Key result
Advanced liver fibrosis in T2DM linked to ~59% higher HFpEF risk versus no steatosis.
Why the study?
HFpEF is a major cause of morbidity and mortality in T2DM and frequently coexists with obesity and poor metabolic control, prompting investigation into associations of NAFLD and advanced fibrosis with HFpEF across metabolic goal achievement.
Does advanced liver fibrosis increase the risk of HFpEF in patients with type 2 diabetes mellitus?
Cross-Sectional (n=2,418)
No
Does advanced liver fibrosis increase the risk of HFpEF in patients with type 2 diabetes mellitus?
Odds Ratio: 1.59 (95% CI 1.22–2.08)
p-value: p=0.001
Advanced liver fibrosis is independently associated with an increased risk of HFpEF in patients with type 2 diabetes, regardless of obesity or metabolic goal attainment.
Supports fibrosis screening for HFpEF risk stratification in T2DM; hypothesis-generating pending prospective validation.
Background: Heart failure with preserved ejection fraction (HFpEF), a major cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM), is frequently coexisted with obesity, poor glycemic, blood pressure (BP), and/or lipid control. We aimed to investigate the associations of nonalcoholic fatty liver disease (NAFLD) and its advanced fibrosis with HFpEF according to obesity, glycated hemoglobin A1c (HbA1c), BP, and low-density lipoprotein cholesterol (LDL-C) goal achievement status in T2DM patients. Methods: A total of 2,418 T2DM patients who were hospitalized were cross-sectionally assessed. Liver fibrosis was evaluated by non-invasive biomarkers. Logistic regression analysis was used to evaluate the independent and combined associations of fibrosis status and diabetic care goal attainments with HFpEF risk. Results: Simple steatosis was not associated with HFpEF risk compared with patients without steatosis, while advanced liver fibrosis was found to have significantly higher odds for HFpEF risk (odds ratio,1.59; 95% confidence interval, 1.22-2.08). Advanced fibrosis in NAFLD was significantly associated with an increased risk of HFpEF, regardless of obesity status, HbA1c, BP, and LDL-C goal achievement status. P values for the interactions between fibrosis status and HbA1c control status, fibrosis status and BP control status, fibrosis status and LDL-C control status, and fibrosis status and body mass index (BMI) status on HFpEF risk were 0.021, 0.13, 0.001, and 0.23, respectively. Conclusion: In patients with T2DM, advanced hepatic fibrosis was significantly associated with HFpEF risk, irrespective of obesity status, HbA1c, BP, and LDL-C goal attainment status. Further, HbA1c and LDL-C goal attainment status modified this association.
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Jiang et al. (2023) conducted a cross-sectional in Type 2 diabetes mellitus (n=2,418). Advanced liver fibrosis vs. No nonalcoholic fatty liver disease (steatosis) was evaluated on Heart failure with preserved ejection fraction (HFpEF) (OR 1.59, 95% CI 1.22-2.08, p=0.001). Advanced liver fibrosis in patients with type 2 diabetes was significantly associated with an increased risk of heart failure with preserved ejection fraction (OR 1.59) compared to patients without steatosis.
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