European Journal of Cardiovascular Medicine

Non-alcoholic fatty liver disease (NAFLD) is increasingly recognized as the most common cause of chronic liver disease worldwide, affecting approximately 25–30% of the global population. It encompasses a spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma (1). The condition is strongly associated with metabolic syndrome components such as central obesity, insulin resistance, dyslipidemia, and type 2 diabetes mellitus (2).

Heart failure (HF), particularly congestive heart failure (CHF), remains a major public health concern, with rising prevalence due to aging populations and improved survival after acute cardiac events. The interaction between HF and the liver is well known, as hepatic congestion and hypoperfusion can result in congestive hepatopathy and ischemic hepatitis (3). However, beyond these hemodynamic effects, metabolic liver disease such as NAFLD may coexist and contribute to adverse cardiovascular outcomes.

NAFLD and HF share multiple pathophysiological pathways including systemic inflammation, oxidative stress, neurohormonal activation, endothelial dysfunction, and insulin resistance (4,5). Moreover, NAFLD itself has been linked with increased risk of subclinical atherosclerosis, left ventricular diastolic dysfunction, and incident heart failure, independent of traditional risk factors (6,7). In turn, the presence of HF can exacerbate hepatic steatosis through chronic venous congestion, altered lipid metabolism, and reduced hepatic oxygenation (8).

Recent studies have reported variable prevalence of NAFLD among patients with heart failure, ranging from 30% to over 50%, depending on the population studied, diagnostic criteria, and imaging methods used (9,10). However, data from South Asian populations remain limited, and the true burden of NAFLD among patients with congestive heart failure in this region is not well established.

Understanding the prevalence and clinical profile of NAFLD in heart failure is essential, as it may influence prognosis, guide monitoring strategies, and identify opportunities for metabolic and lifestyle interventions. Therefore, this observational cohort study was conducted to determine the prevalence of non-alcoholic fatty liver disease among patients with congestive heart failure and to explore its clinical correlates.

