TY - JOUR
T1 - Long-term right ventricular volume overload increases myocardial fluorodeoxyglucose uptake in the interventricular septum in patients with atrial septal defect
AU - Otani, Hiroki
AU - Kagaya, Yutaka
AU - Yamane, Yuriko
AU - Chida, Masanobu
AU - Ito, Kenta
AU - Namiuchi, Shigeto
AU - Shiba, Nobuyuki
AU - Koseki, Yoshito
AU - Ninomiya, Mototsugu
AU - Ikeda, Jun
AU - Saito, Haruo
AU - Maruoka, Shin
AU - Fujiwara, Takehiko
AU - Ido, Tatsuo
AU - Ishide, Nobumasa
AU - Shirato, Kunio
PY - 2000/4/11
Y1 - 2000/4/11
N2 - Background - Several studies have shown that long-term right ventricular (RV) overload in animal models alters myocardial energy substrate metabolism. However, whether long-term RV volume overload alters this metabolism in the human is unclear. Methods and Results - We performed positron emission tomography with [18F]fluorodeoxyglucose (FDG) and single-photon emission tomography (SPECT) with [201Tl] (Tl) and [123I]15-(p-iodophenyl)-3-R,S- methylpentadecanoic acid (BMIPP) in 11 patients with atrial septal defect (ASD) and 11 control subjects. In the FDG study, we calculated myocardial metabolic rate of glucose (MMR) in interventricular septum (IVS) and left ventricular (LV) free wall. MMR was significantly increased in IVS compared with LV free wall in the ASD patients (420±35 versus 333±32 mol · kg-1 · min-1; P<0.05) but not in the control group (347±27 versus 357±25 mol · kg-1 · min-1). In both ASD and control groups, SPECT count was not significantly different between IVS and LV free wall in Tl (ASD, 160±1 versus 177±12; control, 141±12 versus 157±14 counts per 15 minutes) and BMIPP studies (ASD, 203±14 versus 212±18; control, 162±16 versus 176±16 counts per 15 minutes). MMR in the IVS/LV free wall ratio in the ASD group significantly correlated with indices related to RV volume overload. Conclusions - Given the assumption that long-term RV volume overload did not affect the lumped constant, the present study suggests that, unlike myocardial perfusion or fatty acid analogue uptake, myocardial glucose utilization in IVS relative to LV free wall is increased in relation to long- term RV volume overload in patients with ASD.
AB - Background - Several studies have shown that long-term right ventricular (RV) overload in animal models alters myocardial energy substrate metabolism. However, whether long-term RV volume overload alters this metabolism in the human is unclear. Methods and Results - We performed positron emission tomography with [18F]fluorodeoxyglucose (FDG) and single-photon emission tomography (SPECT) with [201Tl] (Tl) and [123I]15-(p-iodophenyl)-3-R,S- methylpentadecanoic acid (BMIPP) in 11 patients with atrial septal defect (ASD) and 11 control subjects. In the FDG study, we calculated myocardial metabolic rate of glucose (MMR) in interventricular septum (IVS) and left ventricular (LV) free wall. MMR was significantly increased in IVS compared with LV free wall in the ASD patients (420±35 versus 333±32 mol · kg-1 · min-1; P<0.05) but not in the control group (347±27 versus 357±25 mol · kg-1 · min-1). In both ASD and control groups, SPECT count was not significantly different between IVS and LV free wall in Tl (ASD, 160±1 versus 177±12; control, 141±12 versus 157±14 counts per 15 minutes) and BMIPP studies (ASD, 203±14 versus 212±18; control, 162±16 versus 176±16 counts per 15 minutes). MMR in the IVS/LV free wall ratio in the ASD group significantly correlated with indices related to RV volume overload. Conclusions - Given the assumption that long-term RV volume overload did not affect the lumped constant, the present study suggests that, unlike myocardial perfusion or fatty acid analogue uptake, myocardial glucose utilization in IVS relative to LV free wall is increased in relation to long- term RV volume overload in patients with ASD.
KW - Glucose
KW - Heart septal defects
KW - Metabolism
KW - Nuclear medicine
UR - http://www.scopus.com/inward/record.url?scp=0034636081&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034636081&partnerID=8YFLogxK
U2 - 10.1161/01.CIR.101.14.1686
DO - 10.1161/01.CIR.101.14.1686
M3 - Article
C2 - 10758051
AN - SCOPUS:0034636081
VL - 101
SP - 1686
EP - 1692
JO - Circulation
JF - Circulation
SN - 0009-7322
IS - 14
ER -