Cholestatic Bradycardia: The Story of Rising Bilirubin and the Slowing Heart – A Case Report of a 74 Years Old Female Patient at University of Nigeria Teaching Hospital, Enugu, Nigeria

Abstract

The association between Cholestatic jaundice and bradycardia has been well documented with reports of a variety of bradyarrhythmias. Although the actual mechanism by which jaundice leads to development of bradycardia or bradyarrhythmia has remained a puzzle to both physicians and surgeons for more than a century, it has however been known to complicate the course and outcome of obstructive jaundice. Case Description: Here we report the case of an elderly woman suffering from obstructive jaundice secondary to pancreatic malignancy (carcinoma of head of pancreas). She subsequently developed progressive bradycardia and other cardiac rhythm disorders as her serum bilirubin and bile acids continued to rise, and was referred to us, the cardiologists. Blood samples were taken about every three days for serum bilirubin and bile acids assay, and serial electrocardiogram (ECG) was done accordingly. The total/direct bilirubin rose progressively from 28.4/17.6 umol/L at the outset to 501.5/234.0 umol/L. The bile acids equally increased steadily from Aspartate Transaminases/ Alanine Transaminases/ Alkaline Phosphatase (AST/ALT/ALP) levels = 96/81/1037 IU/L to as high as AST/ALT/ALP = 580/400/7000 IU/L.Patient manifested cardiac rhythm disorders ranging from sinus bradycardia with first degree atrio-ventricular (AV) block and heart rate (HR) of 54/min, to Mobitz type 2 AV block (HR =40/min), and to Complete heart block (HR=33/min) over two weeks period. She was commenced on drugs that enhance bile acid elimination and counteract excessive vagal stimulation, and later on a decompressive surgery (biliary diversion) was carried out under temporary pace maker support. Consequently, patient showed some improvement in her cardiovascular parameters following intake of those drugs and much further improvement following the biliary decompressive surgery under temporary pace maker support, with the HR increasing steadily up to normal rate of 68 to 86 b/min over 3 weeks period. Conclusion: This case has significantly demonstrated that the postulated mechanisms of cholestatic bradycardia hold some credence.