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The current reperfusion strategy in Japan for acute myocardial infarction (AMI) is that the majority of early arrival patients are treated with primary percutaneous coronary intervention (PCI). However, the efficacy of primary PCI, intravenous thrombolysis (IV-T), intracoronary thrombolysis (IC-T) and rescue PCI has not been compared in the clinical situation. In the present study, 3,258 cases of AMI in 1992-2000 from the data base of the Miyagi Study Group for AMI were analyzed. These patients were hospitalized within 6 h of the onset of symptoms. IV-T and IC-T were initially performed in 120 and 441 patients, respectively, and 41 and 199 rescue PCI procedures, respectively, were needed. Primary PCI was performed in 1,822 cases, and no reperfusion therapy was done in 875 patients. The crude 30-day in-hospital mortality was 12.7% for IV-T, 3.7% for IC-T, 4.8% for primary PCI, 7.9% for rescue PCI, and 14.1% in patients who did not undergo reperfusion therapy. The covariate-adjusted odds ratio (95% confidence interval) was 0.38 (0.28-0.52) for primary PCI, 0.30 (0.15-0.60) for IC-T, 1.04 (0.51-2.10) for IV-T and 0.77 (0.46-1.30) for rescue PCI. The present data verify that primary PCI is superior to other reperfusion strategies in the real clinical situation and justifies the current unique strategy of reperfusion therapy for AMI used in Japan.

We recently reported that myocardial phosphoinositide (PI) metabolism can be visualised by 1-[1-11C]-butyryl-2-palmitoyl-rac-glycerol (11C-DAG) in rats with myocardial infarction (MI). Angiotensin II, the receptors for which are expressed predominantly in infarcted areas with active fibrogenesis rather than in non-infarcted regions, is involved in the upstream signalling systems of PI metabolism and plays an important role in the process of left ventricular (LV) remodelling after MI. We therefore hypothesised that the distribution of 11C-DAG after MI may be affected by the inhibition of angiotensin converting enzyme, which is one of the most important factors in the development of LV remodelling after MI. Rats were injected with 11C-DAG after 3 or 10 weeks of treatment with captopril or no treatment following coronary artery ligation, and quantitative autoradiography was performed. Cells occupying the infarcted region were identified by immunohistochemistry. Compared with untreated rats, treatment with captopril for 3 weeks after MI elicited a reduction in the 11C-DAG uptake in the infarcted region (P<0.05) but not in the non-infarcted region, and was associated with a 22% decrease in the heart weight/body weight ratio. The thallium-201 distribution in the infarcted area was similarly low in the rats with and rats without the 3-week captopril treatment after MI. Abundant macrophages and myofibroblasts occupied the infarcted area in both rats with and rats without the captopril treatment for 3 weeks after MI. The 11C-DAG radioactivity in the infarcted region in the untreated rats was lower 10 weeks after MI than 3 weeks after MI (P<0.01). This finding was in agreement with the results of immunohistochemistry demonstrating that the number and size of macrophages and myofibroblasts were remarkably reduced in rats 10 weeks after MI compared with 3 weeks after MI. Captopril treatment for 10 weeks after MI did not decrease the 11C-DAG radioactivity in the infarcted area further. These data suggest that 11C-DAG is useful for visually detecting regions with activated PI metabolism after MI, and that captopril reduces PI metabolism in the infarcted region in the relatively early phase of MI, which might contribute to the attenuation of ventricular remodelling.

The case-fatality rate from acute myocardial infarction (AMI) appears to have been declining in recent decades, so the present study reviewed the trend in in-hospital case-fatalities from AMI in Miyagi Prefecture, Japan, 1980-1999. The causes of death and the effects of gender and age on the trend were also analyzed. From the AMI registration database of the Miyagi Study Group for AMI, 12,961 cases of AMI were analyzed. The 30-day in-hospital case-fatality was calculated from the data for 1980-1999: data for causes of death were available for 1980-1997, and the data concerning primary percutaneous transluminal coronary angioplasty (PTCA) for AMI were available for 1997-1999. The in-hospital case-fatality rate declined from 17.0% in the early 80s to 7.3% in the late 90s (approximately 57% reduction). The in-hospital case-fatality rate was higher in female patients. Rhythm failure substantially decreased in the late 1980s. Pump failure is decreasing, but is still the biggest problem. The in-hospital case-fatality rate was significantly lower in patients received PTCA. The declining trend in the in-hospital case-fatality rate suggests the benefits of current therapeutic procedures, including primary PTCA, for AMI. Pump failure is an important target for further decreasing the trend.

