Background and Aim: Cardiovascular disease (CVD) is the principal cause of death in patients with type 2 diabetes (T2D). In this study, we assessed whether liver fibrosis predicted the risk of CVD in patients with T2D. Methods: A total of 1481 patients who had commenced oral antidiabetic drugs to treat newly diagnosed T2D between 2006 and 2010 were recruited. The fibrosis-4 index (FIB-4), non-alcoholic fatty liver disease fibrosis score (NFS), and BARD score were used to assess fibrotic burden at the time of T2D diagnosis. Results: During the follow-up period (median 88.1 [interquartile range 36.6–113.6] months), 242 (16.3%) patients developed CVD. CVD occurred frequently in older patients and was associated with hypertension; metabolic syndrome; obesity; smoking; administration of statin, which is an antihyperlipidemic drug; lower platelet counts; lower alanine aminotransferase, total cholesterol, and HbA1c levels; higher C-peptide and homeostatic model assessment of insulin resistance levels; and higher FIB-4, NFS, and BARD score (all P < 0.05). FIB-4 (hazard ratio [HR] = 1.163), NFS (HR = 1.322), BARD score (HR = 1.564), metabolic syndrome (HR = 1.556), smoking (HR = 2.829), and statin use (HR = 0.603) independently predicted the risk of CVD (all P < 0.05). The cumulative incidence of CVD was significantly different among groups stratified by liver fibrotic burden (all P < 0.05, log-rank test). Competing risk analysis showed a significant association between the severity of liver fibrosis and CVD development (all P < 0.001, Gray's test). Conclusions: The severity of liver fibrosis independently predicted CVD in patients with T2D. Thus, assessment of liver fibrosis might allow physicians to optimize the timing of appropriate cardiovascular interventions in such patients.
|Number of pages||11|
|Journal||Journal of Gastroenterology and Hepatology (Australia)|
|Publication status||Published - 2021 Jun|
Bibliographical noteFunding Information:
Financial support: This work was in part supported by the National Research Foundation of Korea (NRF) grant funded by the Korean government (Ministry of Science and ICT, South Korea [MSIT]) (2019R1A2C4070136). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
© 2020 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd
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