Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide. Increasing evidence indicates that sex differences significantly influence the development, progression, and outcomes of CVDs. Recent advances have highlighted the central role of mitochondria, not only as cellular energy hubs but also as key regulators of oxidative stress, inflammation, and apoptosis, in mediating sex-specific cardiovascular responses. This review explores sexual dimorphism in cardiovascular disease, focusing on the interplay between mitochondrial function and sex hormones in cardiovascular tissues. We summarize current evidence on the molecular, hormonal, and cellular mechanisms contributing to sex-based disparities in cardiovascular outcomes. Preclinical studies suggest that female cardiac mitochondria may exhibit greater antioxidant capacity and produce fewer reactive oxygen species than male mitochondria, contributing to enhanced cardioprotection. Estrogen has been shown to influence mitochondrial bioenergetics and gene expression, affecting vascular tone, inflammation, and cardiac remodelling, whereas the role of testosterone remains less well defined. Additionally, sex-specific mitochondrial signalling responses have been reported under cardiac stress conditions, which may underlie differences in disease presentation and progression. A better understanding of how sex modulates mitochondrial function could improve risk stratification and support the development of personalized prevention and treatment strategies. Further research is needed to translate these mechanistic insights into clinical practice.