Delayed recovery of myocardial perfusion in acute myocardial infarction: a scintigraphic study after early thrombolytic treatment.
BACKGROUND
Assessments of compromised myocardium and infarct size early after thrombolytic treatment in acute myocardial infarction (AMI) are important for risk stratification and for treatment management. We have therefore evaluated the clinical usefulness of myocardial perfusion scintigraphy (MIBI-SPECT) for the assessment of myocardial viability early after AMI.


METHODS
Seventy-one patients [53 men and 18 women, aged 64 +/- 9 years (range 45-75 years)] with AMI treated by thrombolysis took part in this prospective study at University Hospital, Stockholm, Sweden. Sixty of them underwent adenosine-stress and resting MIBI-SPECT 2-4 days after AMI, and 11 were examined only at rest. Six months after the AMI, a repeat MIBI-SPECT at rest was obtained for comparison.


RESULTS
All patients had significant perfusion defects compared with an age- and sex-matched healthy reference population. Seventy-six percent of the patients able to undergo a complete adenosine-stress and rest SPECT showed signs of reversible perfusion defects. Defect size (extent) and severity at rest decreased between the tests at 2-5 days and 6 months after AMI (P < 0.001). Reversible perfusion defects early after AMI were not related to spontaneous improvement of myocardial perfusion 6 months later. Early, semiquantitative MIBI-SPECT was not able to predict final infarct size as measured by resting perfusion data 6 months after AMI, regardless of whether the threshold value was set at 30, 40, 50 or 60% of the maximal isotope uptake in the early resting scan.


CONCLUSIONS
Myocardial perfusion scintigraphy with adenosine-stress and resting MIBI-SPECT early after AMI underestimates myocardial viability in the majority of patients treated with thrombolytic agents. Neither reversible perfusion defects nor regional semi-quantitative perfusion data appear to predict spontaneous improvement of perfusion 6 months after AMI.
Bouvier
F
F
Department of Clinical Physiology, Söder Hospital, Stockholm, Sweden. bouvier.info@swipnet.se
Höjer
J
J
Samad
B A
BA
Jensen-Urstad
K
K
Ruiz
H
H
Hulting
J
J
Jensen-Urstad
M
M
D000241:Adenosine; D003326:Coronary Circulation / Q000502:physiology*; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006321:Heart / Q000000981:diagnostic imaging*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging* / Q000188:drug therapy / Q000503:physiopathology; D017682:Myocardial Stunning / Q000000981:diagnostic imaging; D011446:Prospective Studies; D019275:Radiopharmaceuticals; D013300:Streptokinase / Q000627:therapeutic use; D017256:Technetium Tc 99m Sestamibi; D015912:Thrombolytic Therapy; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use; D015899:Tomography, Emission-Computed, Single-Photon; D014665:Vasodilator Agents
D005343:Fibrinolytic Agents; D019275:Radiopharmaceuticals; D014665:Vasodilator Agents; D017256:Technetium Tc 99m Sestamibi; D013300:Streptokinase; D010959:Tissue Plasminogen Activator; D000241:Adenosine