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Macrotroponin complexes commonly cause discordant cardiac troponin elevations in the general population, notably troponin I, without conferring increased cardiovascular risk, underscoring the need to recognize assay interference for accurat
A large multicohort and experimental study suggests the cTnI/cTnT ratio is biologically informative, separates acute from chronic myocardial injury, and modestly improves type 1 versus type 2 MI discrimination.
Switching from high-sensitivity troponin I to T significantly increases diagnoses of myocardial injury and hospital admissions without improving long-term cardiovascular outcomes, while low-threshold troponin I remains a safe tool for rapid
Elevated high-sensitivity cardiac troponin I and T levels, indicative of subclinical myocardial injury in midlife, are associated with accelerated cognitive decline, structural brain changes, and increased dementia risk in later life.