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A study of changes in QTC interval in ECG in cirrhosis of liver.

INTRODUCTION

Cirrhosis of liver results in disorganisation of the lobular and vascular architecture. Portal hypertension develops due to resistance to blood flow through the liver, thereby increase in portosystemic collaterals which pass the liver.

One of the manifestations of portal hypertension is hyperdynamic circulatory state due to activation of neurohumoral pathways that stimulate renal sodium retention, expansion of plasma volume. This hyperdynamic circulatory syndrome is associated with a variety of cardiovascular alterations. [1] In addition, the heart in patients with cirrhosis presents with structural and functional abnormalities that have been termed cirrhotic cardiomyopathy. [2], [3]

"Cirrhotic cardiomyopathy" is a chronic cardiac dysfunction, characterised by blunted contractile responsiveness to stress and altered diastolic relaxation with electrophysiological abnormalities, such as prolongation of the QT interval, all occurring in the absence of any other cardiac disease. [4, 5]

Electrophysiological changes like prolonged repolarisation and impaired cardiac excitation - contraction coupling have been demonstrated in these patients. [6, 7] Repolarisation prolongation is manifested by a prolonged QT interval on the electrocardiogram. Prolongation of QT interval can be associated with an increased risk of certain ventricular arrhythmias, particularly the "Torsade de pointes" type of ventricular tachycardia. Rate-corrected of the QT (>440msec) is found in 30%-60% of patients with cirrhosis. [6, 7]

The exact mechanism leading to these electrophysiological changes is unclear. In clinical studies, severity of liver disease and circulatory dysfunction are related to prolonged QT interval. Moreover, these changes disappear after liver transplantation in most patients. [6, 7]

AIM OF THE STUDY

To assess the prevalence of prolonged QTc interval in ECG in patients with cirrhosis of liver.

MATERIALS AND METHODS Inclusion Criteria

The present study was an observational study conducted in King George Hospital of Andhra Pradesh. Fifty ambulatory hemodynamically stable patients of cirrhosis of liver irrespective of etiology were selected for the study. Age and gender matched control group was selected for comparison with the patients.

All were normal on clinical examination and did not have risk factors for cardiovascular, lung disease, any medications or acute illness.

Exclusion Criteria

Anemia, Hypertension, Diabetes, Dyslipidemia, primary cardiac or pulmonary disease, GI bleed within the previous 3 months, those on B-blocker within the previous 3 weeks, heart disease, those with intercurrent illness and those who were critically ill were excluded from the study.

RESULTS Age and Gender

Among total of 50 patients, 38 were male and 12 were female patients. Out of 50 controls, 32 were male and rest females (Table 1). The mean age of the patients and controls was 44 years and 47 years respectively.

QTc Interval

Out of 50 patients of liver cirrhosis, 21 had prolonged QTc (>440ms) and 29 had normal QTc interval. Among controls only 1 person has prolonged QTc (>440ms) (Table 2).

The difference between cases (21/50 or 42%) compared to controls (1/50 or 2%) is statistically significant (p<0.0001).

QTc Interval between Alcoholics and Non-Alcoholics Prolonged QTc interval was present in 7/18 (38.89%) among alcoholic cirrhotics compared to 14/32 (43.75%) among nonalcoholic cirrhotics (Table 3). The difference is not statistically significant (p=0.74).

DISCUSSION

In this study, the mean age of the patients was comparable with the control group.

The main electrocardiographic change in cirrhosis is a prolongation of the QT interval adjusted for heart rate. Our study had QTc prolongation of 42% vs 2% in patients vs controls. This is comparable to the findings of Bernardi et al., where QTc was prolonged above 440ms in 46.8% of patients and 5.4% of control subjects (P<001). (6)

The difference in the prevalence of prolongation of QTc among alcoholics and non-alcoholics is not statistically significant, similar to the findings noted by Bernardi et al. [6] This is unrelated to the aetiology of the liver disease and effect of alcohol. [8, 9]

A prolonged QTc interval is fundamentally due to a delayed repolarization phase, which is responsible for an increased risk of ventricular arrhythmias and sudden death. [10] More likely, a latent heart failure and cardiac dysfunction are present in some patients with cirrhosis, especially in those patients with a more deranged circulation. Although overt cardiac failure is uncommon in cirrhosis, unexpected cardiac deaths have occurred following surgery in patients with cirrhosis. [11-13) suggesting that better assessment of cardiac function is needed in these patients.

This study has excluded those with very advanced hepatic dysfunction and as only a few patients of hepatic cirrhosis present in the early stage, the results essentially represent the middle of the spectrum of the disease severity. This study included only a limited spectrum of the disease is one of the drawbacks of this study design.