Study Design and Setting: This was an observational cohort study conducted in the Department of Medicine and Cardiology at Konaseema institute of medical sciences Amalapuram AP India a tertiary care teaching hospital, between January 2022 and March 2023. Consecutive adult patients admitted with or attending follow-up for clinically diagnosed congestive heart failure (CHF) were enrolled after obtaining informed consent. The study protocol was approved by the Institutional Ethics Committee, and written informed consent was obtained from all participants prior to inclusion. Study Population: All adult patients aged ≥18 years with a confirmed diagnosis of congestive heart failure, based on the European Society of Cardiology (ESC) criteria—symptoms and/or signs of heart failure with supporting echocardiographic evidence of structural or functional cardiac abnormality—were included (11). Inclusion Criteria: Adults (≥18 years) with clinical and echocardiographic evidence of CHF (HFrEF, HFmrEF, or HFpEF). Willingness to provide informed consent. Exclusion Criteria: History of significant alcohol consumption (>30 g/day for men and >20 g/day for women). Known chronic liver disease of other etiology (viral hepatitis B or C, autoimmune hepatitis, Wilson’s disease, hemochromatosis, cholestatic liver disease). Use of known hepatotoxic or steatogenic drugs (e.g., amiodarone, methotrexate, tamoxifen, corticosteroids). Pregnancy. Critically ill patients unable to undergo abdominal ultrasonography. Sample Size: - Sample size was calculated based on the expected prevalence of NAFLD among patients with CHF. Assuming a prevalence of 40%, a confidence level of 95%, and an allowable error of 10%, the minimum sample size required was calculated using the formula: 𝑛=𝑍2×𝑝(1−𝑝)/𝑑2n where Z = 1.96, p = 0.4, and d = 0.1, yielding n ≈ 92. For the present study, 60 patients were included as a pilot sample due to feasibility considerations. Data Collection: - A predesigned proforma was used to collect demographic, clinical, biochemical, and imaging data. Clinical data: - age, sex, duration of illness, comorbidities (hypertension, diabetes, dyslipidemia), NYHA functional class, and medication history. Anthropometric measurements: weight, height, and body mass index (BMI, kg/m²). Cardiac evaluation: echocardiographic parameters including left ventricular ejection fraction (LVEF), chamber dimensions, and diastolic function. HF was classified as HFrEF (<40%), HFmrEF (40–49%), or HFpEF (≥50%) according to ESC guidelines (11). Laboratory Investigations: All patients underwent routine investigations including complete blood count, fasting blood sugar, liver function tests (AST, ALT, ALP, bilirubin, albumin), renal function tests, and fasting lipid profile. Serum transaminase levels >40 IU/L were considered elevated. Assessment of NAFLD: - All participants underwent abdominal ultrasonography (USG) performed by a single experienced radiologist blinded to the clinical details. NAFLD was diagnosed based on characteristic ultrasonographic findings diffuse hyper echogenicity of liver parenchyma compared with renal cortex, attenuation of ultrasound beam, and poor visualization of intrahepatic vessels—after excluding other causes of liver disease (12). The severity of hepatic steatosis was graded as: Grade I (mild): Slight, diffuse increase in fine echoes in liver parenchyma. Grade II (moderate): Moderate increase in echogenicity with obscured intrahepatic vessels. Grade III (severe): Marked increase in echogenicity and poor penetration of posterior liver segments. Where available, transient elastography (Fibro Scan) was used to estimate hepatic steatosis (Controlled Attenuation Parameter, CAP) and liver stiffness for fibrosis staging. Non-Invasive Fibrosis Assessment: -The following fibrosis indices were calculated: FIB-4 index: - (Age × AST) / (Platelet × √ALT). NAFLD fibrosis score: computed from age, BMI, diabetes status, AST/ALT ratio, platelet count, and albumin (13). Cut-offs for advanced fibrosis: FIB-4 >2.67 and NAFLD fibrosis score >0.676. Statistical Analysis: - Data were entered into Microsoft Excel and analyzed using SPSS version 26.0 (IBM Corp., Armonk, NY, USA). Continuous variables were expressed as mean ± standard deviation (SD) or median (interquartile range) as appropriate. Categorical variables were presented as frequencies and percentages. The prevalence of NAFLD was calculated as a proportion of the total sample. Comparison between groups (NAFLD vs. non-NAFLD) was done using Student’s t-test or Mann–Whitney U test for continuous variables and chi-square test for categorical variables. A p-value <0.05 was considered statistically significant.

A total of 60 patients with clinically and echocardiographically confirmed congestive heart failure were included in the present study. The mean age of the study population was 58.6 ± 10.4 years, ranging from 35 to 78 years. Of these, 38 (63.3%) were males and 22 (36.7%) were females. The majority of patients (40%, n=24) belonged to the age group of 51–60 years.

Prevalence of NAFLD

On abdominal ultrasonography, non-alcoholic fatty liver disease (NAFLD) was detected in 26 patients (43.3%), while 34 patients (56.7%) showed no evidence of hepatic steatosis. Among the NAFLD cases, Grade I steatosis was observed in 14 (53.8%), Grade II in 9 (34.6%), and Grade III in 3 (11.6%) patients.

Table 1:- Baseline Demographic and Clinical Characteristics

*Statistically significant (p < 0.05)

Table 2:- Heart Failure Characteristics

Patients with NAFLD had a trend toward lower ejection fraction and higher NYHA class, though these did not reach statistical significance.

Table: - 3, Liver Function and Metabolic Parameters

*Statistically significant (p < 0.05)

Elevated liver enzymes (ALT and AST) were significantly more common among patients with NAFLD. These patients also had higher BMI, fasting glucose, and triglyceride levels.

Table: - 4, Non-Invasive Fibrosis Scores

*Statistically significant (p < 0.05)

Although most patients had low or indeterminate fibrosis risk, 7 (11.6%) of the total cohort were classified as high-risk for advanced fibrosis.

Outcomes

During the follow-up period of 3 months, 7 patients (11.7%) experienced hospital readmission for heart failure exacerbation, and 3 patients (5%) died. Readmission rates were higher among the NAFLD group (19.2% vs. 5.9%, p = 0.09), though not statistically significant due to limited sample size.

