This review explores the role of vitamin C as a scavenger of reactive oxygen species (ROS) during healing after myocardial infarction (MI). Vitamin C is a well-known antioxidant that neutralizes harmful free radicals, including superoxide anion (O₂⁻·) and hydrogen peroxide (H₂O₂), and can also donate electrons to protect biomolecules from oxidative damage. Despite its antioxidant properties, the clinical use of vitamin C remains controversial due to its complex dose-dependent absorption and release kinetics. The review discusses the mechanisms of vitamin C metabolism, its role in cardiovascular pathologies, and its potential as a therapeutic agent in cardiovascular disease management. Vitamin C is involved in the metabolism of various ROS, including those produced by mitochondrial complexes I, III, and IV. These ROS contribute to oxidative stress, which exacerbates tissue damage and impairs cardiac function after MI. Vitamin C can reduce ROS levels by scavenging these species and enhancing the activity of antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT). Additionally, vitamin C helps maintain intracellular antioxidant levels, including glutathione (GSH), which is crucial for protecting cardiac cells from oxidative damage. The review also highlights the potential of vitamin C in preventing or minimizing heart failure by reducing oxidative stress and improving cardiac function. Animal studies have shown that vitamin C supplementation can reduce infarct size, improve vascular density, and decrease fibrosis after MI. However, the effects of vitamin C are dose- and time-dependent, and excessive intake may increase cardiovascular mortality. Furthermore, vitamin C intake has been associated with an increased risk of kidney stone formation, particularly at high doses. In conclusion, while vitamin C has demonstrated antioxidant properties and potential therapeutic benefits in cardiovascular disease, its clinical application remains controversial. Further research is needed to clarify the role of vitamin C in the prevention and treatment of cardiovascular diseases, particularly in the context of oxidative stress and mitochondrial dysfunction. The review emphasizes the importance of careful dosage management and the need for future studies to explore the potential of vitamin C in combination therapies for cardiovascular diseases.This review explores the role of vitamin C as a scavenger of reactive oxygen species (ROS) during healing after myocardial infarction (MI). Vitamin C is a well-known antioxidant that neutralizes harmful free radicals, including superoxide anion (O₂⁻·) and hydrogen peroxide (H₂O₂), and can also donate electrons to protect biomolecules from oxidative damage. Despite its antioxidant properties, the clinical use of vitamin C remains controversial due to its complex dose-dependent absorption and release kinetics. The review discusses the mechanisms of vitamin C metabolism, its role in cardiovascular pathologies, and its potential as a therapeutic agent in cardiovascular disease management. Vitamin C is involved in the metabolism of various ROS, including those produced by mitochondrial complexes I, III, and IV. These ROS contribute to oxidative stress, which exacerbates tissue damage and impairs cardiac function after MI. Vitamin C can reduce ROS levels by scavenging these species and enhancing the activity of antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT). Additionally, vitamin C helps maintain intracellular antioxidant levels, including glutathione (GSH), which is crucial for protecting cardiac cells from oxidative damage. The review also highlights the potential of vitamin C in preventing or minimizing heart failure by reducing oxidative stress and improving cardiac function. Animal studies have shown that vitamin C supplementation can reduce infarct size, improve vascular density, and decrease fibrosis after MI. However, the effects of vitamin C are dose- and time-dependent, and excessive intake may increase cardiovascular mortality. Furthermore, vitamin C intake has been associated with an increased risk of kidney stone formation, particularly at high doses. In conclusion, while vitamin C has demonstrated antioxidant properties and potential therapeutic benefits in cardiovascular disease, its clinical application remains controversial. Further research is needed to clarify the role of vitamin C in the prevention and treatment of cardiovascular diseases, particularly in the context of oxidative stress and mitochondrial dysfunction. The review emphasizes the importance of careful dosage management and the need for future studies to explore the potential of vitamin C in combination therapies for cardiovascular diseases.