Identifying Hypoxia and Glycolysis in Chemotherapy- and Radiation-Induced Cardiotoxicity by Nuclear Medicine Diagnostic Imaging With 18F-Flurodeoxyglucose – Key Role of Coenzyme Q10 Deficiency in Acquired Mitochondrial Dysfunction

Abstract

Cardiotoxicity is an unwanted side-effect arising from different medications. The term describes a diminution of heart function, affecting especially left ventricular ejection fraction, which can progress to heart failure. Pediatric oncology patients treated with drugs of the anthracycline group, e.g., doxorubicin, can evolve to heart failure patients in adult age. Nuclear Medicine imaging of fatty acid oxidation and glycolysis accurately describes normal and altered heart metabolism. The most common finding is a state of cardiac glycolysis, which is reflected by increased uptake of 18F-desoxyglucose (18F-FDG) at a time when fatty acid oxidation is decreased. Glycolysis has recently been recognized as being the result of coenzyme Q10 deficiency as part of adaptation to hypoxia. Low LEVF correlates with impaired fatty acid oxidation. This deficiency can arise from chemotherapy and radiation and can be corrected by supplementation. Drugs like enalapril can improve fatty acid utilization. We will review relevant Nuclear Medicine imaging studies as well as fundamental biochemical data that demonstrate this pathogenetic path.