<p>Cardiovascular diseases (CVDs) comprise a range of conditions affecting the heart and vasculature, encompassing ischemic heart disease (IHD), stroke, heart failure (HF), peripheral and aortic diseases, arrhythmias, and valvulopathy. Notably, the high prevalence rates of CVDs among younger populations warrant concern, emphasizing the importance of prevention and treatment. In recent years, ferroptosis, a novel form of cell death, has attracted significant research interest across various diseases. Similarly, cuproptosis, another cell death mechanism resulting from copper ion accumulation, has also been extensively studied. Cell death plays a crucial role in the development and maintenance of organisms, with both ferroptosis and cuproptosis closely associated with cell metabolism, signaling pathways, and drug resistance. Emerging evidence suggests that ferroptosis and cuproptosis are closely linked to the occurrence and progression of various diseases, including CVDs. The death of myocardial cells is pivotal in the pathophysiology of CVDs, with the roles of ferroptosis and cuproptosis in this process increasingly recognized. This article aims to summarize the molecular mechanisms and interactions of ferroptosis and cuproptosis, as well as their potential as novel targets for CVD treatment.</p>