“…In right ventricular (RV) pressure overload due to pulmonary artery constriction in rats, we demonstrated not only that myocardial glucose utilization in the RV free wall increased, but the regional profiles of substrate utilization in the interventricular septum and the LV free wall were also altered (5). Our previous clinical study with positron emission tomography (PET) demonstrated that myocardial [ 18 F]fluorodeoxyglucose (FDG) accumulation was increased in the interventricular septum compared with the LV free wall in patients with chronic RV volume overload due to atrial septal defect, and that the FDG accumulation in the RV free wall was also increased in those patients compared with the control subjects, although we did not correct the radioactivity for the RV free wall thickness (7). However, it is unclear whether FDG accumulation in the RV free wall, corrected for the partial volume effect, which is derived from the relatively thin RV free wall thickness, increases in patients with chronic RV pressure overload.…”