RT Book, Section
A1 Ohira, Hiroshi
A1 Renaud, Jennifer
A1 deKemp, Robert A.
A1 Aung, May
A1 Ruddy, Terrence D.
A1 Beanlands, Rob
A2 Heller, Gary V.
A2 Bateman, Timothy M.
A2 Case, James A.
A2 Arumugam, Parthiban
SR Print(0)
ID 1159185178
T1 Patient Preparation for FDG PET Viability Imaging
T2 Cardiovascular PET: Current Concepts
YR 2019
FD 2019
PB McGraw-Hill Education
PP New York, NY
SN 9781259860485
LK accesscardiology.mhmedical.com/content.aspx?aid=1159185178
RD 2024/04/19
AB The  heart  consumes  more  energy  than  any  other  organ  in  order  to  maintain  its  contractile  performance.1  The  healthy  myocardium  possesses  the  superb  ability  to  utilize  a  wide  variety  of  substrates  including:  free  fatty  acids,  glucose,  lactate,  pyruvate,  ketone  bodies,  and  amino  acids  as  energy  sources,  which  makes  it  possible  for  it  to  function  as  a  constant  pump.  In  the  healthy  adult  myocardium,  free  fatty  acids  are  the  major  energy  source;  however,  under  certain  conditions,  such  as  the  postprandial  state  when  glucose  is  more  available,  the  heart  is  capable  of  switching  to  a  glucose-predominant  substrate  utilization  pattern.2,3  During  ischemia,  when  there  is  reduced  oxygen  available  to  the  tissue,  the  heart  must  use  anaerobic  glycolysis  for  ATP  and  energy  production.  As  such,  glucose  becomes  the  primary  substrate  for  ischemic  myocardium.  18F-fluorodeoxyglucose  (FDG)  is  a  glucose  analog  whose  uptake  parallels  glucose  and,  therefore,  can  be  used  to  reflect  glucose  utilization  and  the  metabolic  state  of  the  myocardium.  Viable  myocardium  that  is  ischemic  or  hibernating  will  take  up  glucose  and  thus  FDG.  Likewise  normal  myocardium  (which  is,  of  course,  also  viable)  in  the  postprandial  state  will  take  up  glucose  and  as  such  FDG.