Evidence that programmed cell death contributes to cardiomyocyte loss is substantial for some cardiac pathologies such as myocardial infarction and a variety of cardiomyopathies. For others, such as chronic hibernating and stunned myocardium, its involvement is still debated. Recent studies have indicated that the heart remodels its structure in a rather stereotypical way when subjected to unfavourable conditions such as ischemia and pressure or volume overload. This stereotypical response is characterized by subcellular adaptations in cardiomyocytes whereby the cells switch from an adult (functional) to a fetal (survival) phenotype, a process akin to dedifferentiation. Structural hallmarks of dedifferentiation are reduction of contractile filaments, accumulation of glycogen in the cytosol, dispersion of nuclear heterochromatin, changes in mitochondrial shape and size, and loss of sarcoplasmic reticulum and T-tubules. The changes are accompanied by important alterations in the expression and distribution of structural proteins in these organelles. Today, there is only circumstantial evidence that cardiomyocyte dedifferentiation is an adaptive and reversible phenomenon instead of a degenerative event leading to apoptotic cell death. Indeed, some research groups consider the switch to a fetal phenotype to be a rescue reaction and therefore coined the name 'programmed cell survival', whereas others interpret this as an event on the 'programmed cell death' pathway. It is obvious that resolving this controversial issue is of direct clinical importance as far as prognosis and therapy are concerned.