European Journal of Cardiovascular Medicine

Liver cirrhosis is a disease that can cause several problems, some of which might be fatal in the long run. Numerous alterations in the circulatory system are linked to chronic liver disease. Hyperdynamic circulatory syndrome is a disorder that is observed in patients with advanced cirrhosis. Spontaneous blood pooling, portal systemic collateral opening, arterial vasodilatation, and a compensatory rise in blood volume are its defining features. The events that follow in the autonomic regulatory system lead to a decrease in peripheral vascular resistance and an increase in cardiac output.^[1] Kowalski and Abelmann were the first to report the presence of cardiac dysfunction in liver disease cases, pointing to a lower systemic vascular resistance and a greater resting cardiac output. Numerous investigations were conducted following this discovery, and it was found that there was hyperdynamic circulation, which was defined by elevated cardiac output and peripheral vasodilatation.^[2,3] Typically, the factors that produce chronic liver diseases, whether related to ethanol or not, do not influence its prevalence.^[4]

Early stages of cirrhosis rarely observe or clinically evoke the hyperdynamic form of circulation. But as the illness advances into more advanced phases, there is a general correlation between the degree of hyperdynamic circulation and the severity of the sickness. The venous return and heart rate rise in response to an increase in cardiac output. Patients with cirrhosis experience a disturbed heart rate, which is a circadian variable. Patients with cirrhosis of any source may display poor chronotropic reflexes, and the frequency of these symptoms rises with the severity of the disease.^[5] The majority of these pathophysiological mechanisms are active in advanced cirrhosis. Vasodilatation (low systemic vascular resistance), the presence of arteriovenous connections, expanded blood volume, and enhanced sympathetic nerve activity may further raise the cardiac output.^[6,7]

Blood and plasma volumes will rise in cases of severe cirrhosis as well, but the distribution of these volumes between central and non-central vascular regions will become uneven.^[8] Patients with cirrhosis will have decreased ventricular contractility in addition to hyperdynamic circulation. It was previously believed that this cardiovascular function was a sign of latent alcoholic cardiomyopathy. However, research on patients who were alcoholists and those who were not showed the same type of cardiovascular manifestation, ruling out alcohol as a cause and establishing that the impaired ventricular contractility was caused by cirrhotic changes in the liver, a common etiological factor in both groups.^[9,10,11] We dubbed these modifications "cirrhotic cardiomyopathy."^[12]

The characteristic features of cirrhotic cardiomyopathy include^[12]

• An attenuated systolic or diastolic response to stress stimuli,
• Structural or histological changes in cardiac chambers,
• Electrophysiological abnormalities, and
• Serum markers suggestive of cardiac

Therefore, a number of cardiovascular problems, such as hyperdynamic circulation-which is typified by a higher resting cardiac output, a lower systemic vascular resistance, and impaired ventricular contractility-are commonly linked to cases of liver cirrhosis. This study was conducted to determine the prevalence of diastolic and systolic dysfunction in cirrhosis,

AIMS AND OBJECTIVES

• To study the clinical profile of chronic liver disease cases admitted to Sri Chamundeshwari medical college hospital and Research institute, a tertiary care hospital.
• To investigate the cardiovascular structural and functional status of the aforementioned.

The Department of GENERAL MEDICINE AT Sri Chamundeshwari Medical College Hospital and Research Institute, Channapatna, carried out a hospital-based observational study involving 100 patients with chronic liver disease from August 2023 to January 2024, after receiving the signed informed consent from the study participants.

Inclusion Criteria

• Patients diagnosed with chronic liver disease above the age of 20 years were included in the study

Exclusion Criteria

• Patients with other known etiologies of cardiac
• Patients with severe
• Patients with HIV infection
• Patients with hepatorenal syndrome

Sample Size Calculation

The sample size was estimated by using the proportion of diastolic dysfunction among alcoholic liver disease subjects detected by ECHO as 64% from the study by A. Batra et al. using the formula

P = 64 or 0.64

q = 36 or 0.36

d = 15% or 0.15

Using the above values at a 95% confidence level, a sample size of 40 subjects with chronic   liver disease were included in the study. Considering 10% nonresponse, a sample size of 40 + 4 = 44 subjects were included in the study. However, we have considered 100 samples in this study.

