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 Table of Contents  
Year : 2021  |  Volume : 8  |  Issue : 4  |  Page : 383-389

Echocardiographic abnormalities in patients with chronic liver disease: Observations from Thrissur, Kerala, India

1 Department of Medicine, Government Medical College, Thrissur, Kerala, India
2 Department of Gastroenterology, Government Medical College, Thrissur, Kerala, India
3 Department of Cardiology, Government Medical College, Thrissur, Kerala, India

Date of Submission28-Oct-2021
Date of Acceptance23-Nov-2021
Date of Web Publication22-Dec-2021

Correspondence Address:
Dr. Mukundan Chelakkat
Department of Cardiology, Government Medical College, Thrissur 680596, Kerala.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mgmj.mgmj_84_21

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Background: Chronic liver disease is an important cause of mortality as well as morbidity all over the world. Cirrhosis causes clinical manifestations extending beyond the liver. In patients with chronic liver disease, the cause of mortality is usually related to the liver pathology, but extrahepatic manifestations of chronic liver damage contribute significantly to the morbidity. With regards to the cardiovascular system, the manifestations are due to circulatory disturbances and cardiac dysfunction. Among all etiologies, cirrhotic cardiomyopathy is the cardiac dysfunction secondary to chronic liver disease. Objective: To study the echocardiographic abnormalities in patients with chronic liver disease. Materials and Methods: This was a cross-sectional study that was conducted on 80 patients in a tertiary care center. All etiologies for chronic liver disease were included. The diagnosis was confirmed by clinical features, laboratory and imaging criteria, and endoscopic evidence, and the duration of the abnormalities was to be persistent for more than six months. Echocardiography was done within one week of conducting the investigations. Echocardiography was done by the same cardiologist, who was a part of the study group, for all the patients. Results: The study cohort included 69 males and 11 females. The age ranged from 36 years to 76 years. The most common abnormality noted was left ventricular hypertrophy 48 (60%). Diastolic dysfunction was observed in 33 (41.5%). The other abnormalities noted include: left ventricular dilatation 5 (6.25%), dilated left atrium 13 (16.25%), increase in pulmonary artery pressure 15 (18.75%), and right ventricular dysfunction 10 (12.5%). Conclusion: Cirrhotic cardiomyopathy is a common but silent entity. A high index of suspicion is to be kept for this entity while managing patients with cirrhosis. The existence of this entity, if known, will be helpful in the management of patients during procedures or diseases that place stress on the heart. The use of newer modalities of imaging such as tissue Doppler imaging and two-dimensional speckle tracking echocardiography is more sensitive than conventional echocardiography for identifying cardiac dysfunction.

Keywords: Chronic liver disease, cirrhotic cardiomyopathy, diastolic dysfunction

How to cite this article:
Jacob MG, Sebastian S, Paul G, Chelakkat M, NM A, Joy BA, Afsal M. Echocardiographic abnormalities in patients with chronic liver disease: Observations from Thrissur, Kerala, India. MGM J Med Sci 2021;8:383-9

How to cite this URL:
Jacob MG, Sebastian S, Paul G, Chelakkat M, NM A, Joy BA, Afsal M. Echocardiographic abnormalities in patients with chronic liver disease: Observations from Thrissur, Kerala, India. MGM J Med Sci [serial online] 2021 [cited 2022 Aug 13];8:383-9. Available from: http://www.mgmjms.com/text.asp?2021/8/4/383/333331

  Background Top

Chronic liver disease is an important cause of mortality as well as morbidity all over the world. The same is true for India and especially the state of Kerala, where there is considerable alcohol consumption. Chronic liver disease is characterized by persistent parenchymal damage extending beyond six months. The damage to the hepatic parenchyma is followed by the collapse of the framework and subsequent collagen deposition, fibrosis, nodular formation, and distortion of the vascular bed. The ongoing process of damage and regeneration leads to fibrosis and cirrhosis. The causes of chronic liver disease include genetic, metabolic, alcohol, chronic infections, metabolic syndrome, toxins, and autoimmune diseases.

