Chronic liver disease (CLD) represents a major global health challenge and is an important cause of morbidity, mortality, and healthcare utilization worldwide. It encompasses a heterogeneous group of progressive hepatic disorders characterized by persistent inflammation, fibrosis, and architectural distortion that may ultimately result in cirrhosis, portal hypertension, and hepatic failure [1]. Despite advances in antiviral therapy and increasing recognition of metabolic dysfunction-associated steatotic liver disease (MASLD), the burden of CLD continues to be substantial, particularly in low- and middle-income countries where alcohol-related liver disease and chronic viral hepatitis remain important etiologies [2,3]. In India, alcohol-related liver disease, chronic hepatitis B and C, and MASLD contribute substantially to the burden of chronic liver disease [3]. Although CLD primarily affects the liver, it is increasingly recognized as a systemic disorder involving multiple organ systems [4]. Progressive fibrosis and portal hypertension result in profound hemodynamic and neurohumoral alterations that extend beyond the liver and affect cardiovascular function. Splanchnic vasodilatation, activation of the renin–angiotensin–aldosterone system and sympathetic nervous system, together with chronic inflammation and endothelial dysfunction, contribute to the development of a hyperdynamic circulatory state [4,5]. Persistent exposure to these alterations may result in structural, functional, and electrophysiological myocardial abnormalities collectively described within the spectrum of cirrhotic cardiomyopathy [6]. Cirrhotic cardiomyopathy is characterized by impaired ventricular relaxation, abnormal myocardial contractile reserve, and electrophysiological abnormalities occurring in the setting of cirrhosis and in the absence of other primary cardiac disease [6]. Patients may remain clinically asymptomatic during the compensated stage, while cardiac dysfunction may become clinically apparent during physiological stress such as sepsis, variceal haemorrhage, transjugular intrahepatic portosystemic shunt (TIPS) placement, or liver transplantation [6,7]. Recognition of cardiovascular abnormalities in patients with CLD may therefore be clinically important, particularly in those with advanced hepatic disease or undergoing major interventions. Electrocardiography (ECG) is a simple, accessible, and inexpensive investigation for detecting cardiovascular abnormalities in patients with cirrhosis. QTc prolongation, sinus tachycardia, nonspecific ST-T changes, conduction abnormalities, and cardiac arrhythmias have been reported in patients with advanced liver disease and may reflect autonomic dysfunction and myocardial involvement [8–10]. Because ECG is widely available and relatively inexpensive, it may serve as a useful screening tool for cardiovascular abnormalities in patients with CLD. Two-dimensional echocardiography complements ECG by providing structural and functional assessment of the heart. Left ventricular diastolic dysfunction is among the commonly described echocardiographic abnormalities in cirrhotic cardiomyopathy, while changes in systolic function, left ventricular geometry, left atrial size, pulmonary artery pressure, and cardiac output may provide additional information regarding cardiovascular involvement [11]. Echocardiography may therefore help identify cardiac abnormalities that are not clinically apparent during routine examination. Abdominal ultrasonography remains an important imaging modality in the evaluation of patients with CLD. In addition to demonstrating hepatic parenchymal abnormalities, ultrasonography provides information regarding portal hypertension, splenomegaly, portal vein dilatation, ascites, and other complications of advanced liver disease [12, 13]. These findings may provide useful markers of hepatic disease severity and decompensation. Combining ultrasonographic assessment of hepatic disease with cardiovascular evaluation may therefore provide a broader assessment of the systemic consequences of CLD. Although previous studies have independently evaluated electrocardiographic changes, echocardiographic abnormalities, and ultrasonographic features in patients with chronic liver disease and cirrhosis [8,9,11,13], relatively few studies have examined these three routinely available non-invasive modalities together, particularly in the Indian population. An integrated approach may improve the characterization of cardiovascular involvement in CLD and help identify associations between hepatic disease severity and cardiovascular abnormalities. Therefore, the present study was undertaken to evaluate electrocardiographic, echocardiographic, and ultrasonographic abnormalities in patients with chronic liver disease and to determine their association with hepatic disease severity and decompensation. By integrating these routinely available investigations, the study aimed to provide a comprehensive assessment of cardiovascular and hepatic abnormalities in patients with CLD.