lodine-123 metaiodobenzylguanidine (MIBG) uptake was reported to be reduced compared to Tl-201 (Tl) in acute myocardial infarction (AMI). Within such an area, degrees of both sympathetic neural function and ischemic myocardial cell damage are considered to be greatly dispersed. These kinds of damage were reported to effect reporalization time in myocardial cells, and we evaluated our hypothesis that extension of the discordant MIBG uptake area correlates with recovery time (RT) dispersion and relate ventricular arrhythmias in AMI. MIBG and Tl images were obtained in AMI patients. Regional Tl or MIBG uptake was estimated in 9 segments of SPECT by using four-point scoring. The total score was the sum of scores in 9 SPECT segments. ATI-MIBG was calculated by subtracting the total MIBG score from the total Tl score. Corrected RT (RTc) was measured as a signal-averaged ECG. RTc dispersion was defined as the difference between maximal and minimal RTc. The patients were assigned to two groups (group A; < or = Lown 4a, group B; > or = Lown 4b) according to the results of 24-hour Holter monitoring. A positive correlation between RTc dispersion and ATI-MIBG was found. ATI-MIBG and RTc dispersion in group B were greater than those in group A. These results suggested that ATI-MIBG could be used to predict the development of malignant ventricular arrhythmias.

To investigate the effects of endothelin blockade initiated immediately after the onset of myocardial infarction on survival and left ventricular remodeling, treatment with the nonselective receptor antagonist TAK-044 (n = 22) or saline (n = 19) for 3 weeks was initiated immediately after coronary ligation in rats. The 24-h survival rate was significantly lower in the TAK-044 group than in the saline group. The systolic blood pressure 24 h after the onset of myocardial infarction was similar in the saline and TAK-044 groups, although it was significantly lower in the TAK-044 group during the 3-week protocol. Heart weight/tibial length was significantly increased in the TAK-044 group compared with the saline group. As all deaths in the TAK-044 group occurred within 24 h after myocardial infarction, we performed additional experiments using a separate group of rats 12-16 h after myocardial infarction. Plasma and myocardial endothelin-1 levels were significantly increased, and a bolus injection of TAK-044 significantly reduced left ventricular dP/dtmax in these rats that had had a myocardial infarction compared with sham-operated rats. Endothelin receptor blockade initiated immediately after the onset of myocardial infarction may deteriorate acute-phase survival and left ventricular remodeling. Inhibition of the positive inotropic action of endothlin-1 may partially explain the increased 24-h mortality.

Unlabelled: Phosphoinositide turnover mediates the signaling of angiotensin II, which plays a pivotal role in ventricular remodeling after myocardial infarction (MI). We tested the hypothesis that phosphoinositide turnover can be visualized by 1-[1 -(11)C]butyryl-2-palmitoyl-rac-glycerol (11C-DAG) in both infarcted and noninfarcted myocardium after MI in rats., Methods: Rats received an injection of 11C-DAG 7 d after left coronary artery ligation, and myocardial lipids were extracted from both infarcted and noninfarcted areas of myocardium (n = 3). Metabolites of 11C-DAG were determined by thin-layer chromatography. Quantitative autoradiography of hearts was performed to visualize myocardial phosphoinositide turnover in rats that received an injection of 11C-DAG 1 d (n = 3) and 7 d (n = 5) after MI and 7 d after a sham operation (n = 3). Quantitative autoradiography with 201TlCl was also performed to evaluate myocardial blood flow in rats 7 d after MI (n = 3). Cells occupying the infarcted myocardium were identified by immunohistochemistry., Results: The radioactivity incorporated into the intermediates of phosphoinositide turnover was predominant in both the infarcted (67.1% +/- 5.2% of the total activity) and the noninfarcted (57.4% +/- 3.2%) myocardium. 11C-DAG radioactivity in the infarcted region normalized to that in the noninfarcted region was 1.09 +/- 0.04 in rats 7 d after MI, which was significantly higher than that in rats 1 d after MI (0.38 +/- 0.03, P < 0.001). 201Tl radioactivity in the infarcted region normalized to that in the noninfarcted region was only 0.19 +/- 0.01 7 d after MI. 11C-DAG radioactivity in the noninfarcted region normalized to that in the right ventricular free wall tended to be increased in rats 1 and 7 d after MI compared with the sham-operated rats; the differences, however, were not statistically significant (1.30 +/- 0.15, 1.20 +/- 0.07, and 1.13 +/- 0.02, respectively). Immunohistochemistry revealed that abundant fibroblasts, myofibroblasts, and macrophages occupied the infarcted myocardium 7 d after MI, but the cellularity was low during the first day after MI., Conclusion: These data suggest that 11C-DAG may be useful for visualizing regions with activated phosphoinositide turnover after MI. Because wound healing and fibrogenic processes are important factors of ventricular remodeling, 11C-DAG and PET may offer new information benefiting patient management after MI.