Cirrhosis causes clinical manifestations extending beyond the liver. Neurological, dermatological, hematological, and pulmonary involvement are some of the well-recognized extrahepatic manifestations of cirrhosis.[1] In patients with chronic liver disease, the cause of mortality is usually related to the liver pathology, but extrahepatic manifestations of chronic liver damage contribute significantly to the morbidity.[2] With regards to the cardiovascular system, the manifestations are due to circulatory disturbances and cardiac dysfunction. In liver diseases other than due to chronic hepatitis C and nonalcoholic steatohepatitis, the lipid profile is favorable and protects against the development of ischemic heart disease.[3],[4]

Chronic hepatitis C has an association with myocardial ischemia and cardiomyopathy. The major cause of mortality in nonalcoholic fatty liver disease is cardiovascular events. Wong et al.[5] were able to bring out the strong association between fatty liver and coronary artery disease. Cardiac dysfunction in liver disease was initially attributed to alcohol-related liver disease. However, now it is known that it is seen across the entire spectrum of liver disease, whatever may be the etiology of the liver dysfunction, and is known by the term “cirrhotic cardiomyopathy.”[6],[7] Even though it was previously believed that patients with cirrhosis are protected from the development of coronary artery disease, now studies have shown that these patients are likely to have asymptomatic myocardial ischemia.[8],[9] The existence of cardiomyopathy in patients with liver disease has been recognized for a long time. In the beginning, it was attributed to alcohol-induced cardiomyopathy.

Now the concept has been changed to cirrhotic cardiomyopathy, in which liver disease of any cause has been implicated as the cause of cardiomyopathy. The components of cirrhotic cardiomyopathy are impaired cardiac response to stress, diastolic dysfunction, and electrophysiological abnormalities in the absence of cardiac disease.[10] The circulatory disturbances in cirrhosis include peripheral vasodilatation, low blood pressure, an increase in pulse rate, and cardiac output.[11] This hyperdynamic state is produced by splanchnic vasodilatation mediated by nitric oxide, carbon monoxide, and endogenous cannabinoids. The low effective arterial blood volume leads to decreased cardiac output and decreased renal perfusion, leading to salt and water retention. In cirrhosis, the contractile function of the heart is normal at rest, but under stress, the left ventricular ejection fraction is suboptimal. Most patients with cirrhosis have a normal systolic function on echocardiography.[12] The mechanism of the systolic dysfunction on exertion is decreased myocardial reserve and blunted heart rate response to stress. Similarly, diastolic dysfunction is also found in cirrhotics, which may be evident even at rest. Diastolic dysfunction in cirrhosis is attributed to myocardial fibrosis and hypertrophy.[13] Diastolic dysfunction may be a forerunner of systolic dysfunction in cirrhosis. The hyperdynamic state and peripheral vasodilation mask the adverse consequences of decreased cardiac output. The mediators for the hyperdynamic state, by their inhibitory effects on the myocardium, are believed to be responsible for the cardiomyopathy.[14]

The deleterious effects of cirrhotic cardiomyopathy extend beyond the heart. These are believed to underlie the development of the hepatorenal syndrome and cardiorenal syndrome.[15],[16] Another important aspect of recognizing the presence of cardiac involvement in cirrhosis is the role played by it in the development of various cardiac complications after the TIPS procedure. The most common complication after TIPS is pulmonary edema. Cardiac involvement in cirrhotics is a major contributing factor to the poor outcome after a liver transplant, implying that cardiac function evaluation is an important factor to be considered while considering liver transplant.[17],[18] A detailed evaluation of the cardiac status is, thus, warranted in the treatment algorithm of cirrhosis.

The state of Kerala has a high prevalence of the alcohol-related liver disease. Similar to the rest of India, Kerala also has its share of diabetes, hypertension and coronary artery disease, and chronic kidney disease. Because of the coexistence of these diseases, all of which can affect the heart in their way, dyspnea is a common denominator in many patients. Early investigations and proper accounting of the reason for dyspnea are important in the appropriate management of these patients. Clinical manifestations of the cardiac abnormalities may be evident only on exertion. Patients with cirrhosis can have exertional dyspnea due to other causes such as ascites, Porto-pulmonary hypertension, hepatopulmonary syndrome, and anemia. Echocardiography is a reasonable investigation modality to pick up the cardiac abnormalities in this scenario. So we ventured into this project to determine the echocardiographic abnormalities in patients with chronic liver disease.


To study the echocardiographic abnormalities in patients with chronic liver disease.

  Materials and methods Top

This was a cross-sectional study that was conducted in a tertiary care center. The study setting was the departments of Medicine, Gastroenterology, and Cardiology. Overall, 80 consecutive patients who satisfied the inclusion criteria were studied, after getting their informed consent. The study period was for one year, from January 2020 to January 2021.