Chronic liver disease (CLD) represents a major global health challenge and is an important cause of morbidity, mortality, and healthcare utilization worldwide. It encompasses a heterogeneous group of progressive hepatic disorders characterized by persistent inflammation, fibrosis, and architectural distortion that may ultimately result in cirrhosis, portal hypertension, and hepatic failure [1]. Despite advances in antiviral therapy and increasing recognition of metabolic dysfunction-associated steatotic liver disease (MASLD), the burden of CLD continues to be substantial, particularly in low- and middle-income countries where alcohol-related liver disease and chronic viral hepatitis remain important etiologies [2,3]. In India, alcohol-related liver disease, chronic hepatitis B and C, and MASLD contribute substantially to the burden of chronic liver disease [3]. Although CLD primarily affects the liver, it is increasingly recognized as a systemic disorder involving multiple organ systems [4]. Progressive fibrosis and portal hypertension result in profound hemodynamic and neurohumoral alterations that extend beyond the liver and affect cardiovascular function. Splanchnic vasodilatation, activation of the renin–angiotensin–aldosterone system and sympathetic nervous system, together with chronic inflammation and endothelial dysfunction, contribute to the development of a hyperdynamic circulatory state [4,5]. Persistent exposure to these alterations may result in structural, functional, and electrophysiological myocardial abnormalities collectively described within the spectrum of cirrhotic cardiomyopathy [6]. Cirrhotic cardiomyopathy is characterized by impaired ventricular relaxation, abnormal myocardial contractile reserve, and electrophysiological abnormalities occurring in the setting of cirrhosis and in the absence of other primary cardiac disease [6]. Patients may remain clinically asymptomatic during the compensated stage, while cardiac dysfunction may become clinically apparent during physiological stress such as sepsis, variceal haemorrhage, transjugular intrahepatic portosystemic shunt (TIPS) placement, or liver transplantation [6,7]. Recognition of cardiovascular abnormalities in patients with CLD may therefore be clinically important, particularly in those with advanced hepatic disease or undergoing major interventions. Electrocardiography (ECG) is a simple, accessible, and inexpensive investigation for detecting cardiovascular abnormalities in patients with cirrhosis. QTc prolongation, sinus tachycardia, nonspecific ST-T changes, conduction abnormalities, and cardiac arrhythmias have been reported in patients with advanced liver disease and may reflect autonomic dysfunction and myocardial involvement [8–10]. Because ECG is widely available and relatively inexpensive, it may serve as a useful screening tool for cardiovascular abnormalities in patients with CLD. Two-dimensional echocardiography complements ECG by providing structural and functional assessment of the heart. Left ventricular diastolic dysfunction is among the commonly described echocardiographic abnormalities in cirrhotic cardiomyopathy, while changes in systolic function, left ventricular geometry, left atrial size, pulmonary artery pressure, and cardiac output may provide additional information regarding cardiovascular involvement [11]. Echocardiography may therefore help identify cardiac abnormalities that are not clinically apparent during routine examination. Abdominal ultrasonography remains an important imaging modality in the evaluation of patients with CLD. In addition to demonstrating hepatic parenchymal abnormalities, ultrasonography provides information regarding portal hypertension, splenomegaly, portal vein dilatation, ascites, and other complications of advanced liver disease [12, 13]. These findings may provide useful markers of hepatic disease severity and decompensation. Combining ultrasonographic assessment of hepatic disease with cardiovascular evaluation may therefore provide a broader assessment of the systemic consequences of CLD. Although previous studies have independently evaluated electrocardiographic changes, echocardiographic abnormalities, and ultrasonographic features in patients with chronic liver disease and cirrhosis [8,9,11,13], relatively few studies have examined these three routinely available non-invasive modalities together, particularly in the Indian population. An integrated approach may improve the characterization of cardiovascular involvement in CLD and help identify associations between hepatic disease severity and cardiovascular abnormalities. Therefore, the present study was undertaken to evaluate electrocardiographic, echocardiographic, and ultrasonographic abnormalities in patients with chronic liver disease and to determine their association with hepatic disease severity and decompensation. By integrating these routinely available investigations, the study aimed to provide a comprehensive assessment of cardiovascular and hepatic abnormalities in patients with CLD.