Phosphoinositide turnover and protein kinase C (PKC) mediate the signaling of angiotensin II, which plays a pivotal role in ventricular remodeling after myocardial infarction (MI). To determine whether PKC is activated after MI, rat hearts after MI were subjected to in vitro quantitative autoradiography with [3H]phorbol 12,13-dibutyrate (PDBu), which is highly selective for PKC. [3H]PDBu binding in the infarcted area increased significantly compared with the non-infarcted region 7 and 21 days after MI, but not 1 and 3 days and 10 months after MI. [3H]PDBu binding in the noninfarcted area was similar to that in the sham-operated rats. Immunohistochemical analysis revealed that abundant macrophages (7 days after MI), fibroblasts, and myofibroblasts (7 and 21 days after MI) occupied the infarcted region. To investigate whether myocardial [3H]PDBu binding is affected by captopril, hearts were subjected to in vitro autoradiography with [3H]PDBu after 1- or 3-week captopril treatment or no treatment. Captopril treatment significantly suppressed [3H]PDBu binding in the infarcted area 3 weeks after MI, but not 1 week after MI nor in the noninfarcted areas. These results suggest that PKC is upregulated during the healing and fibrogenic process after MI and that captopril treatment suppresses the upregulation in the infarcted area.

This study qualified the severity and localization of reverse redistribution of technetium-99 m (Tc)-tetrofosmin rest imaging. Both Tc-tetrofosmin and thallium-201 (Tl) rest imaging with early images and delayed images were obtained in the subacute phase of myocardial infarction in 21 patients with first anterior myocardial infarction and with successful transluminal angioplasty (including stenting). Relative myocardial uptake (%uptake), degree of reverse redistribution (%), and washout rate (%) were evaluated quantitatively in 6 left ventricular segments (inferoseptal, anteroseptal, anterior, anterolateral, lateral, inferolateral and inferior) by circumferential profile analysis. The percentage reverse redistribution in the infarct area was larger in Tc-tetrofosmin imaging than in Tl imaging (p = 0.013). Reverse redistribution was most prominent in the anterior wall (anterior > anteroseptal > inferoseptal, p = 0.020). This suggests that infradiaphragmatic scatter is unlikely as the mechanism of reverse redistribution. The washout rate of Tc-tetrofosmin in the infarct area (reverse redistribution area) was higher than that in the normal area (non-reverse redistribution area), and was also higher than the washout rate of Tl imaging in the infarct area. The %uptake of delayed images in the infarct area was larger in Tc-tetrofosmin than that in Tl imaging, whereas %uptake of early images did not differ. The percentage reverse redistribution did not correlate with the degree of collateral circulation and the residual stenosis. In conclusion, reverse redistribution of Tc-tetrofosmin was more prominent in the infarct area, and this was due to the relatively lower uptake of reverse redistribution of Tc-tetrofosmin than delayed Tl images.