CONCLUSIONS

Cardiac evaluation should be a pre-requisite in patients with cirrhosis undergoing stress like surgery, because the presence of cardiac involvement adds to the morbidity and mortality.

Further studies dedicated to this purpose are required to accurately delineate the extent of correlation between severity of hepatic dysfunction and cardiac changes in cirrhotics.

REFERENCES

[1.] Bosch J, Pizcueta P, Feu F, et al. Pathophysiology of portal hypertension. Gastroenterol Clin North Am 1992;21:1-14.

[2.] Ma Z and Lee SS. Cirrhotic cardiomyopathy: getting to the heart of the matter. Hepatology 1996;24:451-9.

[3.] Moller S and Henriksen JH. Cirrhotic cardiomyopathy: a pathophysiological review of circulatory dysfunction in liver disease. Heart 2002;87:9-15 4.

[4.] Zambruni A, Trevisani F, Caraceni P, et al. Cardiac electrophysiological abnormalities in patients with cirrhosis. J Hepatol 2006;44:994-1002.

[5.] Moller S, Henriksen JH. Cardiovascular complications of cirrhosis. Gut 2008;57:268-78.

[6.] Bernardi M, Calandra S, Colantoni A, Trevisani F, Raimondo ML, Sica G, et al. Q-T interval prolongation in cirrhosis: prevalence, relationship with severity and etiology of the disease and possible pathogenetic factors. Hepatology 1998;27:28-34.

[7.] Bal JS, Thuluvath PJ. Prolongation of QTc interval: relationship with etiology and severity of liver disease, mortality and liver transplantation. Liver Int 2003;23:243-248.

[8.] Alexander J, Mishra P, Desai N, Ambadekar S, Gala B, Sawant P. Cirrhotic cardiomyopathy: Indian scenario. J Gastroenterol Hepatol 2007;22:395-9.

[9.] Lazzeri C, Lavilla G, Laffi G, Vecchiarino S, Gambilonghi F, Gentilini P, et al. Autonomic regulation of heart rate and QT interval in non-alcoholic cirrhosis with ascites. Digestion 1997;58:580-6.

[10.] Tan HL, Hou CJ, Lauer MR, et al. Electrophysiologic mechanisms of 29. The long QT interval syndromes and torsade de pointes. Ann Intern Med 1995;122(9):701-14.

[11.] Rayes N, Bechstein WO, Keck H, Blumhardt G, Lohmann R and Neuhaus P. (1995) Causes of death after liver transplantation: an analysis of 41 cases in 382 patients. Zentralbl Chir 120, 435-8.

[12.] Lebrec D, Giuily N, Hadenque A, et al. (1996) Transjugular intrahepatic portosystemic shunt: comparison with paracentesis in patients with cirrhosis and refractory ascites: a randomized trial. J Hepatol 25, 135-44.

[13.] Franco D, Vons C, Traynor O, et al. (1988). Should portocaval shunt be reconsidered in the treatment of intractable ascites in cirrhosis? Arch Surg 123, 987-91.

V. C. Srinivas Reddy (1), Jyotirmayi Boddu (2)

(1) Assistant Professor, Department of General Medicine, Andhra Medical College, Visakhapatnam, Andhra Pradesh.

(2) Assistant Professor, Department of General Medicine, Andhra Medical College, Visakhapatnam, Andhra Pradesh.

Financial or Other, Competing Interest: None.

Submission 10-11-2015, Peer Review 11-11-2015, Acceptance 19-11-2015, Published 19-12-2015.

Corresponding Author: Dr. V. C. Srinivas Reddy, Assistant Professor in Medicine, Andhra Medical College, Visakhapatnam-530002, Andhra Pradesh.

E-mail: drvcsr@yahoo.co.in

DOI:10.14260/jemds/2015/2510
Table 1: Age and Gender Distribution

             CASES   CONTROLS

AGE (Mean)   44.26    47.14
  MALES       38        32
 FEMALES      12        18

Table 2: QTc Interval between Cases and Controls

     Study Subjects         Cases   Controls

QTc Prolonged (>440 msec)    21        1
 QTc Normal (<440 msec)      29        49

Table 3: QTc Interval--Alcoholics Ks Non-Alcoholics

   Cases      QTc-Prolonged   QTc- Normal   Total

ALCOHOLICS          7             11         18
   NON-            14             18         32
 ALCOHOLIC
   TOTAL           21             29         50
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Title Annotation:Original Article
Author:Reddy, V.C. Srinivas; Boddu, Jyotirmayi
Publication:Journal of Evolution of Medical and Dental Sciences
Date:Dec 21, 2015
Words:1302
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