Chirantan Banerjee, MD

Saura H, Ogasawara K, Beppu T, Yoshida K, Kobayashi M, Yoshida K, et al. Hypoxic Viable Tissue in Human Chronic Cerebral Ischemia Because of Unilateral Major Cerebral Artery Steno-Occlusive Disease. Stroke. 2015

Cerebral autoregulation is a unique and powerful feature of the intracranial vasculature. Powers in a seminal article in 1991 described the stages of intracranial hemodynamic failure with progressively decreasing cerebral perfusion pressures (CPP). In Stage 1, cerebral blood flow (CBF) is maintained despite falling CPPs by vasodilation of resistance arterioles. In Stage 2, with further reductions in CPP, the autoregulatory capacity is exhausted and CBF falls as a function of pressure. However, a compensatory increase in the oxygen extraction fraction (OEF) maintains cerebral oxygen metabolism and tissue function. In Stage 3, further CPP reduction leads to true ischemia and possible permanent injury. Several PET studies over the years have replicated these findings. 

15O tracer in PET has been used as a correlate of OEF in prior studies, which may correlate with future stroke risk. However, OEF might not be the best marker as in stage 3, as OEF may actually decrease in this stage due to tissue damage from ischemia. 18F-FRP170 is a nitroimidazole PET tracer which is a marker of hypoxic but viable brain tissue. In the current study by Saura et al, the authors use PET with this 18F-FRP170 tracer in 52 patients with unilateral symptomatic MCA or ICA high-grade stenosis/occlusion and 20 healthy controls. The authors were able to show the presence of hypoxic but viable tissue in chronic hypoperfusion, and found that the 18F-FRP170 ratio correlated well with OEF. Also, the combination of an elevated 18F-FRP170 ratio and OEF together had much higher positive predictive value and specificity than individual markers. This is an important finding, as it may prove to be a reliable modality to stratify stroke risk in these patients in the future, as well as provide further insights into cerebral hemodynamics.