Advances in pharmacotherapy as well as device therapy in common cardiovascular
diseases, especially implementation of rapid coronary reperfusion as a key management
strategy in acute ischemic disease, improved overall survival. Yet, this success contributes
to increased number of patients susceptible to heart failure development due to damaged
myocardium. Although survival after heart failure diagnosis has improved over time, the
death rate remains high: ≈50% of people diagnosed with this disease will die within 5 years.
Thus, not only there is a space for novel concepts and strategies in the treatment of symptomatic
heart failure, but also they are urgently needed. The mechanisms underlying the development
of heart failure are multiple, complex, and not well understood. However, regardless
of the cause of heart failure, or whether its presentation is acute or chronic, altered
mitochondrial function/bioenergetics appears to play a substantial role in its pathophysiology.
As such, the mitochondria are potentially promising, but still underused, target for new
This review will focus on changes that occur in the mitochondria of failing myocardium, as well as on targets and
approaches that suggest potential therapeutic effect in this ominous disease.