Cardiac changes in patients with
chronic liver disease: A prospective descriptive study
Sukhwani N 1, Nayak O.
P.2, Kumbhkar T 3
1Dr Nitesh Sukhwani, Assistant Professor, 2Dr Om Prakash Nayak,
Assistant Professor, Department of General Medicine, Peoples College of
Medical Sciences and Research center, Bhopal, 3Dr Tapas Kumbhkar,
Senior Resident Department of General Medicine. Peoples College of
Medical Sciences and Research Center Bhopal, MP, India
Address for
correspondence: Dr Nitesh Sukhwani, Email:
roshanchanchlani@gmail.com
Abstract
Background:
The systemic circulation in patients with cirrhosis is hyperdynamic
with an increased cardiac output and heart rate and a reduced systemic
vascular resistance as the most pronounced alterations. The concomitant
cardiac dysfunction has recently been termed “cirrhotic
cardiomyopathy”, which is an entity different from that seen
in alcoholic heart muscle disease. Objective:
To study cardiac changes in patients with chronic liver disease. Methodology: The
present study was a prospective descriptive clinical study consisting
of thirty five patients with cirrhosis who were inpatients in the
department of Medicine, tertiary care Institute, from Oct 2011 to Oct
2013.The patients were evaluated for presence of cirrhotic
cardiomyopathy. Results:
In A group there is no patient, while in Child- Pugh Score- B group 14
subjects have cirrhotic cardiomyopathy out of 16 and in C group 18 have
cirrhotic cardiomyopathy out of 19. We analyzed that there was no
relation between severity of liver disease and cirrhotic cardiomyopathy
(p value- 0.446). Conclusion:
Indian patients with cirrhosis do have diastolic dysfunction. In the
absence of other risk factors for cardiac disease, this dysfunction can
be attributed only to cirrhotic cardiomyopathy.
Keywords: Cardiomyopathy,
Cirrhosis, chronic liver disease
Manuscript received: 25th
Feb 2016, Reviewed:
13th March 2016
Author Corrected:
22nd March 2016, Accepted
for Publication: 7th April 2016
Introduction
The clinical picture of patients with cirrhosis is dominated by the
classical complications such as ascites, bleeding from oesophageal
varices, portal hypertension and encephalopathy. In addition,
a considerable number of patients show signs of peripheral
vasodilatation with palmar erythema and reddish skin, raised and
bounding pulse, and a low systemic blood pressure indicating a
hyperdynamic circulation. The hyperdynamic syndrome comprises an
increased heart rate, cardiac output, and plasma volume, and a reduced
systemic vascular resistance and arterial blood pressure. Increased
cardiac output in cirrhosis was described more than 50 years ago and a
hyperdynamic, hyporeactive circulation is today a well¬
characterized element in the clinical appearance of these patients. In
addition, patients with cirrhosis develop complications from a variety
of organs including the heart, lungs, and kidneys, and other organ
systems. Besides the hepatorenal syndrome, this has led to the
recognition of new clinical entities, such as cirrhotic cardiomyopathy
and the hepatopulmonary syndrome. Cirrhotic cardiomyopathy was
initially thought to be of little clinical relevance. However, with the
frequent use of invasive procedures like surgical portocaval shunts,
transjugular intrahepatic portosystemic shunt and liver
transplantation, the adverse consequences of cardiac dysfunction became
evident. These procedures put additional stress on the dysfunctional
heart, precipitating overt cardiac failure. Unexpected deaths due to
heart failure following these procedures became a cause of concern in
centers where these procedures were regularly performed.
Past decades have seen the appearance of new techniques for the study
of different aspects of cardiac function. Our knowledge of
cardiovascular pathophysiology has improved considerably, including our
understanding of cardiovascular complications of liver disease.
Kowalski et al [1] were the first to report that patients
with cirrhosis had abnormal cardiovascular function and a prolonged QT
interval. The systemic circulation in patients with decompensated
cirrhosis is hyperdynamic and characterised by increased heart rate and
cardiac output (CO) and decreased systemic vascular resistance with low
normal or decreased arterial blood pressure [2–4]. Among the
factors that may increase the CO in patients with cirrhosis are
increased sympathetic nervous activity, increased blood volume
(increased preload), and the presence of arteriovenous communications
[5–7]. Many of the patients present with dyspnoea, fluid
retention, and limited exercise capacity [4,8,9]. There is paucity of
data from the Indian subcontinent on cirrhotic cardiomyopathy. Apart
from a study by Jacob Alexander et al, there is scanty information on
the status of cardiac abnormalities in Indian patients with cirrhosis.
Just as the etiological spectrum of cirrhosis varies in different parts
of the world, data from one population may not be valid in a different
population.
We undertook to study cardiac status in patients with cirrhosis of
liver at rest and stress to assess the occurrence of cirrhotic
cardiomyopathy, to study if echocardiographic parameters of cardiac
dysfunction correlate with the severity of liver dysfunction, and to
appraise whether or not there are significant differences in these
parameters between alcoholic and non-¬alcoholic cirrhosis.
