Association Between Vascular Cell Adhesion Molecule 1 and Atrial Fibrillation
JAMA Cardiology, 2017
Willeit K., Pechlaner R., Willeit P., Skroblin P., Paulweber B., Schernthaner C., Toell T., Egger G., Weger S., Oberhollenzer M., Kedenko L., Iglseder B., Bonora E., Schett G., Mayr M., Willeit J., Kiechl S.
Disease area | Application area | Sample type | Products |
---|---|---|---|
CVD | Pathophysiology | Blood | Olink Target 96 |
Abstract
Arterial fibrillation (AF) is a major contributor to thromboembolic stroke and associated with significant morbidity and mortality. Systemic inflammation has been suggested to be a contributory factor, but this view is controversial. This study aimed to examine proteins involved in systemic or arterial inflammation as potential markers for AF. The discovery Bruneck cohort was examined in 1990, using ELISAs for 13 candidate inflammatory markers, and followed up more recently in the SAPHIR validation cohort – an Olink panel (probably INF) was also run in the latter cohort.
Of the 13 principle markers of interest, VCAM-1 showed significant association with AF after rigorous statistical analysis and adjustment for other known risk factors. VCAM-1 is associated with arterial, not systemic inflammation, which may be relevant for the pathophysiology of AF. Although only a relatively small number of systemic inflammation markers could be excluded from the principle analysis, the Olink panel used in the validation cohort included many such proteins, and none of these showed significant association with AF. This study therefore 1) identified VCAM-1 as an important marker for AF and 2) provided strong indications that systemic inflammation is not a contributory factor. Although the Olink data in this paper was only shown in the supplementary materials, it was actually important in reaching this second conclusion regarding the roles of atrial vs systemic inflammation.