 Oxidative stress is a common mediator in cardiovascular disease pathogenesis and likely contributes to residual risk, not explained by traditional factors. Functional oxidative modifications of cellular proteins are a causal step in cellular dysfunction, but accurately quantifying reactive oxygen species and measuring stable byproducts modified under conditions of oxidative stress can be challenging. Redox-sensitive proteins with important cellular functions are confined to signaling microdomains in cardiovascular cells and may not be readily available for quantification. New methodologies for high throughput measurement of selected biomarkers of oxidative stress, such as redox-cysteine modifications, show promise in cardiovascular medicine, but further studies are required to examine their utility in predicting prognosis or response to treatment. This article was authored by Edwin Ho, Kevan Karimi-Galugahi, Chia-Chi Lu, and others.