Material
Methods
Present prospective descriptive clinical study was approved by the
institutional ethics committee and consent was obtained from each
patient. Thirty five consecutive patients with cirrhosis of liver
presenting to the Department of Medicine, tertiary care Institute,
Bhopal from October 2011 to October 2013 were included in the study.
Diagnosis of cirrhosis of the liver was made on clinical, biochemical,
serological, and ultrasound imaging. . All patients were ambulatory and
hemodynamically stable.
Inclusion criteria were:
Diagnosed cases of chronic liver disease irrespective of age and sex.
Exclusion criteria were K/C of CAD, hypertension, RHD, NIDDM,
cardiomyopathy. Known cases of hyperthyroidism, hypothyroidism.
Detail history was takenusing Pre-designed and pretested questionnaire.
Investigation included complete blood count, Liver and Renal function,
Blood sugar, Urine- R/M, HBsAg, Lipid profile, Chest X- ray, USG, ECG
and Echocardiography. Echocardiography was performed at rest and also
after stress. From the 2D echocardiography ejection fraction was
calculated by using Modified Simpson rule. All valves of heart were
seen in detail, Regional wall motion abnormalities was look in every
patient. The M mode echocardiogram was used for the measurement of end
diastolic and systolic dimensions. All the four chambers were look
individually for chamber enlargement. For the stress echocardiography
we performed 6MWT (6 minute walk test). In this test we advised to walk
around 100ft. On flat hard surface. This test is easy to perform and
well tolerated by the patients. Two-dimensional and M¬ mode
echocardiographic studies were performed by an experienced cardiologist
using a commercially available cardiac ultrasound machine(GE- Vivid3).
Echocardiographic images were obtained from the parasternal and apical
windows with the patient reclining on the left side, according to the
recommendations of American Echocardiography Committee. In Doppler
echocardiography accompanied by electrocardiogram, peak early filling
velocity (E wave), peak atrial systolic velocity (A wave), early and
late mitral diastolic flow ratio (E/A), ratio of E and A velocity time
integrals was measured. With M¬ mode measurements,
Isolvulmetric relaxation time (IVRT) was measured.
Statistical
Methods
The Statistical software namely SPSS 15.0, Stata 8.0, MedCalc 9.0.1 and
Systat 11.0 were used for the analysis of the data and Microsoft word
and Excel were used to generate graphs, tables. A p value of
<0.05 was considered as significant. Analysis of variance
(ANOVA) has been used to find the significance of study parameters
between three or more groups of patients, Student t test (two tailed,
independent) has been used to find the significance of study parameters
on continuous scale between two groups Inter group analysis) and
Student t test (two tailed, dependent) was used to find the
significance of study parameters on continuous scale within each group.
Results
In the study thirty five patients were included, age group ranging from
30 to 70 yrs, which included 31 males and 4 females constituting 89%
and 11%, Ratio of male /female was 7.75/1. Maximum age of the patient
was 70 yrs and minimum was 30 yrs. Maximum patients come under the
50-59yrs age group (40%). The most common presentation was decrease
appetite (88.5%), abdominal distension (88.5%), hematemesis and malena
in 54.2%. There were no patients with advanced features of cirrhosis.
Among the 35 patients common clinical signs were ascitis (94.2%),
splenomegaly (80%) edema (68.5%), icterus (48.5%) and pallor (42.8%).
Ascitis was minimal to gross was included in our study. Among the
patients in the study majority of the patients had alcohol has etiology
(51%). Non alcoholicetiologies were Hepatitis B (43%) and Hepatitis C
(6%). None of the patients in the study had other etiologies like
autoimmune, biliary causes. There were no patients of multiple
etiologies. Severity of cirrhosis was calculated based on Child- Pugh
criteria, Majority of the subjects were in severity group of Child B
(54%) or Child C (46.0%). In our study we compare Child- Pugh Score
with Cirrhotic cardiomyopathy. In A group there is no patient, while in
B group 14 subjects have cirrhotic cardiomyopathy out of 16 and in C
group 18 have cirrhotic cardiomyopathy out of 19.We analyzed that there
was no relation between severity of liver disease and cirrhotic
cardiomyopathy(p value- 0.446). Table no. 1 In our study we compare the
occurrence of LVH in cirrhotic cardiomyopathy patients. We found that
LVH is present in 2 subjects (5.7%) and absent in 33 subjects (94.2%).
P value was also insignificant i.e. 0.65. Ejection fraction was
increase in 23 patients (65.2%) and decrease in 12 patients (34.2%)
after stress. None of the patient had same ejection fraction after
stress.
