Cardiovascular disease (CVD) is a significant public health issue due to its high prevalence and considerable contribution to the global disease burden. Recent studies suggest that genetic factors, including noncoding RNAs, have an important role in the progression of CVD. Noncoding RNA plays a critical role in genetic programming and gene regulation during development. Ferroptosis is a form of iron-dependent regulated cell death (RCD), which is mainly caused by increased lipid hydroperoxide and redox imbalance. Ferroptosis is essentially different from other forms of RCD in morphology and mechanism, such as apoptosis, autophagic cell death, pyroptosis, and necroptosis. Much evidence suggested ferroptosis is involved in the development of various CVDs, especially in cardiac ischemia/reperfusion injury, heart failure, and aortic dissection. Here, we review the latest findings based on noncoding RNA regulation of ferroptosis and its involvement in the pathogenesis of CVD and related treatments, aimed at providing insights into the impact of noncoding RNA regulation of ferroptosis for CVD.