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visualization of the infarct size (i.e., SPECT, contrast-enhanced MRI) or indirect
method of measuring systolic dysfunction in the infarct zone as an indicator of
extent of scar tissue. Though certain studies showed decrease in the infarct size over
period of time [ 50 – 52 ] the results of the other studies was not conclusive [ 49 , 56 ].
As far as imaging techniques is concerned contrast enhanced MRI provides more
accurate results as compared to SPECT. MRI and SPECT detect transmural myo-
cardial infarcts at similar rates. However, MRI systematically detects subendocar-
dial infarcts that are missed by SPECT [ 57 ]. Considering variable results further
randomized controlled trials are needed to evaluate changes in infarct size after stem
cell therapy.
8.5.3 Myocardial Perfusion
Studies have used cardiac imaging tools to assess myocardial perfusion following
stem cell therapy [ 51 , 54 , 55 ]. Changes in perfusion following acute myocardial
infarction as well as chronic ischemic disease can be evaluated. These techniques
mostly include nuclear imaging with PET or SPECT. While SPECT is predomi-
nantly used non-invasive imaging and provides information on relative changes in
tracer uptake, PET measures absolute quantification of myocardial perfusion.
Doppler flow wire can be used invasively to assess coronary blood flow at rest and
stress [ 58 ]. Studies have shown improvement in perfusion defect following stem
cell therapy with decrease in size of the defect seen over 3–12 months using resting
Tc-99m sestamibi SPECT [ 59 ]. Also some studies have reported decrease in stress-
inducible ischemia [ 60 ] in patients with refractory angina.
8.5.4 Myocardial Viability
Myocardial viability can be evaluated using nuclear imaging with PET (mainly
using F18-FDG ) or SPECT (with F18-FDG or Tc-99m-labeled agents), or low-
dose dobutamine echocardiography or MRI. These techniques can be used to evalu-
ate viability in the infarct zone with increased F18-FDG seen after cell therapy [ 51 ,
61 ] within 3–6 month of follow up. Also catheter-based electromechanical mapping
can be used for identification and localization of viable myocardial tissue. Other
marker of myocardial viability is contractile reserve with most studies not being
able to show significant improvement following stem cell therapy. This may be
because in patients with severe myocardial dysfunction and injury on the cellular
level, contractile reserve is frequently lost, whereas glucose utilization is preserved.
The substantial number of myocardial segments with preserved glucose and fatty
acid utilization but without contractile reserve, suggests an underestimation of myo-
cardial viability by dobutamine echocardiography [ 62 ]. Further studies would be
needed to evaluate changes in myocardial viability following stem cell therapy.
S. Raina et al.