A total of 204 patients with chronic liver disease were included in the study. The mean age was 46.2 ± 11.8 years (range 19–75 years). The majority of patients were males (178; 87.3%), while females constituted 26 (12.7%) of the study population. Alcohol-related liver disease (ALD) was the predominant etiology (57.8%), followed by hepatitis C virus (HCV) infection (26.5%), hepatitis B virus (HBV) infection (8.8%), metabolic dysfunction-associated steatotic liver disease (MASLD) (3.9%), and other causes (2.9%). Most patients presented with decompensated chronic liver disease (82.4%), whereas only 17.6% had compensated disease. Table 1. Baseline Characteristics of the Study Population Variable Value Number of patients 204 Age (years), mean ± SD 46.2 ± 11.8 Male 178 (87.3%) Female 26 (12.7%) Alcohol-related liver disease 118 (57.8%) Hepatitis C 54 (26.5%) Hepatitis B 18 (8.8%) MASLD 8 (3.9%) Other etiologies 6 (2.9%) Compensated CLD 36 (17.6%) Decompensated CLD 168 (82.4%) Clinical Profile Ascites was the commonest clinical manifestation and was observed in 178 patients (87.3%). Upper gastrointestinal bleeding occurred in 64 patients (31.4%), hepatic encephalopathy in 52 (25.5%), acute kidney injury in 38 (18.6%), spontaneous bacterial peritonitis in 12 (5.9%), and hepatorenal syndrome in 8 (3.9%). Electrocardiographic Findings Electrocardiographic abnormalities were present in 186 patients (91.2%), whereas only 18 patients (8.8%) had a normal ECG. QTc prolongation was the most frequent abnormality (62.7%), followed by sinus tachycardia (46.1%), ST-T changes (40.2%), short PR interval (37.3%), and left axis deviation (25.5%). Less frequent findings included supraventricular ectopics (7.8%), sinus arrhythmia (5.9%), atrial fibrillation (2.0%), junctional rhythm (2.9%), premature ventricular complexes (2.0%), and atrial tachycardia (1.0%). Table 2. Electrocardiographic Findings ECG finding n (%) Any ECG abnormality 186 (91.2) QTc prolongation 128 (62.7) Sinus tachycardia 94 (46.1) ST-T changes 82 (40.2) Short PR interval 76 (37.3) Left axis deviation 52 (25.5) Supraventricular ectopics 16 (7.8) Sinus arrhythmia 12 (5.9) Junctional rhythm 6 (2.9) Atrial fibrillation 4 (2.0) Premature ventricular complexes 4 (2.0) Atrial tachycardia 2 (1.0) Echocardiographic Findings Echocardiography demonstrated a broad spectrum of cardiac abnormalities. Normal left ventricular ejection fraction (≥50%) was observed in 37.3% of patients, whereas 46.1% had mildly reduced (40–49%) ejection fraction and 16.6% had an ejection fraction below 40%. The mean left ventricular ejection fraction was 48.6 ± 9.2%. Left ventricular diastolic dysfunction was identified in 150 patients (73.5%), including Grade I dysfunction in 62.7% and Grade II dysfunction in 10.8%. Hyperdynamic circulation was noted in 18.6%, left ventricular hypertrophy in 8.8%, left atrial enlargement in 7.8%, elevated pulmonary artery systolic pressure in 5.9%, and right ventricular dilatation in 2.9%. Table 3. Echocardiographic Findings Parameter n (%) Normal LVEF(>50%) 76 (37.3) LVEF 40–49% 94 (46.1) LVEF <40% 34 (16.6) Grade I LV diastolic dysfunction 128 (62.7) Grade II LV diastolic dysfunction 22 (10.8) Hyperdynamic circulation 38 (18.6) Left ventricular hypertrophy 18 (8.8) Left atrial enlargement 16 (7.8) Elevated PASP 12 (5.9) Right ventricular dilatation 6 (2.9) Ultrasonographic Findings Abdominal ultrasonography demonstrated characteristic features of chronic liver disease and portal hypertension. Bright liver was present in 79.4%, coarse hepatic echotexture in 72.5%, irregular liver surface in 47.1%, hepatomegaly in 38.2%, and a small shrunken liver in 16.7%. Portal vein dilatation (>13 mm) was observed in 54.9%, splenomegaly in 82.4%, splenic vein enlargement in 13.7%, and portal vein thrombosis in 3.9%. Ascites was present in 87.3%, including mild ascites in 20.6%, moderate ascites in 41.2%, and gross ascites in 25.5%. Gallbladder wall thickening was seen in 16.7%, cholelithiasis in 8.8%, and pleural effusion in 13.7%.. Table 4. Ultrasonographic Findings Finding n (%) Bright liver 162 (79.4) Coarse echotexture 148 (72.5) Splenomegaly 168 (82.4) Ascites 178 (87.3) Portal vein dilatation 112 (54.9) Hepatomegaly 78 (38.2) Irregular liver surface 96 (47.1) Small shrunken liver 34 (16.7) Gallbladder wall thickening 34 (16.7) Pleural effusion 28 (13.7) Splenic vein enlargement 28 (13.7) Cholelithiasis 18 (8.8) Portal vein thrombosis 8 (3.9) Correlation Between Cardiac and Hepatic Findings Cardiovascular abnormalities increased with worsening liver disease. QTc prolongation was significantly more frequent in patients with decompensated CLD than in those with compensated disease (73.8% vs. 38.9%; p < 0.001). Similarly, sinus tachycardia occurred significantly more often in decompensated patients (68.4% vs. 22.2%; p < 0.001). The prevalence of left ventricular diastolic dysfunction increased progressively with the severity of ascites, being highest among patients with gross ascites (82.1%) compared with those without significant ascites (48.3%; p < 0.001). Overall, 127 patients (62.3%) demonstrated concomitant abnormalities on ECG, echocardiography, and abdominal ultrasonography, highlighting the close association between hepatic decompensation and cardiovascular dysfunction. Table 5. Significant Correlations Variable Result QTc prolongation in decompensated CLD 73.8% vs. 38.9% (p < 0.001) Sinus tachycardia in decompensated CLD 68.4% vs. 22.2% (p < 0.001) LVDD in gross ascites 82.1% vs. 48.3% (p < 0.001) Integrated ECG + ECHO + USG abnormalities 127 (62.3%)