Inclusion criteria

  1. Patients with chronic liver disease confirmed by clinical features, laboratory, and imaging evidence.

  2. All etiologies for liver disease were included in the study.

Exclusion criteria

  1. Patients younger than 18 years.

  2. Patients with associated diseases that could contribute to systolic or diastolic dysfunction such as hypertension, diabetes mellitus, valvular heart disease, congenital heart disease, ischemic heart disease, or cardiomyopathy.

  3. Those patients on drugs that could impair cardiac function were also not included.

The diagnosis was confirmed by clinical features, laboratory and imaging criteria, and endoscopic evidence. The duration of the abnormalities was to be persistent for more than six months. The clinical features included jaundice, upper gastrointestinal bleeding, ascites, and hepatic encephalopathy. The blood investigations done included complete blood count, liver function tests, renal function tests, fasting and postprandial blood sugars, and coagulation profile. The laboratory investigations to diagnose chronic liver disease included hypoalbuminemia, thrombocytopenia, and coagulopathy. Serum albumin value less than 3.5g % was considered hypoalbuminemia. Platelet count less than 1 lakh/mm3 and Prothrombin time more than 3 sec beyond the control value were considered the cutoff points. Ultrasound evidence of chronic liver disease included changes in the echotexture of the liver, dilatation of portal vein, ascites, splenomegaly, and the presence of portosystemic collaterals. Endoscopy was done if needed to confirm the presence of portal hypertension. Whenever possible, the upper gastrointestinal scope was performed to look for varices. The size of the varices was classified as small or large varices. The evidence of band ligation of the varices was also considered. Echocardiography was done within one week of doing the investigations. Echocardiography was done by the same cardiologist, who was a part of the study group, for all the patients. Echocardiography was done for all patients, and the following details were looked into:

  1. Left ventricular (LV) function was done by M mode and by Simpsons technique.

  2. LV diastolic dysfunction was assessed by mitral Doppler, E/A ratio, Tissue Doppler of both lateral and medial annulus of Mitral valve, and E/e’ ratio.

  3. The presence of mitral regurgitation was assessed by color Doppler examination.

  4. The presence of PAH was assessed by the gradient of the tricuspid regurgitation jet.

  5. The presence of RV dysfunction was assessed by TAPSE.

  6. The presence of pericardial effusion was noted.

  7. Any other abnormality present was also noted.

Statistical analysis

All data were entered into the proforma and then into a Microsoft Excel 2007 spreadsheet. The data were analyzed by using Statistical Package for the Social Sciences (SPSS) software. Continuous variables were expressed as the appropriate means and standard deviations or medians and interquartile ranges. Categorical variables were summarized as the counts and percentages in each category. Informed consent from the patients and clearance from the Institutional Ethical Committee were obtained.

  Results Top

The total number of patients studied was 80: Among these, 69 were males (86.2%) and 11 were females (13.75%). The age distribution of the patients was from 36 to 76 years. The mean age of the patients was 55 years. There were 27 patients in the age group 30–50 years, 36 in the age group 51–60 years, and 17 patients older than 60 years. The maximum number of patients were in the age group 30–60 years [Table 1].
Table 1: Echocardiographic findings of the study cohort

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Left ventricular hypertrophy, as measured by either left ventricular interventricular septum dimensions or left ventricular posterior wall dimensions more than 11 mm, was observed in 48 (60%) patients. Left ventricular dilatation as evidenced by left ventricular internal dimensions in a diastole more than 59 mm or end-diastolic volume more than 150 mL was seen in five (6.25%) patients. Systolic dysfunction at rest was seen in only one patient, who also had diastolic dysfunction. Overall, 33 patients (41.25%) had diastolic dysfunction. Of the 33 patients with diastolic dysfunction, 24 had only ventricular dysfunction without an associated increase in pulmonary artery pressure. Increased pulmonary artery systolic pressure was seen in 15 (18.75%) patients, of whom seven had isolated raised pulmonary artery pressure without any abnormality of the left heart. Right ventricular dysfunction was seen in 10 (12.5%) patients, among whom six had right ventricular dysfunction with normal pulmonary artery pressure.

