Narasingarao S.1, Kanaka Mahalakshmi A.2, Manojna Beesetty3
BACKGROUND Coronary Vascular Disease is currently the leading cause of death in India and its prevalence is projected to rise. In 2000, there were an estimated 30 million people with coronary heart disease (CHD) alone in India, or a nearly 3% prevalence. The prevalence of other risk factors of HF is also rising in India. One of the most common manifestations of congestive heart failure is enlargement of the liver. This fact has led several investigators such as Jollife and Robertson to study liver function tests in an attempt to evaluate hepatic dysfunction in congestive heart failure. Historically, the first association of liver pathology and congestive heart failure was noted by Keirnan who described the nutmeg liver. Seventy-eight years later Mallory described the typical microscopic appearance of central congestion with focal necrosis. The three main theories of the pathogenesis of the altered liver anatomy were: infection, mechanical compression, and hypoxia with secondary nutritional deficiency. The deficiency in oxygen supply to liver cells in heart failure seems to be due not only to the slowing of blood flow through the liver but even more so to arterial unsaturation resulting from pulmonary lesions. METHODS All cases of congestive cardiac failure admitted at King George Hospital (N= 75), of varied aetiologies from May 2017 to May 2018 (12 months) were taken up for study. Liver function tests were performed in all CCF cases, namely, serum bilirubin, AST, ALT, SAP, serum proteins and prothrombin time both on day 1 and day 7 of admission. This study was a cross sectional descriptive study, comparing the liver function tests between cases of various causes of heart failure. Results were entered in Microsoft Excel Spread sheet and analysed. Significance values were analysed using Minitab software, Epi Info software. Chisquare test. Students ‘t’ test values were applied for significance. A p value below 0.05 was considered significant. RESULTS The profile of LFTs on day 1 and day 7 showed a strong correlation of serum bilirubin and serum alkaline phosphatase levels with disease activity with a p value of <0.00001 and a p value of <0.001 respectively. Aminotransferase levels paralleled the severity and indicated poor prognosis associated with low serum albumin levels. CONCLUSIONS Liver function abnormalities were mostly present in patients with coronary artery disease developing heart failure. Liver function abnormalities were least in patients with cardiomyopathy developing heart failure. The serum bilirubin, serum alkaline phosphatase and serum transaminases returned to normal with remission. The serum bilirubin, serum enzymes and prothrombin time were elevated with exacerbation. Severe congestive cardiac failure with hypotension leads to a gross elevation of serum aspartate transaminase and alanine transaminase. Serum alkaline phosphatase elevation correlated with the presence of hepatomegaly. Serum bilirubin levels at presentation of more than 5 mg and presence of hypoalbuminemia were associated with a poor prognosis.