Background: Iodine 123-labeled 15-(p-iodophenyl)-3R,S-methylpentadecanoic acid (BMIPP) has recently been developed, since normal myocardium metabolizes free fatty acids. This study investigated the clinical usefulness of BMIPP imaging in patients with acute myocardial infarction (MI), particularly in the detection of stunned myocardium in patients who underwent acute coronary revascularization., Methods: The subjects were 41 patients with acute MI who had undergone emergency coronary revascularization. Both BMIPP and thallium-201 images at rest were obtained during the subacute phase. The myocardial distribution of radiotracers was quantified by generating circumferential count-distribution profile analysis. Initial 201Tl imaging, delayed 201Tl imaging, and BMIPP imaging were performed, and the mean count densities in the infarct region (initial 201Tl images [TL1], delayed 201Tl images [TL2], and BMIPP images in the infarct region [BM], respectively) were obtained. The differences between mean count densities (TL1-BM: BM subtracted from TL1; TL2-BM: BM subtracted from TL2) were also calculated., Results: BM showed a higher correlation with wall motion data by echocardiography (WM) in the acute phase than other nuclear imaging tests, whereas TL2 showed the highest correlation with WM in the chronic phase. Acute to chronic WM improvement showed a good correlation with TL2-BM., Conclusion: Single photon emission computed tomography imaging with BMIPP is a candidate for providing the "memory image" of ischemic damage, whereas TL2 reflects all viable tissue. The mismatch between the tracers can serve as an indicator of myocardial stunning.

Myocardial imaging using beta-methyl-p-[123I]-iodophenylpentadecanoic acid (BMIPP) of 15 patients with acute myocardial infarction was performed to assess "fill-in" and "washout" defects in the delayed myocardial image. The initial and delayed images were evaluated by a visual and quantitative washout rate method. Visual judgement found 8/180 (4%) segments showed "fill-in" defects, and 24/180 segments (13%) showed "washout" defects. There was no relationship between days from onset to the study and the frequency of fill-in and washout defects. The mean washout rate in the segments with "fill-in" defects was 9.0 +/- 16.6%, and that of "washout" defects was 24.9 +/- 18.1% which was significantly higher than in controls (8.7 +/- 15.4%, p < 0.05). There was no correlation between mean washout rate and total blood lipids, total cholesterol, triglyceride and HDL-cholesterol. Therefore, neither time from onset nor blood lipids level was related to changes from the initial image to the delayed image. These changes may be due to relative (false) findings due to changes in circumference, and may be based on myocardial characteristics after myocardial infarction and/or reperfusion.

Quantitative evaluation of 111In-antimyosin Fab myocardial (InAM) imaging was performed in 15 patients with acute myocardial infarction to evaluate which organ is the most appropriate for the control of myocardial accumulation, to compare the quantitative method with the conventional visual method, and to study which clinical indices correlate with the InAM quantitative evaluations. InAM images demonstrated the myocardium with 31 +/- 6 mean counts/pixel, lung with 14 +/- 4, upper mediastinum with 20 +/- 5, middle mediastinum with 26 +/- 5, and liver with 75 +/- 10. We considered the lung to be the most appropriate control organ for quantitative evaluations of InAM imaging, because it could be separated from the myocardium, and the measurement range was narrow. The InAM uptake index [IUI = (myocardial counts-lung counts)/lung counts] was calculated as the index of myocardial accumulation. Visual evaluations of myocardial accumulation on InAM images were classified into three grades. The IUI of grade 1 (slight) was 0.98 +/- 0.19, grade 2 (moderate) was 1.34 +/- 0.38, and grade 3 (severe) was 1.97 +/- 0.19. Visual grading was nearly in accordance with the IUI, although it was difficult to distinguish visually between grades 1 and 2. Measurement of wall motion by left ventriculography showed that reduced wall motion was associated with an IUI of 1.01 +/- 0.18 and dyskinesis with an IUI of 1.92 +/- 0.16, showing IUI can indicate regional myocardial damage. However, IUI was not correlated with indices of the overall left ventricular function, such as ejection fraction, cardiac index, and peak creatine kinase level.

