Molecular Imaging of the Failing Heart: Assessment of Cardiac Sympathetic Nerve and Mitochondrial Function

Patients with heart failure have a high morbidity and mortality despite the advancement of recent heart failure treatment. It is important to evaluate the mechanism of the failing myocardium for decision making appropriate managements or the prediction of prognosis in patients with heart failure. Myocardium mainly utilizes fatty acid or glucose as the energy substrate of oxidative regeneration of ATP in the mitochondria. Intracellular calcium handling, that needs an amount of ATPs in several processes, induces myocardial contraction and relaxation by the sliding of the actin-myosin filament. Moreover, beta adrenal-stimulus also regulates intracellular calcium handling. In the failing myocardium, these components related to the myocardial work are variedly impaired, by various etiologies, including ischemia, inflammation, oxidative stress, metabolic or structural disorder, mechanical stress, or various other factors, and could become the imaging targets. In this review article, we focus on the clinical usefulness of 2 radionuclide imaging in evaluating sympathetic nerve function using myocardial 123I-MIBG SPECT and mitochondrial function using myocardial 99mTc-sestamibi SPECT in the failing heart. We summarize the relationship between each scintigraphic finding derived from the above mentioned tracers and myocardial functional properties of force frequency relations, the molecular mechanism of mitochondrial function, calcium handling, or beta-adrenal signaling in patient with cardiomyopathy.