Molecular Imaging of Apoptosis and Atheromatous Plaques: Current and Future Applications in Heart Failure

Nowadays, chronic heart failure patients are assessed by various modalities in order to investigate the extent of jeopardized myocardium. This is extremely important for cardiac remodeling prevention. Radionuclide studies have been extensively used for more than 30 years in the evaluation of these patients. In chronic heart failure, the extent, severity and localization of myocardial damage, as well as the underlying pathology, affect clinical decision-making, including the selection of the optimal therapeutic intervention. A significant portion of heart failure cases is associated with atherosclerotic cardiovascular disease. Plaque rupture represents the main pathophysiological mechanism in these patients, leading to myocardial necrosis and apoptosis. Even though myocardial necrosis and apoptosis almost always co-exist, necrosis is considered as a non-reversible state, whereas apoptosis can be reversed and the affected myocardium may be salvaged. Notably, nuclear medicine techniques can detect and quantitate the amount of myocardial mass that has entered the apoptotic process. On the other hand, while classic imaging modalities have failed to identify the prone to rupture plaques, breakthroughs in molecular imaging may achieve early identification of vulnerable plaques and, therefore, recognition of patients at risk. This chapter focuses on the pathophysiology of apoptosis and plaque rupture, as well as on the available imaging techniques for these phenomena.

Keywords: Anexin-V, Anti-apoptotic therapy, Apoptosis imaging, Atherogenesis, Endothelial dysfunction, Matrix remodeling, Myocardial apoptosis, Neovascularization, Thrombosis, Vulnerable plaque.