Cardiomyocyte Apoptosis as a Risk Factor for Ischemic Heart Disease Development (Literature Review)

Ischemic heart disease (IHD) is a common pathology that plays a key role in cardiovascular mortality. Cardiovascular diseases affect people of all ages, including the actively working population, which can have a negative impact on the social and economic status of society. In this research work the processes of cardiomyocyte apoptosis and their impact on myocardial damage during ischaemia is analyzed. A systematic review of published relevant studies on the role of cardiomyocyte apoptosis in the mechanism of IHD was conducted. The information was searched in the electronic scientific bibliographic databases PubMed. The key words used to select publications were “ischemic heart disease”, “apoptosis of cardiomyocytes”, “cell death”. The search covered studies over the past 10 years (2015–2025). The main inclusion criteria were: studies containing experimental data or clinical observations on cardiomyocyte apoptosis in IHD; publications in peer-reviewed journals in English or Ukrainian. The review did not include publications with missing full text, articles without clear data on research methods, or review articles without new experimental data. The analysis showed that preventing cardiomyocyte apoptosis is an extremely important therapeutic goal today. Ischaemia/reperfusion, overload-induced hypertrophy, and myocardial remodelling after infarction are associated with myocyte apoptosis. This suggests that modern treatment approaches that have proven effective in these diseases can achieve their effect, in particular, by influencing the processes of apoptosis. Thus, the study of apoptosis and its regulation is important not only for understanding the development of cardiovascular diseases, but also for creating new therapeutic approaches. Apoptosis is a controlled process of cell death and is of great importance in the field of cardiac pathology, namely, in ischaemia/reperfusion, myocardial hypertrophy, and post-infarction remodelling.