|Year : 2017 | Volume
| Issue : 1 | Page : 26-30
Echocardiographic study of left ventricular structure and function in Nigerian patients with chronic liver disease
Adewole A Adebiyi1, Okechukwu S Ogah1, Adegboyega Akere2, Jesse A Otegbayo2
1 Department of Medicine, Cardiology Unit, University College Hospital, Ibadan, Oyo State, Nigeria
2 Department of Medicine, Gastrointestinal Tract/Liver Unit, University College Hospital, Ibadan, Oyo State, Nigeria
|Date of Web Publication||10-Mar-2017|
Jesse A Otegbayo
Department of Medicine, Gastrointestinal Tract/Liver Unit, University College Hospital, Ibadan, Oyo State
Source of Support: None, Conflict of Interest: None
Background: The concept of cirrhotic cardiomyopathy includes impaired cardiac contractility, decreased beta-adrenergic receptor function, abnormal beta-adrenergic postreceptor function, defective excitation-contraction coupling, and cardiac conduction abnormalities. This study was aimed to assess the cardiac structure and function in adult Nigerians with chronic liver disease (CLD).
Methods: This was a cross-sectional descriptive study of consecutive patients with CLD without any known cardiac disease attending the Liver Clinic of the Medical Out-patient Department of the University College Hospital. Apparently, normal individuals with comparable age and sex distribution were recruited as controls. The subjects and controls underwent two-dimensional, M-mode and Doppler echocardiographic studies to determine the cardiac structure in relation to both systolic and diastolic cardiac functions.
Results: A total of 46 subjects and 50 normal controls were recruited. There was no difference in the blood pressure parameters of the two groups. The septal wall thickness was statistically higher in control, but this difference was lost when adjusted for body mass index. On the other hand, the adjusted left atrial diameter and aortic root dimension were statistically larger in the subjects than the controls. There was no difference in the left ventricular (LV) fractional shortening or ejection fraction, relative wall thickness, and deceleration time of the E-wave.
Conclusions: We demonstrated an increase in cardiac index at rest in the subjects, but there was no significant difference in the LV diastolic or systolic dysfunction using traditional methods. Studies using newer modalities of the assessment of cardiac structure and function are needed in our environment.
Keywords: Chronic liver disease, echocardiography, heart disease, Nigeria
|How to cite this article:|
Adebiyi AA, Ogah OS, Akere A, Otegbayo JA. Echocardiographic study of left ventricular structure and function in Nigerian patients with chronic liver disease. Nig J Cardiol 2017;14:26-30
|How to cite this URL:|
Adebiyi AA, Ogah OS, Akere A, Otegbayo JA. Echocardiographic study of left ventricular structure and function in Nigerian patients with chronic liver disease. Nig J Cardiol [serial online] 2017 [cited 2018 Jul 19];14:26-30. Available from: http://www.nigjcardiol.org/text.asp?2017/14/1/26/201907
| Introduction|| |
Chronic liver disease (CLD) is a major health problem in many developing countries such as Nigeria.,,,,, Although it is well-known that heart failure can lead to abnormalities of hepatic function as well as hepatic damage,, the full understanding that liver diseases can also cause cardiac dysfunction is relatively recent.,,,,,, This is as a result of advances in imaging and diagnostic techniques.
Kowalski and his colleagues were the first to report that, patients with cirrhosis have an abnormal cardiac function as well as prolonged QT interval., Patients with CLD have increased heart rate and cardiac output as well as decreased vascular resistance with normal or reduced arterial blood pressure.,,,, Factors responsible for increased cardiac output include increased sympathetic nervous activity, increased preload, and presence of arteriovenous malformations. The concept of cirrhotic cardiomyopathy, therefore, includes impaired cardiac contractility, decreased beta-adrenergic receptor function, abnormal beta-adrenergic postreceptor function, defective excitation-contraction coupling, and cardiac conduction abnormalities.,,,,, There are conflicting reports on the size of the heart chambers in CLD. Although some authors reported normal heart mass,, others have reported increased left ventricular mass (LVM).,
Most studies on the impact of CLD on cardiac structure and function have emanated from developed countries.,,, There are very few studies in Africa, and to the best of our knowledge, there has not been any similar study in Nigeria. The aim of this study, therefore, was to assess cardiac structure and function in adult Nigerians with CLD.
