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.
