Cureus. 2025 Nov 27;17(11):e97927. doi: 10.7759/cureus.97927. eCollection 2025 Nov.
ABSTRACT
Background Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and is closely linked to metabolic risk factors that also predispose to ischemic heart disease (IHD). Evaluating the relationship between NAFLD severity and IHD may improve cardiovascular risk assessment. Objective To compare the severity of NAFLD, assessed by FibroScan, in patients with and without IHD. Methods A cross-sectional study was conducted at Liaquat National Hospital, Karachi (Sept 2023-Feb 2024). Adults with NAFLD confirmed by FibroScan were enrolled (n=300), including 100 IHD patients and 200 non-IHD controls. Anthropometric, biochemical, and FibroScan parameters (Controlled Attenuation Parameter (CAP) and Liver Stiffness Measurement (LSM)) were recorded. Between-group differences were analyzed using t-tests and Chi-square tests, and logistic regression was used to estimate associations, adjusting for age, sex, and BMI. Results Among the 300 patients (mean age 51.4 ± 8.5 years; 62.2% female), obesity (99.1%), diabetes (54.8%), and dyslipidemia (62.7%) were prevalent comorbidities. Mean FibroScan values did not differ significantly between IHD and control groups (7.2±2.05 vs 7.03±2.16 kPa, p=0.507). CAP scores were also comparable (273.3±65.0 vs 282.2±66.6 dB/m, p=0.276). Logistic regression showed mild CAP associated with higher IHD odds (OR 2.21, 95% CI 1.04-4.72, p=0.04), but no consistent associations were observed with fibrosis stage. Conclusions The severity of non-alcoholic fatty liver disease (NAFLD), assessed non-invasively by FibroScan, did not differ significantly between patients with and without ischemic heart disease (IHD). A borderline association between mild hepatic steatosis (CAP) and IHD was observed; however, this finding should be interpreted with caution, as it lacked a dose-response pattern and histologic (biopsy) confirmation. Given the cross-sectional design, the results indicate an association rather than causation, underscoring the need for longitudinal, biopsy-validated studies to better clarify the hepatic-cardiovascular relationship.
PMID:41466930 | PMC:PMC12744314 | DOI:10.7759/cureus.97927