| Methods|| |
The study was cross-sectional case–controlled. Consecutive patients with CLD attending the Liver Clinic of the Medical Out-patient Department of the University College Hospital, Ibadan were recruited into the study. Subjects with coexisting medical conditions such as hypertension, congestive cardiac failure, arrhythmias, sickle cell disease, chronic renal disease, and those who did not give consent were excluded from the study. Apparently, normal individuals with comparable age and sex distribution as the subjects were recruited from health workers and relations of patients in our institution as controls. All the controls had a complete physical examination to exclude medical illnesses. Cases and controls gave informed consent before they were enrolled into the study. Ethical clearance was obtained from the institution's ethics review committee.
Baseline clinical and demographic characteristics were obtained from the subjects using a structured questionnaire. Information obtained included age, gender, occupation, marital status, history of diabetes mellitus, hypertension, history of smoking, and alcohol consumption. Other information obtained were past or present history of angina pectoris, myocardial infarction, transient ischemic attacks, cerebrovascular disease, hypertensive encephalopathy, renal failure, and left ventricular (LV) failure. This was followed by a complete physical examination. Their blood pressures were measured in the right arm with the subjects seated and rested for 5 min before the procedure and according to standard guidelines. Body mass index (BMI) and body surface area were calculated using standard formulae.
Two-dimensional guided M-mode echocardiography with the use of commercially available echo-machine (ALOKA SSD-1700) and a 2.5–5.0 MHz linear array transducer was performed on each subject in the left lateral decubitus position. Two experienced physicians performed the echocardiography. In our laboratory, the intraobserver concordance correlation coefficient has been reported and ranged from 0.76 to 0.98 while that of the inter-observer concordance ranged from 0.82 to 0.96. All measurements were made according to the American Society of Echocardiography leading edge to leading edge convention. The LV measurements taken include interventricular septal thickness at end-diastole, the posterior wall thickness at end diastole, and the LV internal dimensions at end systole and end diastole. Measurements were taken in three cardiac cycles and average of the three values calculated.
The LV inflow velocities were measured from the apical four-chamber view with the pulsed-wave Doppler sample volume positioned at the tips of the mitral leaflets. LV diastolic filling pattern was determined by the analyses of the mitral inflow velocities.
LVM was calculated using the formula that has been shown to yield values closely related to necropsy LV weight, and that has good inter-study reproducibility (r = 0.90). LV hypertrophy was considered present when LVM index exceeded 46.7 g/m 2.7 in women and 49.2 g/m 2.7 in men. LV systolic performance was calculated by Teichholz formula  Ejection fraction <50% was taken as impaired LV systolic function. Abnormal LV diastolic function (abnormal LV relaxation) was defined according to the European society of echocardiography guidelines  using the combination of E/A ratio (<1 up to 50 years, <0.5 over 50 years) and deceleration time of E-velocity (>220 ms up to 50 years, >280 over 50 years) or using IVRT (>92 ms up to 30 years, >100 ms between 31 and 50 years, and >105 ms over 50 years).
All data generated were entered into a standard pro forma. Continuous variables were expressed as mean (standard deviation), and categorical variables were expressed as percentages. Normality was assessed with Shappiro–Wilks test. Differences in categorical variables were assessed using Chi-square analysis. Comparison of continuous variables among the two groups was performed using Student's t-test for independent groups. Where the assumption of normality was not satisfied, Kruskal–Wallis test was used to compare continuous variables. A two-tailed P < 0.05 was considered statistically significant. The statistical program used was R, version 3.0.2.
| Results|| |
A total of 46 subjects and 50 normal controls were recruited. [Table 1] shows the physical characteristics of the subjects. The cases were taller than controls but weighed less. The BMI was significantly higher in the controls. There was no difference in the blood pressure parameters of the two groups.
