Role of Glycogen Phosphorylase in Prediction of Cardiotoxicity Associated with Acute Carbon Monoxide Poisoning

Abstract

Introduction: Carbon monoxide (CO) poisoning is a leading cause of death from intoxication. The heart is extremely susceptible to CO-induced hypoxia due to its high oxygen demand. Cardiovascular involvement in CO poisoning could be clinically occult and undiagnosed due to lack of overt symptoms or specific electrocardiogram (ECG) changes. There is an emerging need for early and specific markers for myocardial hypoxia. One potential candidate is the glycogen phosphorylase BB isoenzyme (GPBB). Aim of the study: The study was planned to assess the role of glycogen phosphorylase in early prediction of myocardial toxicity due to CO poisoning. Methods: This prospective study included 2 groups; Control group and Patient group. Control group included 15 non-smokers healthy adults aged between 20 and 35 years old selected from patients’companions presented to Zagazig University Hospitals. Patient group included 30 adults aged 20-35 years old with history of CO exposure within 6 hrs. They were sub- divided into mild & moderate CO poisoning groups according to COHB% & clinical manifestations. The study was performed during the period between January 2015 to April 2016. All the subjects enrolled in the study were subjected to clinical examination, ECG, echocardiogram (Echo), cardiac troponin I (cTn-I) and GPBB assessment. Results: There was a significant increase in heart rate between patient and control groups. Also, a significant increase in GPBB was found between patient and control groups and this was associated with a significant decrease of ejection fraction evaluated by Echo in moderate CO poisoning group when compared with control group. No significant differences were found as regard serum cTn-1 level or ECG findings between patient and control groups. Conclusion: GPBB can be used as an early predictor of CO-induced myocardial ischemia which in turn may modify management plan to avoid later sequelae affecting ventricular function.