Antiarrhythmic and electrophysiological effects of SD-3212, a novel antiarrhythmic agent, which has both Na+ channel and Ca++ channel blocking activities, were compared with those of its (+)-stereoisomer, SD-3211, which has only a Ca++ channel blocking activity, and bepridil, a known Ca++ channel blocker with additional Na+ channel blocking activity, using the two-stage coronary ligation induced arrhythmia (24 h after the ligation of the left anterior descending coronary artery) and 7 day-old myocardial infarcted hearts in anaesthetized dogs. SD-3212 showed a dose-dependent antiarrhythmic effect on the two-stage coronary ligation induced arrhythmia. SD-3212 at a dose of 3 mg/kg reduced the arrhythmic ratio, i.e. ectopic beats per min divided by the sum of ectopic beats and sinus beats per min, significantly from 1 up to 12 min after the administration. Neither bepridil (1-6 mg/kg) nor SD-3211 (1 mg/kg) had an antiarrhythmic effect. SD-3212 (0.3-3 mg/kg) prolonged both the conduction time in the normal myocardium and the delayed potential in the infarcted myocardium in the 7 day-old myocardial infarcted hearts in anaesthetized dogs in a dose-dependent manner. This effect of SD-3212 was shown at coupling intervals of 150-1000 ms increasing with decreasing interval. In this respect, SD-3212 is similar to drugs which show fast recovery of Vmax from use-dependent block such as lidocaine. Bepidril (1-6 mg/kg) also prolonged these parameters in a dose-dependent manner, however, the prolongation induced by bedripil was limited to shorter coupling intervals as compared with that induced by SD-3212. SD-3212 (0.1-1 mg/kg) did not show this prolonging effect.(ABSTRACT TRUNCATED AT 250 WORDS)

201Tl stress myocardial scintigraphy was performed in convalescent patients with acute myocardial infarction, to evaluate the influence of stenosis and collateral circulation of coronary artery in acute phase, on myocardial salvage in chronic phase. In 14 cases of unsuccessful coronary revascularization (complete occlusion), a complete defect of thallium imaging in chronic phase was seen in only one case of four cases with good collateral circulation, while eight of 10 cases with poor collateral circulation. In 16 cases of poor collateral circulation, six cases showed a complete defect, although the target vessel had improved to less than 75% of stenosis. However, in cases of good collateral circulation, no case showed a complete defect when the target vessel had improved to less than 75% of stenosis. The myocardial salvage is quite possible (p less than 0.05), when the coronary angiography in acute phase showed the forward flow (99% or 90% of stenosis) before coronary revascularization and/or good collateral circulation (Rentrop 2 degrees or 3 degrees).

Myocardial accumulation of In-111-antimyosin (InAM) was evaluated in comparison with circulating serum myosin light chain I (LCI) level at the time of InAM injection. Seventeen consecutive patients were studied at various stages ranging from 6 days to 34 days after myocardial infarction (MI). The infarct area was positive for InAM uptake in all patients (100%), and significant myocardial uptake was observed in 14 patients (82.4%). The intensity of InAM uptake correlated with the infarct location shown by ECG and CAG. In contrast, 12 patients (70.6%) had normal or undetectable serum myosin LCI levels, with 5 being normal (0.42-2.5 ng/ml) and 7 undetectable (0.42 ng/ml or less). Only 5 patients (29.4%) had elevated serum myosin LCI levels at the time of InAM injection, and this elevation was slight, ranging from 3.4 to 4.5 ng/ml (mean: 3.75 ng/ml). Among patients with undetectable, normal, and elevated serum myosin LCI levels, there was no significant correlation between InAM uptake and the serum myosin LCI level. Thus, even after the serum myosin LCI level has decreased to normal, InAM can still bind to cardiac myosin in patients with MI, presumably until there is complete recovery from the hibernating myocardium due to ischemic damage.

The myocardial uptake and redistribution in thallium scintigraphy and the regional wall motion by echocardiography were evaluated by a semi-quantitative method in 42 patients who previously had myocardial infarction (50 target vessels) and underwent coronary revascularization. The aim of this study was to elucidate the significance of the initial image, delayed image and redistribution on thallium-201 scintigraphy for clinical diagnosis of the myocardial viability. As a semi-quantitative analysis, we used a bull's-eye display for thallium image and centerline method for echocardiographic wall motion, and compared the results before and after revascularization. As a result, the thallium grade improved postoperatively in all 17 areas which preoperative had showed redistribution, and also in 11 of the 32 areas without preoperative redistribution. The sensitivity, specificity and accuracy of preoperative thallium redistribution for predicting myocardial viability were 61%, 100% and 78%, respectively, when the postoperative improvement in the thallium grade was used as the standard. The postoperative probability of improvement in the thallium grade increased in proportion to the preoperative thallium grade (delayed image) (p less than 0.01). There was no correlation between the preoperative thallium delayed image and postoperative improvement in wall motion. Postoperative improvement in thallium image and wall motion could not be predicted from the preoperative wall motion. Thus, postoperative improvement in thallium images can be anticipated if redistribution is present on the preoperative thallium image, and the preoperative thallium delayed image is useful for predicting myocardial viability. Improvement in wall motion could not be predicted preoperatively by these methods.

