Quantification of myocardial infarct size by thallium-201 single-photon emission computed tomography: experimental validation in the dog.

Abstract

To evaluate the potential advantages of thallium-201 (201T1) single-photon emission computerized tomography (SPECT) to assess myocardial infarct size in the experimental animal, six normal dogs and 14 dogs with 6 to 8 hr closed-chest coronary occlusion (eight left anterior descending and six left circumflex) were studied. Ten minutes after intravenous administration of 2 mCi of 201T1, 30 projections were obtained over 180 degrees. The dogs were killed and their hearts sliced and stained by triphenyl tetrazolium chloride (TTC). Pathologic infarct size was calculated for each slice and for the entire left ventricular myocardium as percent weight. Tomograms were quantified by automatically generating maximum-count circumferential profiles, which were compared with normal limit profiles derived from the six normal dogs. Tomographic infarct size was defined as the percentage of circumferential points falling below normal for each tomogram. SPECT and TTC infarct size on 71 slices correlated highly (mean SD 27.9 ± 23.4% and 26.7 25.3%, respectively; r = .93, p < .001, SEE = 9.4%). To determine SPECT infarct size as percent total left ventricular myocardial weight, infarct sizes from each slice were added to one another after each was multiplied by a coefficient that reflected the contribution of that slice to the total left ventricular weight. SPECT and TTC infarct size for the entire left ventricle correlated closely (mean ± SD 20.5 ± 7.6% and 19.3 ± 8.3%, respectively; r = .86, p < .001, SEE = 4.5%). It is concluded that 201T1 SPECT is a valid method for the noninvasive assessment of experimental myocardial infarct size. Circulation 74, No. 4, 852-861, 1986. PROGNOSIS in acute myocardial infarction has been shown to be related to the extent of the necrotic myocardium.1-t Several noninvasive, nonimaging,6-8 and imaging5' 121 methods have been developed for measurement of infarct size. With planar imaging or limited-angle tomography,9-13 thallium-201 (201T1) myocardial perfusion and technetium-99m-pyrophosphate infarct-avid scintigraphy are suboptimal for quantita-

Quantification of infarct size by 201Tl single-photon emission computed tomography during acute myocardial infarction in humans. Comparison with enzymatic estimates.

“…Radionuclide perfusion scintigraphy is an alternative noninvasive method that may provide this important anatomic information. In [17][18][19] This technique is highly reproducible and does not rely on subjective edge detection of the outer myocardial border or that of the perfusion defect.…”

Lack of correlation after reperfusion between ventricular function and infarct size estimated by thallium single-photon emission computed tomography

“…Experimental [7,13,14,15] and clinical thallium tomographic studies [11,16,17] have found a correlation between anatomical and enzymatic or ventriculographic infarct size. Patients in whom reperfusion was achieved, however, were only studied by Tamaki et al [9] who found that the correlation between thallium defect size and CK-MB release was not as good in reperfused as compared to nonreperfused patients.…”

“…After thrombolytic therapy, in many patients subendocardial regions of myocardium are recovered and therefore no clear-cut thallium defect remains. These subendocardial infarctions might have been missed by scintigraphy, as was the case for infarctions involving less than 50% of myocardial wall thickness in an experimental study using a very similar method for quantification of infarct size [15]. Thus, the lack of correlation between ventricular function and thallium distribution may actually reflect the complex pathophysiology involved in tissue recovery following ischemic injury.…”

Diabetes mellitus impairs myocardial oxygen metabolism even in non-infarct-related areas in patients with acute myocardial infarction

“…Although the local myocardial oxygen metabolism without ischemia is dependent on the global myocardial work, which correlates closely with the rate pressure product [23] and the extent of myocardial damage due to infarction might have affected the myocardial oxygen metabolism in non infarct-related area, no significant differences were found between group A and group B in the rate pressure products, the indices of the amount of myocardial necrosis (the peak level of serum creatine phosphokinase and summed rest score of technetium-99m tetrofosmin) [24] or the index of the extent of the area at risk (summed rest score of iodine-123 betamethyliodophenylpentadecanoic acid) [15], and besides, these data did not correlate with the myocardial oxygen metabolism in non infarct-related area in all patients with acute myocardial infarction (group A and group B). Moreover, plasma glucose concentrations, serum concentrations of insulin and free fatty acids at the carbon-11 acetate positron emission tomography scan, which might affect the myocardial oxygen metabolism, were not different between group A and group B.…”