The present study demonstrated a high burden of cardiovascular and hepatic abnormalities among patients with chronic liver disease (CLD), with cardiovascular involvement becoming more prominent with hepatic decompensation. Overall, ECG abnormalities were very common, with QTc prolongation and sinus tachycardia being the predominant findings. Echocardiography demonstrated left ventricular diastolic dysfunction as the major cardiac abnormality, accompanied by impairment of systolic function in a substantial proportion of patients. Ultrasonography showed frequent features of portal hypertension and hepatic decompensation, particularly ascites and splenomegaly. Importantly, ECG and echocardiographic abnormalities were significantly more frequent with worsening hepatic decompensation, and a substantial proportion of patients demonstrated abnormalities simultaneously across ECG, echocardiography, and ultrasonography. The predominance of cardiovascular abnormalities in the present study is consistent with the growing evidence that CLD is associated with clinically important myocardial and electrophysiological alterations. In the present study, ECG abnormalities were observed in the great majority of patients, with QTc prolongation being the most frequent abnormality. This finding is particularly relevant because QTc prolongation is considered an important electrophysiological manifestation of cirrhotic cardiomyopathy. Toma et al. (2020) similarly demonstrated progressive QTc prolongation across increasing Child-Pugh classes, with cirrhotic patients having substantially longer QTc intervals than patients with chronic hepatitis. Their findings further showed that QTc prolongation was associated with biochemical markers of more advanced liver dysfunction, including lower albumin and higher bilirubin and ammonia concentrations in decompensated disease [9]. The findings are also strongly supported by Gollamudi et al. (2024), who reported that prolonged QTc was associated with more severe liver dysfunction, particularly advanced Child-Pugh and MELD categories. Their observation that patients with prolonged QTc had greater hepatic impairment is comparable to the present finding that QTc prolongation was considerably more common in decompensated CLD [15]. Similarly, Karagiannakis et al. (2023) found significantly longer QTc intervals among patients with Child-Pugh B/C disease compared with Child-Pugh A patients [16]. Collectively, these studies suggest that QTc prolongation is not merely an incidental ECG finding but may reflect the severity of systemic cardiovascular involvement accompanying progressive liver disease. The present finding of sinus tachycardia as another common ECG abnormality is also compatible with the pathophysiology of advanced CLD. Although the cited studies primarily emphasized QTc rather than sinus tachycardia, the findings of Premkumar et al. (2021) provide a relevant physiological context. Their review described the importance of altered circulatory physiology and bedside haemodynamic assessment in cirrhosis and highlighted the frequent presence of cirrhotic cardiomyopathy in advanced disease [13]. Thus, the increased prevalence of tachycardia in decompensated patients in the present study may represent part of the broader haemodynamic and autonomic alterations associated with advanced CLD. Left ventricular diastolic dysfunction was the predominant echocardiographic abnormality, while a substantial proportion of patients also demonstrated reduced or mid-range ejection fraction. These findings are consistent with the concept of cirrhotic cardiomyopathy, in which impaired relaxation and abnormalities of myocardial function may occur before overt clinical heart failure. Karagiannakis et al. (2023) reported LVDD in cirrhotic patients, although its prevalence varied considerably according to the diagnostic criteria used [16]. The results also agree with Reddy et al. (2026), who evaluated patients with NAFLD and demonstrated progressive echocardiographic abnormalities with increasing sonographic severity of fatty liver [17]. Their study showed increasing ventricular dimensions and LV mass together with reductions in ejection fraction and E/A ratio, while the prevalence of LVDD progressively increased with increasing NAFLD grade [17]. Elsawaby et al. (2019) similarly identified LV diastolic dysfunction among patients with NAFLD and demonstrated a significantly prolonged QTc interval compared with healthy controls. Their finding that QTc correlated with liver size, steatosis grade, and NAFLD activity score is particularly relevant to the present study because it supports an association between the severity of