To evaluate the extent and characteristics of infarct areas, we performed indium-111 monoclonal antimyosin Fab (InAM), thallium-201 (TL) and Tc-99m pyrophosphate (PYP) imagings in 17 patients with acute myocardial infarction, and tried to find out the mechanism that causes difference of these imagings. In each study, the extent scores as an index of the infarct area were obtained by single photon emission computed tomography (SPECT), and comparisons were made between the results obtained. The overlap between InAM and TL imagings obtained by SPECT was evaluated. Location, severity, extent and patterns of accumulation were compared between InAM and PYP with both planar image and SPECT. The extent scores of InAM correlated well with those of TL (r = 0.73, p < 0.01). However, the overlap of both methods was recognized in 8 of 17 patients, in whom wall thickness of the infarct area as obtained by echocardiography was well preserved. The left ventricular regional asynergy was mild in 6 of these 8 patients. Coronary angiography showed poor or no collateral circulation in these cases. Although there were generally close correlations of the extent scores between InAM and PYP, discrepancy was noted in 2 cases for location; 2 for severity, 5 for extent, and 3 for patterns of accumulation. These differences may be attributed to the timings of imaging, coronary reperfusion and different mechanisms of accumulation. In conclusion, the extent of acute myocardial infarction obtained by InAM correlates well with those obtained by TL and PYP, with some exceptions.

To assess the diagnostic accuracy, extent, and characteristics of 111In-antimyosin Fab scintigraphy (In-AM) in acute myocardial infarction (AMI), we studied In-AM in 17 patients with AMI and compared with In-AM, 99mTc-PYP and 201Tl scintigraphy. Intensity of In-AM uptake was classified into 3 grades. Fourteen of 17 patients (82%) showed positive uptake of In-AM. The locations of infarct area diagnosed by In-AM were in accordance with those by electrocardiography. There was a good correlation between the extent score of In-AM planar and that of SPECT (r = 0.72), In-AM SPECT and Tl SPECT (r = 0.79), In-AM planar and PYP planar (r = 0.92), In-AM SPECT and PYP SPECT (r = 0.76), respectively (p less than 0.01). Thus, In-AM is a useful method for diagnosis of AMI.

For quantitative evaluation of acute myocardial infarction, In-111 antimyosin Fab myocardial imaging (InAM) was performed in 17 patients with myocardial infarction who underwent Tl-201 (TL) and Tc-99m pyrophosphate (PYP) myocardial imaging in acute phase. For calculating the infarct size, voxel counter method was used for analysis in PYP and InAM, and extent and severity score were used on bull's-eye polar map in TL. The most appropriate cut-off level ranged from 65 to 80% by the fundamental experiment using cardiac phantom. The cut-off level of 0.70 (InAM) and 0.65 (PYP) were used for clinical application of voxel counter analysis. The infarct size calculated by InAM and PYP was compared with wall motion abnormality index by echocardiography (WMAI), TL extent score, TL severity score, peak CK and sigma CK. Infarct size by InAM showed the following correlations with other indices. PYP: r = 0.26 (ns), TL extent score: r = 0.72 (p less than 0.01), TL severity score: r = 0.65 (p less than 0.05), WMAI: r = 0.69 (p less than 0.05). The infarct size by PYP did not show any correlations with these indices. Therefore, the infarct size by InAM showed better correlations with TL and WMAI than that of PYP. So InAM was considered superior to PYP for quantitative evaluation of acute myocardial infarction.

