Abstract

An abrupt elevation in aminotransferases without clear etiology may be attributed to hypoxic hepatitis. Underlying cardiac dysfunction, an important clinical clue, is often overlooked as a cause of hypoxic hepatitis, and understanding the interdependence of the heart and liver is crucial in making this diagnosis. Causes of cardiac dysfunction may include any of many different diagnoses; infiltrative heart disease is a rare cause of cardiac dysfunction, with amyloidosis being the most common among this category of pathologies. More advanced imaging techniques have improved the ability to diagnose infiltrative heart disease, thus allowing quicker diagnosis of conditions such as amyloidosis.

Highlights

  • An abrupt elevation in aminotransferases has a limited differential diagnosis

  • In the context of the patient’s cardiac history, the clinical picture was diagnostic for ischemic hepatitis, and shifted attention to the heart

  • Known as shock liver or hypoxic hepatitis, was described as early as 1901 in a series of autopsies that revealed homogenous hepatic necrosis distributed around the central veins.[1]

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Summary

Introduction

An abrupt elevation in aminotransferases has a limited differential diagnosis. A thorough investigation into the cause of the elevation can lead to the discovery of other systemic processes. The past medical history was remarkable for type 2 diabetes mellitus, hyperlipidemia, paroxysmal atrial fibrillation, nonischemic cardiomyopathy (ejection fraction of approximately 40%) with stage III diastolic dysfunction, and chronic kidney disease (baseline creatinine 2.2) He smoked 4 cigarettes daily for 25 years, but not the last 20 years. The patient’s electrocardiogram (ECG; Figure 1) revealed multiple conduction defects including a right bundle branch block, left anterior fascicular block, and a first-degree atrioventricular block He had inferior Q waves and T wave inversions in leads I, aVL, and V3. He was seen in cardiology clinic during which time he had further evaluation with cardiac magnetic resonance imaging (MRI; Figure 3) This revealed diffuse myocardial thickening of both left and right ventricles with delayed hyperenhancement in a pattern consistent with amyloidosis (Figure 3A and B, asterisks). The patient declined endomyocardial biopsy and further invasive investigation or therapy

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