  Discussion Top

Dyspnea is a common symptom in patients with cirrhosis and there are several mechanisms for the same. The presence of ascites and subsequent elevation of the diaphragm is the common cause. Respiratory complications such as hepatopulmonary syndrome and portopulmonary hypertension and left ventricular dysfunction secondary to myocardial ischemia or cardiomyopathy can also contribute to dyspnea. Patients with chronic hepatitis C have an association with idiopathic pulmonary fibrosis.[19]

The concept of cardiac involvement in chronic liver disease was first considered in 1953.[20] The initial connection between the liver and the heart was attributed to the toxic effect of alcohol on the heart. The hyperdynamic circulatory state was observed by Kowalski et al.[20] The clinical entity of cirrhotic cardiomyopathy was first put forward by Lee et al.,[21] and now it is a well-recognized entity. Cirrhotic cardiomyopathy is characterized by hyperdynamic circulatory state, systolic dysfunction during periods of stress, diastolic dysfunction, prolonged ventricular repolarization, and a lack of response of heart rate to stress.[10],[22],[23] These changes occur in cirrhotics in the absence of other causes for cardiac dysfunction. Cirrhotic cardiomyopathy is seen in up to 50% of patients with cirrhosis. The fact that cardiac involvement is seen in chronic liver disease of all etiologies, and not only in alcoholic liver disease was an important landmark. This made it obvious that the reason for the cardiac involvement is not alcohol-related toxins. Cardiac abnormalities may be seen in all stages of liver disease. The development of hepatorenal dysfunction may herald the presence of underlying cardiac disease.[24] The reasons postulated for these changes include a defect in the beta receptor signaling downregulation of beta1 and beta2 receptors,[1] impairment in the cardiac myocyte plasma membrane function,[25] abnormalities in the calcium kinetics, and the role of factors such as nitric oxide, carbon monoxide, and endogenous cannabinoids. Patients with cirrhosis have high levels of nitric oxide, carbon monoxide, endocannabinoids, and other vasodilators. There are increased levels of cGMP, which, in turn, inhibits cAMP. cAMP is responsible for the influx of calcium and myocardial contractility. Thus, patients with cirrhosis have impaired systolic function and blunted heart rate response to stress.[26],[27],[28] Another postulated mechanism is the increased sympathetic activity, secondary to splanchnic vasodilation, causing downregulation of the cardiac receptors and impaired calcium channel function.[26] Diastolic dysfunction usually precedes the development of systolic abnormality. Diastolic dysfunction is believed to be due to impaired potassium channel activity, leading to impaired relaxation. Cirrhotics with deranged cardiac function are asymptomatic for long periods unless they are exposed to stress such as bacterial infections, liver transplantation etc. Besides the implications on cardiac function, it is also postulated to contribute to the development of hepatorenal syndrome, making the recognition of this entity all the more important. A high level of suspicion for this entity should be maintained because the symptoms may be attributable to other conditions inherent to the liver disease. Early intervention, before the development of overt cardiac dysfunction, may have the capacity to alter the prognosis. The echocardiographic findings are also nearly normal in the resting state. Thus, altogether the confirmation of cardiac involvement in cirrhosis is difficult. Hence, the exact epidemiology and natural history are also difficult to ascertain. The biomarkers that may help in the diagnosis include BNP, adrenomedullin, Galectin- 3, and QT prolongation in the electrocardiography (ECG).

The most common abnormality observed in echocardiography in cirrhotics is left ventricular hypertrophy. For us also, the most common abnormality noted was left ventricular hypertrophy (n = 48, 60%). In the study by Anish et al.,[29] left ventricular hypertrophy was seen in 47% of patients. Other investigators also noticed a common occurrence of left ventricular hypertrophy.[30],[31]

Diastolic dysfunction is more frequent and occurs earlier than systolic dysfunction in cirrhotic cardiomyopathy. The mechanism of diastolic dysfunction is the left ventricular hypertrophy, fibrosis, and subendothelial edema,[6],[28] retention of sodium and water, and alteration of titin protein modulation.[32] The diastolic dysfunction in cirrhosis is seen both at rest and on exertion.[6],[33] In this study, 33 (41.25%) patients had diastolic dysfunction. In other studies, the presence of diastolic dysfunction ranged between 30% and 40%.[12],[29],[34],[35],[36] In the study by Asmaa et al.,[37]where cirrhotics were compared with normal controls, there were significantly higher values of E, A, and deceleration time in cirrhotics, and 30% of patients had diastolic dysfunction.

In cirrhotics, due to the hyperdynamic circulatory state, the ejection fraction may be higher when compared with normal. By conventional echocardiography, Asmaa et al.[37] noted a significant increase in LV systolic function as reflected in the ejection fraction by the M-mode in patients with cirrhosis; however, such a significant increase was not noted with 2D. Others also have noted an increase in the ejection fraction, but which was not statistically significant.[29],[36] Majority of the studies have shown that systolic function is normal at rest. The mechanism postulated for the normal systolic function is the peripheral vasodilation and the reduced afterload, which compensates for the decrease in preload and contractile dysfunction. In fact, during rest, the ejection fraction in cirrhosis may be supranormal. When put under stress, these compensatory mechanisms become inadequate.