Statistical Methods

SPSS 22 version software was used for data analysis after the data was entered into a Microsoft Excel data sheet. Frequencies and proportions were used to depict categorical data. Chi-square was employed as a significance test. The mean and standard deviation were used to depict continuous data. A p-value (probability that the result is true) of <0.05 was considered statistically significant after assuming all the rules of statistical tests. MS Excel and SPSS version 22 (IBM SPSS Statistics, Somers NY, USA) were used to analyse the data.

34% of the study participants were under 40 years old, 40% belonged to the 41–60 age group, and 26% belonged to the 61–80 age group. In the study, there were 4% female participants and 96% male participants.

Throughout the trial, there were increases in total bilirubin (79%), direct bilirubin (92%), albumin levels (96%), AST (84%), and ALT (56%).

A total of 22% had increased LA diameter, 78% had increased PWd, 70% had diastolic diameter, 26% had decreased ejection fraction (<50%), 26% had RWMA, 12% had increased IV Sd, 46% had increased IV Ss, 52% had LV hypertrophy, and 100% had normal LV diameter, both systolic and diastolic.

The study found significant relationships between the etiology of LV hypertrophy, diastolic dysfunction, EF%, and RWMA.

Twenty percent had EF <50%, 17.5% had RWMA, 45% had LVH, and 72.5% had diastolic dysfunction among those with alcohol as the cause.

66.7% of patients with LVH, 100% with diastolic dysfunction, 66.7% with EF <50%, and 0% with RWMA had alcohol + HBsAg as the cause.

100% of patients with LVH, 25% with diastolic dysfunction, 50% with EF <50%, and 75% with RWMA had HBsAg as the cause.

HCV was the cause for 66.7% of patients with LVH, 33.3% with diastolic dysfunction, 66.7% with EF <50%, and 100% with RWMA.

Nearly 96% of the 100 patients with chronic liver disease in our study were male, and the bulk of them were in the 41–60 age range. The prevalence of chronic liver disease in that age range and among men suggests that alcohol intake is higher in men and middle-aged people, and as a result, alcoholic-related liver disease is more common in those populations.

The age range of liver disease patients in our investigation was comparable to that of Wong F. et al. findings.^[13] Similar to the results of our investigation, other studies conducted by Wong F. et al., Liu P. et al., and Pozzi M.^[14] et al also demonstrated the male preponderance of liver disease. These investigations also revealed a link between male alcohol use and the liver illness that affects them.

In our study, alcohol consumption was the cause of nearly 80% of the cases, and 6% of the patients tested positive for hepatitis B. In the Wong F. et al., study, alcohol intake was the cause of chronic liver disease in 68.5% of patients, while chronic hepatitis was the cause in 17.1% of cases.

There was no discernible relationship between any specific cause and the cardiac anomalies observed in the cohort. This highlights the significance of latent cardiac anomalies in individuals with cirrhosis, regardless of the reason for screening.

This observation is also consistent with the findings of the Pozzi M. et al. study, which indicated that the diastolic dysfunction in the subjects was unlikely to be due to the harmful effects of ethanol on the heart and that there was no difference between the cardiac abnormalities caused by alcoholic cirrhosis and those caused by post-viral cirrhosis.

Cirrhosis causes peripheral vasodilatation, which "treats" the ventricle by lowering afterload through systemic vasodilation and reducing inhibitory factors like the cardiac muscarinic system to make up for it. This means that overt heart failure symptoms are not common.^[15] Patients complained of ascites, peripheral fluid retention (dependent edema), dyspnea, and impaired exercise capacity; nevertheless, these symptoms are typical of advanced cirrhosis as well as heart failure. Therefore, it can be challenging to diagnose people with symptomatic heart failure based just on their symptoms. The sole distinguishing characteristic is that, rather than being linked to pulmonary vascular congestion or overt pulmonary edema, dyspnea in cirrhosis is typically associated with hydrothorax from ascetic fluid tracking into the pleural cavity or tense ascites pressing up against the respiratory diaphragms. Such pulmonary congestion, whether from cirrhotic cardiomyopathy or other reasons, strongly suggests a diagnosis of heart failure.

One of the effects of chronic liver illness is liver injury. All forms of liver injury will result in elevated AST and ALT levels, both directly and indirectly.

