular Medicine
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Anmerkungen:
Beschreibung: <jats:sec xml:lang="en"> <jats:title>Background</jats:title> <jats:p xml:lang="en"> Preclinical data have indicated a link between use of vitamin K antagonists ( <jats:styled-content style="fixed-case">VKA</jats:styled-content> ) and detrimental effects on vascular structure and function. The objective of the present study was to determine the relationship between <jats:styled-content style="fixed-case">VKA</jats:styled-content> intake and different phenotypes of subclinical cardiovascular disease in the population. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Methods and Results</jats:title> <jats:p xml:lang="en"> Clinical and laboratory data, as well as medical–technical examinations were assessed from 15 010 individuals aged 35 to 74 years during a highly standardized 5‐hour visit at the study center of the population‐based Gutenberg Health Study. In total, the study sample comprised 287 <jats:styled-content style="fixed-case">VKA</jats:styled-content> users and 14 564 <jats:styled-content style="fixed-case">VKA</jats:styled-content> nonusers. Multivariable analysis revealed an independent association between <jats:styled-content style="fixed-case">VKA</jats:styled-content> intake and stiffness index (β=+2.54 m/s; [0.41/4.66]; <jats:italic>P</jats:italic> =0.019), ankle‐brachial index (β=−0.03; [−0.04/−0.01]; <jats:italic>P</jats:italic> <0.0001), intima‐media thickness (β=+0.03 mm [0.01/0.05]; <jats:italic>P</jats:italic> =0.0098), left ventricular ejection fraction (β=−4.02% [−4.70/−3.33]; <jats:italic>P</jats:italic> <0.0001), E/E′ (β=+0.04 [0.01/0.08]; <jats:italic>P</jats:italic> =0.014) left ventricular mass (β=+5.34 g/m <jats:sup>2.7</jats:sup> [4.26/6.44]; <jats:italic>P</jats:italic> <0.0001), and humoral markers of cardiac function and inflammation (midregional pro‐atrial natriuretic peptide: β=+0.58 pmol/L [0.50/0.65]; <jats:italic>P</jats:italic> <0.0001; midregional pro‐adrenomedullin: β=+0.18 nmol/L [0.14/0.22]; <jats:italic>P</jats:italic> <0.0001; N‐terminal pro B‐type natriuretic peptide: β=+1.90 pg/mL [1.63/2.17]; <jats:italic>P</jats:italic> <0.0001; fibrinogen: β=+143 mg/dL [132/153]; <jats:italic>P</jats:italic> <0.0001; C‐reactive protein: β=+0.31 mg/L [0.20/0.43]; <jats:italic>P</jats:italic> <0.0001). Sensitivity analysis in the subsample of participants with atrial fibrillation stratified by intake of <jats:styled-content style="fixed-case">VKA</jats:styled-content> demonstrated consistent and robust results. Genetic variants in <jats:italic> <jats:styled-content style="fixed-case">CYP</jats:styled-content> 2C9 </jats:italic> , <jats:italic> <jats:styled-content style="fixed-case">CYP</jats:styled-content> 4F2 </jats:italic> , and <jats:italic> <jats:styled-content style="fixed-case">VKORC</jats:styled-content> 1 </jats:italic> were modulating effects of <jats:styled-content style="fixed-case">VKA</jats:styled-content> on subclinical markers of cardiovascular disease. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Conclusions</jats:title> <jats:p xml:lang="en"> These data demonstrate negative effects of <jats:styled-content style="fixed-case">VKA</jats:styled-content> on vascular and cardiac phenotypes of subclinical cardiovascular disease, indicating a possible influence on long‐term disease development. These findings may be clinically relevant for the provision of individually tailored antithrombotic therapy. </jats:p> </jats:sec>
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