The theories put forward for the impaired systolic function during stress include downregulation of the beta receptors,[38] increased cannabinoid signaling pathway,[39] and increased bacterial translocation.[40] During stress, the failure of the heart rate to increase, the reduced myocardial contractility due to downregulated beta receptors along with the skeletal muscle wasting seen in cirrhosis, is responsible for the decreased ejection fraction.[28] In the 2005 World Congress of Gastroenterology, Montreal, the criteria for systolic dysfunction were set as an ejection fraction below 55% and failure of an adequate rise in cardiac output after stress.[41] We observed systolic dysfunction at rest in only one patient. A similar observation was also noticed by many others.[12],[29],[35],[42] On the contrary, Kazankov et al.[43] have opined that even at rest, the systolic function is impaired in cirrhotics.

We noticed left ventricular dilatation in five patients (6.25%) and increased left atrial diameter in 13 (16.25%). Vandana et al.[42] noted higher diameters of the atria in cirrhotics when compared with controls, but no difference in the ventricular diastolic diameters. The LV dimensions were normal in other studies.[12],[35] Alcoholic cardiomyopathy is an entity that closely mimics cirrhotic cardiomyopathy. One of the differences between the two entities is the dilated left ventricle seen in alcohol-related cardiomyopathy. Alcoholic cardiomyopathy has a lesser prevalence than alcoholic liver disease. However, the two can coexist in 10%–20% of cirrhotics.[41]

Many studies have noted an increase in pulmonary artery pressure in cirrhotics. We observed increased pulmonary artery pressure in 15 patients (18.75%). Of the 15 patients, seven had isolated elevation of pulmonary artery pressure, whereas eight had associated diastolic dysfunction. Anish et al.[29] noted pulmonary artery hypertension in 33% of patients. Others also have noticed similar findings.[36],[42],[44]

We observed right ventricular dysfunction in 10 patients (12.5%). Previous studies have not observed right ventricular abnormal function by routine echocardiography.[45] By employing newer modalities such as global and layer-specific strains, Zhang et al.[46] were able to demonstrate right ventricular abnormalities.[46] It may be difficult to get a clinical correlate for this echocardiographic finding in patients with cirrhosis, because the presence of edema and breathlessness may be attributed to ascites. Among the 10 patients, six had right ventricular dysfunction with normal pulmonary artery pressure, of whom three had isolated right ventricular dysfunction without left ventricular abnormality. As a contradistinction to the observation made by Zhang et al.,[46] we observed right ventricular dysfunction in the absence of coexistent elevated pulmonary artery pressure.

Normal echocardiographic findings were observed in 10 patients (12.5%). Prahlad et al.[12] noted normal echocardiogram in 23%. Asmaa et al.[37] have noticed that by conventional echo all the parameters are normal in cirrhotics. They were able to pick up more cases of diastolic dysfunction by the advanced modes of echo. The usual echocardiography is not sensitive enough to pick up systolic dysfunction. This needs more sophisticated measures such as tissue Doppler imaging and speckle tracking echocardiography.[47],[48],[49] Such advanced techniques have thrown more insight into the cardiac changes occurring in cirrhotic cardiomyopathy, such as right ventricular diastolic dysfunction.

  Conclusion Top

Cirrhotic cardiomyopathy is a common but silent entity. A high index of suspicion is to be kept for this entity while managing patients with cirrhosis. The existence of this entity, if known, will be helpful in the management of the patient during procedures or diseases that place stress on the heart. Diastolic dysfunction is more common than systolic dysfunction. These abnormalities need not have any relation to the severity of the laboratory and imaging abnormalities. This diagnosis should be diligently sought, especially in those patients in whom liver transplantation is considered. The use of newer modalities of imaging such as tissue Doppler imaging and two-dimensional speckle tracking echocardiography is more sensitive than conventional echocardiography to pick up cardiac dysfunction. The presence of cirrhotic cardiomyopathy cannot be picked up well by routine echocardiography. The use of advanced modalities and stress echocardiography is needed for this purpose.

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Conflicts of interest

There are no conflicts of interest.

Ethical consideration

The present study, the informed consent documents from the patients, and any subsequent modifications were reviewed and approved by the Institutional Ethics Committee, Government Medical College, Thrissur, Kerala, India vide their letter dated 07-11-2021.

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