The septal wall thickness was statistically higher in the controls, but this difference was lost when adjusted for BMI. On the other hand, the adjusted left atrial diameter and aortic root dimension were statistically larger in the cases than the controls [Table 2].
[Table 3] depicts the derived LV parameters. The indexed LVM was smaller in the cases than the controls (P = 0.01). The cardiac index was larger in the cases (P = 0.02). The mitral E-wave velocity was lower in the subjects, but there was no difference in the mitral A-velocity or E/A ratio. There was no difference in the LV fractional shortening or ejection fraction, relative wall thickness, and deceleration time of the E-wave.
| Discussion|| |
The main findings of this study were that patients with CLD weighed less compared to the age- and sex-matched controls. Furthermore, CLD patients had a higher cardiac index but smaller LVM. We did not find a significant difference in the systolic and diastolic function between the cases and controls.
Our findings although similar to the reported observations in the systolic function parameters by Dadhich et al., was different from observed alteration in the diastolic function parameters in their report. They found that over 60% of their patients with CLD had diastolic dysfunction.
The probable reason why we could not demonstrate abnormal LV diastolic dysfunction may be because we did not employ newer methods of assessment of LV or RV diastolic function such as tissue Doppler imaging (TDI). Other workers have also used tissue Doppler method to demonstrate diastolic dysfunction in cirrhotic patients with or without ascites., This is because the use of traditional transmitral E/A ratio is preload dependent and also often require age correction. On the other hand, TDI directly measures myocardial displacement velocity as the LV relax in diastole. It is, therefore, volume independent and less affected by the left atrial pressure. In addition, we did not study the right ventricle for functional alterations.
The increase in cardiac index in CLD subjects documented in this study has been reported by other workers. Some others did not find any change in the stroke volume at rest.
It is, however, well-documented that conditions such as the presence of renal failure, drug infusion, blood loss, and exercise may be associated with impaired LV function in this group of patients compared to normal controls.,
The absence of systolic dysfunction in our cohort may also be related to the selection of our subjects. We excluded subjects with advanced CLD, those with encephalopathy as well as those with associated renal failure.
Some of the limitations inherent in this study has been highlighted earlier on especially the fact that we did not use newer methods of assessment of LV systolic and diastolic functions such as TDI, and spectral tracking as these facilities were not available at our center at the time we conducted this study. The sample size is also small. A larger sample is needed in future studies in our environment. Finally, we did not correlate our findings with the degree of liver failure.
| Conclusions|| |
Our cohort of CLD patients demonstrated an increase in cardiac index at rest. We did not demonstrate any significant difference in the LV diastolic or systolic dysfunctions using traditional methods. Studies using newer modalities of assessment of cardiac structure and function are needed in our environment.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Lesi OA, Kehinde MO, Anomneze EE. Chronic liver disease in Lagos: A clinicopathological study. Niger Postgrad Med J 2004;11:91-6. [Full text]
Ndububa DA, Ojo OS, Aladegbaiye AO, Adebayo RA, Adetiloye VA, Durosinmi MA. Liver cirrhosis: Child-Pugh grading of cases seen in Nigeria. Trop Doct 2005;35:169-71.
Olubuyide IO. Natural history of liver cirrhosis in 116 Nigerians. East Afr Med J 1996;73:233-5.
Olumide F, Sowemimo GO, Mordi VP. Cirrhosis of the liver in Lagos, Nigeria: A post mortem study. Niger Med J 1978;8:108-11.
Onyekwere CA, Ogbera AO, Hameed L. Chronic liver disease and hepatic encephalopathy: Clinical profile and outcomes. Niger J Clin Pract 2011;14:181-5.
] [Full text]
Sudhakaran P, Attah EB. Observations on cirrhosis and carcinoma liver in Ibadan, Nigeria. Indian J Cancer 1982;19:231-3.
Cohen CD, Kirsch RE, Saunders SJ, Terblanche J. Hepatic sequelae of congestive cardiac failure. Evidence for a liver lesion in patients in whom cardiac function has been restored to normal. S Afr Med J 1981;59:213-6.
