Ischemic heart disease (IHD) remains one of the leading causes of morbidity and mortality worldwide. One of the potential risk factors for its development is elevated levels of homocysteine–a sulfur-containing amino acid involved in methionine metabolism. Numerous studies have confirmed the role of hyperhomocysteinemia in the pathogenesis of atherosclerosis, endothelial dysfunction, thrombosis, and vascular calcification. Although the exact mechanisms are still being studied, it is known that homocysteine may contribute to oxidative stress, impair nitric oxide synthesis, and activate procoagulant processes. This makes it a potentially significant biomarker for cardiovascular risk assessment. Laboratory determination of homocysteine levels in blood plays an important role in identifying individuals at high risk of cardiovascular events, as well as in the differential diagnosis of genetic or acquired metabolic disorders. While the effectiveness of homocysteine-lowering therapy in preventing cardiovascular events remains debatable, the inclusion of hyperhomocysteinemia in the group of modifiable risk factors is supported by data from multiple clinical and population studies.
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M. M. Shchurko (2025) studied this question.
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