Serum bilirubin levels were higher in approximately 79% of the cases, while direct bilirubin levels were higher in 92% of the cases. Additionally, we found higher than normal AST and ALT readings in between 84% and 56% of the instances.

Serum albumin is a crucial factor in determining how well the heart works since fluctuations in albumin levels that result in hypoalbuminia can lead to increased preload on the heart from fluid retention in the body, which can induce cardiac diastolic dysfunction. In our investigation, hypoalbuminea was also observed in close to 96% of the cases. According to Huonker M et al,^[16] hypoalbuminemia also raises the heart's preload.

In most cases, the echocardiographic values in cirrhosis were higher than normal. All of the cases in our investigation had normal left ventricular diastolic and systolic dimensions, with no statistically significant difference observed in either. Our study's results were in line with those of Valeriano et al.^[17] and J. Alexander et al.,^[18] but they differed from those of previous studies that found reduced left ventricular sizes.

In 74% of the instances, the left ventricular ejection fraction was determined to be greater than 50%. A small number of research has reported that the presence of subclinical alcohol cardiomyopathy in alcoholic individuals has been linked to a larger ejection fraction in cirrhosis due to pure viruses than in cirrhosis caused by alcohol.

In another study, Wong et al. and Pozzi et al. discovered that the mean left ventricular ejection percent was within normal bounds.

In our study, we observed left ventricular hypertrophy in approximately 52% of the cases; Wong et al. and Pozzi et al. also reported left ventricular hypertrophy in instances involving liver illness.

Nearly 30% of the cases in our study had diastolic dysfunction; similar findings were reported by Alexander et al. and Ajmal M. R. et al. in their studies on liver illness. Batra A et al. found diastolic dysfunction in approximately 64% of cirrhosis cases.

Echocardiographic alterations such as left ventricular hypertrophy, left ventricular diastolic and systolic diameter, left arterial diameter, and even a considerable LVEF indicating hyperdynamic circulation were also detected in the study conducted by Ajmal M. R. et al.,^[19] Finnuci G. et al.,^[20] and Alexandaer et al.

It is crucial to remember that cardiac dysfunction in cirrhosis might still exist, even in cases where echocardiographic values are normal. Individuals diagnosed with cirrhosis exhibit elevated nitric oxide production. This vasodilator substance not only contributes to the pathophysiology of cardiac contractile failure, but it also causes systemic arterial vasodilatation. Thus, even in the event of contractile failure and lower preload, the heart is able to sustain a normal cardiac output due to the reduction in afterload.

Chronic liver disease affects practically every other organ in the body, including the cardiovascular system. It is a systemic illness with broad functional implications. Certain cirrhosis-related systemic consequences, like hepatopulmonary syndrome, acute and chronic encephalopathy, and HRS, have clear diagnostic and therapeutic criteria in place.

Cardiovascular dysfunction in liver cirrhosis patients has been observed since 1960; however, it hasn't been thoroughly described or characterized until recently.

Cardiocirculatory dysfunction is typically a subclinical condition during the natural course of liver disease and only becomes apparent in specific clinical scenarios. For instance, cirrhotic cardiomyopathy plays a significant role in the etiology of HRS. Furthermore, after TIPS implantation, individuals with cirrhosis experience cardiovascular problems due to pre-existing diastolic dysfunction. Candidates for LT who are cirrhotic patients have a significant prevalence of asymptomatic CAD, according to recent cohort studies. The primary cause of non-graft-related mortality following LT is cardiovascular problems, while the prevalence of CAD is the primary contributor to post-LT outcomes. Furthermore, NAFLD—a significant contributor to liver disease-is a stand-alone risk factor for cardiovascular incidents. The necessity of a thorough cardiovascular risk assessment in individuals with chronic liver disease is highlighted by all of these results. It has been proposed that compared to the general population, people with advanced liver disease have a distinct risk-factor profile for cardiovascular disease. For the diagnosis and management of cardiovascular disease in this patient population, there aren't any particular recommendations in place at the moment. Therefore, more prospective studies are needed to come up with more accurate criteria and a consistent way to test for and treat cardiovascular dysfunction in people with liver cirrhosis.

It is crucial that doctors take note of the clinical manifestations of chronic liver disease, assess cardiac dysfunction using two-dimensional echocardiography, and begin treating diastolic dysfunction.

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