hepatic pathology and electrophysiological cardiac abnormalities [18]. The ultrasonographic findings in the present study demonstrated frequent evidence of advanced hepatic disease and portal hypertension, particularly ascites, splenomegaly, coarse hepatic echotexture, and portal vein dilatation. These findings provide an important hepatic context for interpreting the cardiovascular abnormalities. The association between increasing ascites severity and LVDD in the present study suggests that ultrasonographic markers of hepatic decompensation may also identify patients at greater risk of cardiac dysfunction. Premkumar et al. (2026) provided complementary evidence in a much larger cohort of cirrhotic patients with AKI, where cirrhotic cardiomyopathy was particularly frequent among patients with HRS-AKI and was associated with adverse outcomes [13]. Their findings emphasize that cardiac dysfunction in advanced cirrhosis has clinical consequences extending beyond echocardiographic abnormalities, particularly in patients with renal dysfunction and haemodynamic instability [19]. The findings of Premkumar et al. (2021) further support the clinical relevance of integrated ultrasonographic and cardiac assessment. Their review emphasized point-of-care echocardiography and inferior vena cava assessment for volume status and haemodynamic management in critically ill patients with cirrhosis [13]. The integrated nature of the present study is further supported by the work of Lopez Alcaraz et al. (2025) [8]. Using large ECG databases and machine-learning models, they demonstrated that ECG features could discriminate alcoholic liver disease and hepatic failure, with QTc duration consistently identified as an important predictive feature. Although their approach differs substantially from the conventional clinical assessment used in the present study, both studies reinforce the potential of ECG-derived information as a non-invasive marker of liver disease. Not all previous studies have demonstrated an equally strong relationship between cardiac abnormalities and liver disease severity. Somani et al. (2014), for example, reported mild diastolic dysfunction in a proportion of cirrhotic patients but did not find significant differences in echocardiographic parameters between compensated and decompensated disease or a significant relationship with MELD scores. Their 12-month follow-up also did not demonstrate a significant survival difference according to the presence of diastolic dysfunction [11]. This contrasts with the present study, in which LVDD was significantly associated with the severity of ascites and ECG abnormalities were significantly more frequent in decompensated disease. Differences in sample size, disease spectrum, diagnostic definitions, study design, and the proportion of patients with advanced decompensation may account for these differing observations. This study was limited by its cross-sectional, single-center design, which precludes establishing causal relationships or assessing the long-term prognostic significance of the observed cardio-hepatic abnormalities. The relatively small sample size and predominance of decompensated CLD may limit generalizability to compensated disease and other populations. Furthermore, advanced echocardiographic techniques such as strain imaging and stress echocardiography were not performed, which may have limited detection of subtle myocardial dysfunction. Further multicenter prospective studies incorporating advanced echocardiographic techniques and long-term follow-up are warranted to validate these findings and determine their prognostic significance.

he present study demonstrates that cardiovascular abnormalities are highly prevalent among patients with chronic liver disease and become increasingly common with advancing hepatic decompensation. Electrocardiographic abnormalities, particularly QTc prolongation and sinus tachycardia, were observed in the majority of patients, while echocardiography identified left ventricular diastolic dysfunction as the predominant manifestation of cirrhotic cardiomyopathy. Abdominal ultrasonography revealed advanced portal hypertension and hepatic decompensation in a substantial proportion of the study population. Importantly, significant correlations were observed between electrocardiographic abnormalities, echocardiographic dysfunction, and ultrasonographic markers of advanced liver disease. The coexistence of abnormalities across all three modalities in a large proportion of patients highlights the close pathophysiological relationship between hepatic dysfunction and cardiovascular impairment. These findings support the routine incorporation of electrocardiography, transthoracic echocardiography, and abdominal ultrasonography into the evaluation of patients with chronic liver disease. Early identification of subclinical cardiac involvement may improve risk stratification, guide peri-procedural evaluation before interventions such as TIPS or liver transplantation, and facilitate timely management to reduce morbidity and mortality.

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