Yorifuji S. Hepatic circulation and ascites in congestive heart failure. Jpn Circ J 1964;28:88-92.
Li XP, Yu SS, Li L, Han DG, Dai SJ, Gao Y. Changes of left ventricular function in cirrhotic patients and their correlation with the model for end-stage liver disease score. J South Med Univ 2015;35:557-61.
Cassidy S, Hallsworth K, Thoma C, MacGowan GA, Hollingsworth KG, Day CP, et al.
Cardiac structure and function are altered in type 2 diabetes and non-alcoholic fatty liver disease and associate with glycemic control. Cardiovasc Diabetol 2015;14:23.
Li X, Yu S, Li L, Han D, Dai S, Gao Y. Cirrhosis-related changes in left ventricular function and correlation with the model for end-stage liver disease score. Int J Clin Exp Med 2014;7:5751-7.
Sert A, Aypar E, Pirgon O, Yilmaz H, Odabas D, Tolu I. Left ventricular function by echocardiography, tissue Doppler imaging, and carotid intima-media thickness in obese adolescents with nonalcoholic fatty liver disease. Am J Cardiol 2013;112:436-43.
Merli M, Calicchia A, Ruffa A, Pellicori P, Riggio O, Giusto M, et al.
Cardiac dysfunction in cirrhosis is not associated with the severity of liver disease. Eur J Intern Med 2013;24:172-6.
Hallsworth K, Hollingsworth KG, Thoma C, Jakovljevic D, MacGowan GA, Anstee QM, et al.
Cardiac structure and function are altered in adults with non-alcoholic fatty liver disease. J Hepatol 2013;58:757-62.
Theocharidou E, Krag A, Bendtsen F, Møller S, Burroughs AK. Cardiac dysfunction in cirrhosis – Does adrenal function play a role? A hypothesis. Liver Int 2012;32:1327-32.
Abelmann WH, Kowalski HJ, Mcneely WF. The circulation of the blood in alcohol addicts; the cardiac output at rest and during moderate exercise. Q J Stud Alcohol 1954;15:1-8.
Kowalski HJ, Abelmann WH. The cardiac output at rest in Laennec's cirrhosis. J Clin Invest 1953;32:1025-33.
Møller S, Hove JD, Dixen U, Bendtsen F. New insights into cirrhotic cardiomyopathy. Int J Cardiol 2013 20;167:1101-8.
Møller S, Henriksen JH. Cirrhotic cardiomyopathy. J Hepatol 2010;53:179-90.
Møller S, Henriksen JH. Cardiovascular complications of cirrhosis. Gut 2008;57:268-78.
Møller S, Henriksen JH. Cirrhotic cardiomyopathy: A pathophysiological review of circulatory dysfunction in liver disease. Heart 2002;87:9-15.
Moller S, Henriksen JH. Cardiovascular dysfunction in cirrhosis. Pathophysiological evidence of a cirrhotic cardiomyopathy. Scand J Gastroenterol 2001;36:785-94.
Liu H, Song D, Lee SS. Cirrhotic cardiomyopathy. Gastroenterol Clin Biol 2002;26:842-7.
Nam SW, Liu H, Wong JZ, Feng AY, Chu G, Merchant N, et al.
Cardiomyocyte apoptosis contributes to pathogenesis of cirrhotic cardiomyopathy in bile duct-ligated mice. Clin Sci (Lond) 2014;127:519-26.
Gaskari SA, Liu H, Moezi L, Li Y, Baik SK, Lee SS. Role of endocannabinoids in the pathogenesis of cirrhotic cardiomyopathy in bile duct-ligated rats. Br J Pharmacol 2005;146:315-23.
Ward CA, Liu H, Lee SS. Altered cellular calcium regulatory systems in a rat model of cirrhotic cardiomyopathy. Gastroenterology 2001;121:1209-18.
Liu H, Song D, Lee SS. Role of heme oxygenase-carbon monoxide pathway in pathogenesis of cirrhotic cardiomyopathy in the rat. Am J Physiol Gastrointest Liver Physiol 2001;280:G68-74.
