Author information
1Center for Translational and Molecular Medicine, INSERM UMR 1231, Dijon, France.
2Department of Clinical Biochemistry, Dijon Bourgogne University Hospital, Dijon, France.
3Institute of Cardiometabolism and Nutrition (ICAN), Paris, France.
4Sorbonne Université, Paris, France.
5Department of Diabetology, Assistance Publique-Hôpitaux de Paris (APHP), Pitié-Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris, France.
6Centre de Recherche des Cordeliers, INSERM UMR_S 1138, Paris, France.
7Laboratoire d'Imagerie Biomédicale INSERM_1146, CNRS_7371, Paris, France.
8ICT Cardiovascular and Thoracic Imaging Unit, Assistance Publique-Hôpitaux de Paris (APHP), Pitié Salpêtrière University Hospital, Paris, France.
9Sorbonne Université, Paris, France. olivier.bourron@aphp.fr.
10Centre de Recherche des Cordeliers, INSERM UMR_S 1138, Paris, France. olivier.bourron@aphp.fr.
11Department of Diabetology, Assistance Publique-Hôpitaux de Paris (APHP), Pitié-Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris, France. olivier.bourron@aphp.fr.
Abstract
Background: Studies have demonstrated that coronary artery calcification on one hand and non-alcoholic fatty liver disease (NAFLD) on the other hand are strongly associated with cardiovascular events. However, it remains unclear whether NAFLD biomarkers could help estimate cardiovascular risk in individuals with type 2 diabetes (T2D). The primary objective of the present study was to investigate whether the biomarkers of NAFLD included in the FibroMax® panels are associated with the degree of coronary artery calcification in patients with T2D.
Methods: A total of 157 and 460 patients with T2D were included from the DIACART and ACCoDiab cohorts, respectively. The coronary artery calcium score (CACS) was measured in both cohorts using computed tomography. FibroMax® panels (i.e., SteatoTest®, FibroTest®, NashTest®, and ActiTest®) were determined from blood samples as scores and stages in the DIACART cohort and as stages in the ACCoDiab cohort.
Results: CACS significantly increased with the FibroTest® stages in both the DIACART and ACCoDiab cohorts (p-value for trend = 0.0009 and 0.0001, respectively). In DIACART, the FibroTest® score was positively correlated with CACS in univariate analysis (r = 0.293, p = 0.0002) and remained associated with CACS independently of the traditional cardiovascular risk factors included in the SCORE2-Diabetes model [β = 941 ± 425 (estimate ± standard error), p = 0.028]. In the ACCoDiab cohort, the FibroTest® F3-F4 stage was positively correlated with CACS in point-biserial analysis (rpbi = 0.104, p = 0.024) and remained associated with CACS after adjustment for the traditional cardiovascular risk factors included in the SCORE2-Diabetes model (β = 234 ± 97, p = 0.016). Finally, the prediction of CACS was improved by adding FibroTest® to the traditional cardiovascular risk factors included in the SCORE2-Diabetes model (goodness-of-fit of prediction models multiplied by 4.1 and 6.7 in the DIACART and ACCoDiab cohorts, respectively). In contrast, no significant relationship was found between FibroMax® panels other than FibroTest® and CACS in either cohort.
Conclusions: FibroTest® is independently and positively associated with the degree of coronary artery calcification in patients with T2D, suggesting that FibroTest® could be a relevant biomarker of coronary calcification and cardiovascular risk.
Trial registration: ClinicalTrials.gov identifiers NCT02431234 and NCT03920683.