In the present observational cohort study, the prevalence of non-alcoholic fatty liver disease (NAFLD) among patients with congestive heart failure (CHF) was found to be 43.3%. This finding is consistent with prior reports indicating a substantial coexistence of hepatic steatosis in patients with heart failure, suggesting shared pathophysiological mechanisms linking both conditions.

The prevalence of NAFLD in the general population is estimated to be around 25–30% globally (1), and higher in individuals with metabolic syndrome and cardiovascular disease (2). In our study, the prevalence among CHF patients was nearly 1.5 times higher, reflecting the close metabolic association between these two entities. Targher et al. demonstrated that NAFLD prevalence among patients with chronic heart failure ranges between 30–50%, depending on diagnostic modality and population characteristics (9). Zhang et al. similarly reported a prevalence of 45% among hospitalized CHF patients in China (14), comparable to our findings.

The coexistence of NAFLD and CHF is biologically plausible. Both conditions share common risk factors including obesity, insulin resistance, diabetes mellitus, and dyslipidemia (4,5). In our cohort, NAFLD patients had significantly higher body mass index, fasting glucose, and triglyceride levels than non-NAFLD patients. This supports the hypothesis that NAFLD may be a hepatic manifestation of systemic metabolic dysfunction. Diabetes mellitus was observed in 69.2% of NAFLD patients, consistent with earlier studies showing a strong association between insulin resistance and hepatic steatosis (15).

The observed elevation of liver enzymes (ALT and AST) among NAFLD patients in our study is in agreement with previous reports suggesting that subclinical hepatic inflammation is common in CHF patients with fatty liver (16). Chronic passive hepatic congestion and hypoxia in CHF may worsen hepatic injury and fibrosis risk (8). Although most of our patients had mild to moderate steatosis, around 11.6% were categorized as high-risk for advanced fibrosis based on FIB-4 and NAFLD fibrosis score, indicating the need for early identification and management.

In terms of cardiac characteristics, patients with NAFLD had a trend toward lower left ventricular ejection fraction and higher NYHA functional class, though not statistically significant. Prior studies have reported similar associations, suggesting that NAFLD may contribute to myocardial remodeling, diastolic dysfunction, and increased cardiac stiffness through systemic inflammation and lipid accumulation (17). Bonapace et al. reported that NAFLD was independently associated with left ventricular diastolic dysfunction in diabetic patients (6), while Simon et al. found that NAFLD increased the risk of incident heart failure in a community cohort (7).

The pathophysiological link between NAFLD and heart failure likely involves multiple mechanisms, including increased oxidative stress, endothelial dysfunction, and activation of renin–angiotensin–aldosterone and sympathetic systems (19). Moreover, NAFLD may exacerbate cardiac remodeling through hepatic secretion of pro-inflammatory cytokines (IL-6, TNF-α) and hepatokines such as fetuin-A, which have deleterious effects on myocardial metabolism .

Our study adds to the limited data from South Asian populations, where metabolic risk factors are highly prevalent but hepatic comorbidities in heart failure are often under-recognized. The relatively high prevalence of NAFLD in this cohort underscores the importance of screening CHF patients for hepatic steatosis, particularly those with obesity, diabetes, or dyslipidemia.

Limitations:

The study was conducted in a single tertiary care center with a modest sample size, limiting generalizability. Diagnosis of NAFLD was based on ultrasonography, which, although widely used and practical, has limited sensitivity for mild steatosis and cannot distinguish NASH from simple steatosis. Fibrosis assessment relied on non-invasive scores, and liver biopsy or elastography was not available for all patients. A larger, multicentric study with longitudinal follow-up could provide better insights into prognostic implications.

NAFLD is highly prevalent among patients with congestive heart failure and is strongly associated with metabolic risk factors such as obesity, diabetes, and dyslipidemia. Early identification of NAFLD in CHF patients is essential, as it may influence disease progression, management, and long-term cardiovascular outcomes. Routine screening using ultrasonography and non-invasive fibrosis indices should be considered part of comprehensive heart failure evaluation.

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