Table No 1: Comparison
between presences of LVH in Cirrhotic cardiomyopathy
LVH
|
Cirrhotic cardiomyopathy
|
Total
|
Present
|
Absent
|
Yes
|
2
|
0
|
2
|
NO
|
30
|
3
|
33
|
Total
|
32
|
3
|
35
|
Discussion
The present study was a prospective descriptive clinical study
consisting of thirty five patients with cirrhosis who were inpatients
in the department of Medicine, tertiary care Institute, from Oct 2011
to Oct 2013. All patients were ambulant patients thus eliminating the
effect of cardiac deconditioning due to bed rest.
The patients were evaluated for presence of cirrhotic cardiomyopathy.
Cirrhotic cardiomyopathy is defined as chronic cardiac dysfunction in
patients with cirrhosis, characterized by blunted contractile
responsiveness to stress and/or altered diastolic relaxation with
electrophysiological abnormalities in the absence of known cardiac
disease. In our study, male patients outnumbered females (89% vs. 11%).
This is due to the distribution of cirrhosis in between the genders as
well as life style difference. The mean age of the patients in our
study was around fifty four years and subjects in the age group
30-¬70 years were included. Majority presented with history of
decrease appetite (88.5%), abdominal distension (88.5%) as chief
complaint. From our 35 patients, 31 (approximately 88.5%) presented
with decrease appetite and 31 (88.5%) had presented with abdominal
distension. Clinically ascitis was found in 33 of our patients (94.2%)
and Edema was detected in 24 (68.5%),due to activated RAAS,
hypoproteinemia and ascitis compressing the abdominal inferior
venacava. Icterus was detected in 17 (48.5%) of the study population,
this was due to the inclusive criteria used in the study. Cirrhotic
patients of our study had liver dysfunction of intermediate &
late severity (Sixteen patients (46%) were in Child Pugh class B,
nineteen Patients (54%) were in severity class C. Detection of child
class B were due to aggressive investigation and symptoms suggestive of
liver dysfunction. Child C patients presented with features of gross
ascitis or recent GI bleeding. Only ambulated patients were enrolled to
eliminate the effect of cardiac decondition due to rest. In our study
there was no significant association between the severity of hepatic
dysfunction and cardiac changes was seen which is consistent with one
published report from India [10]. But there are reports that cardiac
changes parallel the severity of hepatic dysfunction.
In our study we found that left ventricular hypertrophy is present in 2
subjects (5.7%) and absent in 33subjects (94.2%). So we can say there
is no relationship between presences of LVH in cirrhotic cardiomyopathy
and similar reports also published from India [10]. In most studies of
patients with cirrhosis, the heart mass has been found to be within the
normal range [11,12]. However, some have reported an increased left
ventricular mass [13,14] and in a recent experimental study of portal
hypertensive rats, left eccentric hypertrophy was found to correlate
directly with the degree of hyperdynamic circulation [15]. The
determination of heart volumes in patients with cirrhosis has given
somewhat different results depending on the methods used.
[16–18] In echocardiographic studies, Kelbæk et al
[19] and Rector et al [17] found the size of the left ventricle to be
normal and that of the left atrium enlarged [20,21]. Others, however,
have reported increases in both the end diastolic and the end systolic
volumes of the left ventricle [13,22–25]. Wong et al [16]
used radionuclide angiography and they reported normal left ventricular
systolic and diastolic volumes, including the stroke volume. Normal and
increased right ventricular and atrial volumes have been found by
echocardiography [17,20,21,26,27]. In contrast, magnetic resonance
imaging has shown reduced right ventricular and atrial dimensions and
slightly increased left ventricular and atrial volumes [12]. Reduced
right heart volumes could reflect a general contraction of the central
blood compartment in patients with cirrhosis, as previously suggested
by other techniques [28]. The change in the left ventricular dimensions
in cirrhosis is related to haemodynamic dysfunction. Thus, Lewis et al
[28] found significant correlations between the left ventricular end
diastolic diameters on one hand and CO, stroke volume, mean arterial
blood pressure, and blood volume on the other. Moreover, significant
direct correlations between plasma atrial natriuretic peptide and left
atrial volume and left ventricular end diastolic diameter have been
reported [20,21]. Future pathophysiological and clinical research is
needed to assess the prognostic implications of cirrhotic
cardiomyopathy.
Conclusion
This study demonstrates that Indian patients with cirrhosis do have
diastolic dysfunction. In the absence of other risk factors for cardiac
disease, this dysfunction can be attributed only to cirrhotic
cardiomyopathy. No correlation of cardiac status with severity of liver
dysfunction was established. There were no significant differences in
cardiac structural and functional parameters between alcoholic and non
alcoholic cirrhosis. Echocardiography plays a significant role in
detecting early cardiac changes in cirrhosis however these changes do
not seen to be predictor of increased mortality in patients of
cirrhosis.
Funding:
Nil, Conflict of
interest: None initiated.
Permission from IRB:
Yes
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How to cite this article?
Sukhwani N, Nayak O. P., Kumbhkar T, Cardiac changes in patients with
chronic liver disease: A prospective descriptive study : Int J Med Res
Rev 2016;4(4):569-574. doi: 10.17511/ijmrr.2016.i04.16.