Liu H, Ma Z, Lee SS. Contribution of nitric oxide to the pathogenesis of cirrhotic cardiomyopathy in bile duct-ligated rats. Gastroenterology 2000;118:937-44.
Liu H, Lee SS. What happens to cirrhotic cardiomyopathy after liver transplantation? Hepatology 2005;42:1203-5.
Friedman HS, Fernando H. Ascites as a marker for the hyperdynamic heart of Laennec's cirrhosis. Alcohol Clin Exp Res 1992;16:968-70.
Inserte J, Perelló A, Agulló L, Ruiz-Meana M, Schlüter KD, Escalona N, et al.
Left ventricular hypertrophy in rats with biliary cirrhosis. Hepatology 2003;38:589-98.
Huonker M, Schumacher YO, Ochs A, Sorichter S, Keul J, Rössle M. Cardiac function and haemodynamics in alcoholic cirrhosis and effects of the transjugular intrahepatic portosystemic stent shunt. Gut 1999;44:743-8.
Morace G, Malfanti PL, Porciani MC, Barletta GA, Bellandi F, Bisi G, et al.
Cardiac function in hepatic cirrhosis. Cardiologia 1983;28:523-6.
Adebiyi AA, Aje A, Ogah OS, Ojji DB, Dada A, Oladapo OO, et al.
Correlates of left atrial size in Nigerian hypertensives. Cardiovasc J S Afr 2005;16:158-61.
Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: Results of a survey of echocardiographic measurements. Circulation 1978;58:1072-83.
Nishimura RA, Tajik AJ. Evaluation of diastolic filling of left ventricle in health and disease: Doppler echocardiography is the clinician's Rosetta Stone. J Am Coll Cardiol 1997;30:8-18.
Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, et al.
Echocardiographic assessment of left ventricular hypertrophy: Comparison to necropsy findings. Am J Cardiol 1986;57:450-8.
Teichholz LE, Kreulen T, Herman MV, Gorlin R. Problems in echocardiographic volume determinations: Echocardiographic-angiographic correlations in the presence of absence of asynergy. Am J Cardiol 1976;37:7-11.
How to diagnose diastolic heart failure. European Study Group on Diastolic Heart Failure. Eur Heart J 1998;19:990-1003.
Dadhich S, Goswami A, Jain VK, Gahlot A, Kulamarva G, Bhargava N. Cardiac dysfunction in cirrhotic portal hypertension with or without ascites. Ann Gastroenterol 2014;27:244-9.
Finucci G, Desideri A, Sacerdoti D, Bolognesi M, Merkel C, Angeli P, et al.
Left ventricular diastolic function in liver cirrhosis. Scand J Gastroenterol 1996;31:279-84.
Salerno F, Cazzaniga M, Pagnozzi G, Cirello I, Nicolini A, Meregaglia D, et al.
Humoral and cardiac effects of TIPS in cirrhotic patients with different “effective” blood volume. Hepatology 2003;38:1370-7.
Ruíz-del-Árbol L, Achécar L, Serradilla R, Rodríguez-Gandía MÁ, Rivero M, Garrido E, et al.
Diastolic dysfunction is a predictor of poor outcomes in patients with cirrhosis, portal hypertension, and a normal creatinine. Hepatology 2013;58:1732-41.
Kelbaek H, Eriksen J, Brynjolf I, Raboel A, Lund JO, Munck O, et al.
Cardiac performance in patients with asymptomatic alcoholic cirrhosis of the liver. Am J Cardiol 1984;54:852-5.
Wong F, Liu P, Lilly L, Bomzon A, Blendis L. Role of cardiac structural and functional abnormalities in the pathogenesis of hyperdynamic circulation and renal sodium retention in cirrhosis. Clin Sci (Lond) 1999;97:259-67.
Grose RD, Nolan J, Dillon JF, Errington M, Hannan WJ, Bouchier IA, et al.
Exercise-induced left ventricular dysfunction in alcoholic and non-alcoholic cirrhosis. J Hepatol 1995;22:326-32.
[Table 1], [Table 2], [Table 3]