Edward S. Weiss

Detection of remote myocardial infarction in patients with positron emission transaxial tomography and intravenous 11C-palmitate.

Ischemic myocardial injury has been detected recently in isolated perfused hearts and intact experimental animals with positron-emitting “C-paImitate and reconstructive tomography providing cross-sectional images of the heart free from superimposed activity in overlying structures. To evaluate the applicability of positron emission transaxial tomography in detecting infarction in man, 10 normal human subjects and 12 patients who sustained documented acute myocardial infarction three to 12 months previously were studied. Tomograms were obtained after intravenous injection of 5 to 10 mCi of “C-labeled palmitate, a physiological substrate of myocardium. Tomograms from all normal subjects ex- hibited homogeneous distribution of “IC-palmitate throughout each 1.5 cm thick cross section of the ventricle. Tomograms from all patients with remote anterior or inferior and posterior myocardial infarction exhibited diminished accumulation of “IC-palmitate delineating regions corresponding to the electrocardiographic locus of infarction. The distribution of “IC-palmitate detectable by positron emission transaxial tomography in a series of cross sections from apex to base in the same normal subject or patient with remote myocardial infarction was analogous to that observed in normal dogs and animals with experimentally induced myocardial infarction.

Quantification of infarction in cross sections of canine myocardium in vivo with positron emission transaxial tomography and 11C-palmitate.

SUMMARYTo assess myocardial infarction quantitatively in 15 mm thick transverse sections of the canine heart in vivo we utilized a new technique, positron emission transaxial tomography (PETT) and cyclotron-produced 11C-palmitate (11C-P) injected intravenously. Results were compared to regional myocardial creatine phosphokinase (CPK) depletion, diminished 144C-palmitate accumulation in tissue extracts, and infarction estimated morphometrically 48 hours after coronary occlusion. CPK activity and 14C-P content declined in parallel In transmural biopsies (N = 44) from normal and ischemic zones (r = .92) in six dogs; and infarct in 10 mm thick cross sections of the entire left ventricle estimated morphometrically (N 26) in six other animals correlated with CPK depletion in contiguous 2.5 mm thick slices (r = .92). When the percentage of infarction in 15 mm thick cross sections was assessed tomographically in six other dogs 48 hours after coronary occlusion with 11C-P injected intravenously, results correlated with infarction in corresponding cross sections from the same hearts estimated morphometrically (r = .97, N = 9) and by analysis of CPK depletion (r = .93, N = 9). ThIls, PETT permits estimation of infarction in cross sections of the left ventricle In vivo after intravenous injection of 11C-palmitate.

Evaluation of myocardial metabolism and perfusion with positron-emitting radionuclides.

Unfortunately, in spite of vigorous research efforts and some very promising successes, to date conventional nuclear medicine technology has not provided a totally satisfactory method for the regional, noninvasive differentiation of dead myocardium from ischemic but still viable tissue. This lack of success stems from the physical limitations of the imaging methods used and from the inadequacies of the radiopharmaceuticals administered. At present, most conventional myocardial

Imaging of the inflammatory response in ischemic canine myocardium with 111indium-labeled leukocytes

Myocardial leukocyte infiltration is one hallmark of acute myocardial infarction. In order to detect noninvasively this inflammatory response associated with acute myocardial infarction, we produced coronary occlusion in eight dogs, intravenously administered autologously labeled indium-111 (111In) leukocytes and scintigraphically monitored accumulation of radionuclide in myocardium. Seventy-two hours after coronary occlusion, 111In-labeled white cells accumulated in regions corresponding to myocardial infarcts, and positive images with 111In-labeled leukocytes correlated well with images obtained with technetium-99m pyrophosphate and computer-reconstructed tomograms obtained with nitrogen-13-labeled ammonia. In contrast, two control dogs subjected to sham operation did not exhibit positive 111In-leukocyte images. Scintigraphic results with 111In-labeled leukocytes were verified in vitro by analysis of radioactivity in normal myocardium and in infarcts. Thus, leukocytic infiltration associated with acute myocardial infarction can be detected noninvasively in vivo.

Positron Emission Reconstruction Tomography For The Assessment Of Regional Myocardial Metabolism By The Administration Of Substrates Labeled With Cyclotron Produced Radionuclides

The conventional methods for the assess-ment of myocardial functional integrity, which rely on the external detection of an administered radiopharmaceutical, share the following crippling limitations. (1) The field of view of the radiation detector always encompasses the contribution of activity contained in tissues overlying and underlying the plane of interest. This contribution, which in general cannot be subtracted from the measured signal, contributes noise, and in general considerably depresses the contrast in the plane of interest between tissues containing different activities. (2) The attenuation of the gamma radiation originating from the activity in the myocardium is dependent upon the amount of tissue interposed between the myocardium and the radiation detector. This effect is difficult to compensate for. The combination of the above two defects seriously depresses contrast in myocardial nuclear imaging, and all but precludes the reliable quantitative assessment of the distribution of a radio-active label in the myocardium.