Hypoxia, a condition of insufficient oxygen availability to support metabolism, occurs when
the vascular supply is interrupted, as in stroke. The identification of the hypoxic and viable tissue in
stroke as compared with irreversible lesions (necrosis) has relevant implications for the treatment of
ischemic stroke. Traditionally, imaging by positron emission tomography (PET), using 15O-based radiotracers,
allowed the measurement of perfusion and oxygen extraction in stroke, providing important
insights in its pathophysiology. However, these multitracer evaluations are of limited applicability in
clinical settings. More recently, specific tracers have been developed, which accumulate with an inverse
relationship to oxygen concentration and thus allow visualizing the hypoxic tissue non invasively.
These belong to two main groups: nitroimidazoles, and among these the 18F-Fluoroimidazole (18F-FMISO) is the
most widely used, and the copper-based tracers, represented mainly by Cu-ATSM. While these tracers have been at first
developed and tested in order to image hypoxia in tumors, they have also shown promising results in stroke models and
preliminary clinical studies in patients with cardiovascular disorders, allowing the detection of hypoxic tissue and the prediction
of the extent of subsequent ischemia and clinical outcome. These tracers have therefore the potential to select an
appropriate subgroup of patients who could benefit from a hypoxia-directed treatment and provide prognosis relevant imaging.
The molecular imaging of hypoxia made important progress over the last decade and has a potential for integration
into the diagnostic and therapeutic workup of patients with ischemic stroke.