Heart failure is a complex pathological condition characterized by various mechanisms of cellular death, among which programmed cell death (PCD) plays a crucial role in the pathophysiology of cardiac dysfunction. This review delves into the different forms of PCD present in heart failure, including apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis, and examines the mechanisms of action involved and the potential therapeutic targets for treating cardiac failure. By analyzing the latest research findings, we reveal the pivotal role of PCD in the progression of heart failure and discuss the preclinical prospects of intervening in these processes to develop novel therapeutic strategies. For instance, pharmacological agents that inhibit receptor-interacting protein kinases (RIPK1 and RIPK3) involved in necroptosis have been demonstrated to reduce cardiac injury and improve functional outcomes. Additionally, targeting the inflammatory responses associated with necrotic cell death, such as using interleukin (IL)-1β inhibitors, may provide a dual benefit by reducing cell death and inflammation. Thus, combining current knowledge will enhance our understanding in this field and promote innovative approaches to managing heart failure more effectively.