To elucidate changes with time in T1-201 scintigraphy after coronary revascularization, T1-201 stress myocardial scintigraphy was performed at least twice during the follow-up period (from one to 12 months) in 58 patients with ischemic heart disease (12 with angina, and 46 with myocardial infarction) who had undergone PTCA or A-C bypass surgery. The perfusion defects were classified in 4 grades, and scintigraphic changes over grade 1 were judged significant. We evaluated; 1) time of scintigraphic improvement after revascularization, 2) presence of reverse redistribution, and 3) assessment of coronary restenosis. Scintigraphic improvement was observed in 21 of 58 patients during a 3- to 12- month follow-up period, 7 of whom improved within one month. Reverse redistribution after coronary revascularization was observed in 8 of the 58 patients (14%), including 6 who showed scintigraphic improvement in 3 to 12 months (2 were not examined). Among 29 patients whose coronary angiogram and Tl-201 scintigram were compared, 11 had angiographic evidence of restenosis and 4 of them showed deterioration of scintigraphic findings (sensitivity 57%, specificity 68%, and accuracy 66%). In conclusion, scintigraphic improvement was observed over various periods (immediately after and up to 12 months) after coronary revascularization. Reverse redistribution appears to be a predictor of good prognosis. Coronary restenosis cannot always be reliably assessed by Tl-201 scintigraphy.

The diagnosis of post myocardial infarction syndrome (PMIS) is sometimes difficult because of the absence of a specific test. We report a 68-year-old man with PMIS who had a persistent accumulation of indium-111 oxine labeled leukocytes in the infarcted myocardium for 1 month. The uptake of leukocytes preceded the appearance of the main symptoms and disappeared with the clinical improvement after the therapy with steroids. Leukocyte imaging has a potential as a useful tool for early diagnosis, evaluation of therapy and assessing the mechanism of PMIS.

Indium-111 antimyosin (InAM) scintigraphy was performed in 17 patients with acute myocardial infarction (on 15 +/- 6 days from the onset). The degree of myocardial uptake was classified into 3 groups. They were ranged from low intensity as in bone marrow to high intensity as in liver. All of 17 cases showed positive myocardial uptake including low intensity. The locations of infarction judged by InAM were in agreement with those by electrocardiography, coronary angiography (CAG), and 99mTc-pyrophosphate scintigraphy (PYP, performed on 5 +/- 2 days from the onset). In 5 cases, the uptake of InAM showed doughnuts or diffuse pattern which was occasionally observed on PYP. These cases showed myocardial uptake of 4th degree of Parkey's classification with doughnuts-like pattern on PYP, and showed involvement of left anterior descending artery on CAG. In some cases, the extent of myocardial uptake on InAM did not agree with those on PYP.

Measurements of O2 consumption during treadmill exercise tests and Tl-201 myocardial scintigraphy were performed in 17 cases of myocardial infarction to elucidate O2 consumption at an anaerobic threshold ATVO2 as an adequate index of exercise tolerance, and the scintigraphic indices influencing the exercise tolerance. ATVO2 was obtained using the method of Wasserman and Davisand corrected by body weight. The scintigraphic indices such as the location, extent (residual myocardium), and severity (% uptake) of myocardial infarction were obtained from SPECT and bull's eye displays on Tl-201 myocardial scintigraphy. ATVO2 was correlated with theoretical VO2max as obtained by the predicted maximal heart rate (r = 0.56, p less than 0.01) and with left ventricular ejection fraction as obtained by radionuclide left ventriculography (r = 0.59, p less than 0.01). There was no significant difference between ATVO2 in cases of anterior wall infarction and those of inferior (and/or lateral wall) infarction. There was no significant correlation between % uptake and ATVO2. However, the residual myocardium showed a significant correlation with ATVO2 (r = 0.61, p less than 0.01). In conclusion, 1) ATVO2 is an adequate index of exercise tolerance and reflects cardiac function. 2) The extent of the residual myocardium is most strongly influenced by ATVO2 among the indices of myocardial damage as obtained by Tl-201 myocardial scintigraphy.

Emission computed tomography with 99mTc-PYP was used to estimate infarct size in 38 patients with documented acute myocardial infarction. In the present study, the effect of thrombolysis with Urokinase on infarct size and on left ventricular function was assessed. Fourteen patients with acute myocardial infarction who underwent intracoronary thrombolysis within six hours after the onset of symptoms, and 24 patients who underwent conventional therapy were the subjects of this study. Infarct size was measured by drawing a region of interest around the myocardial pyrophosphate uptake for each tomographic slice. The boundary was then defined as 65% of the maximal count within the region of interest as determined by phantom volume studies. The total number of voxels was obtained by adding those in all slices and multiplying the sum by the voxel volume (0.205 ml per one voxel) to determine the infarct volume. Measurement of the 99mTc-PYP uptake on the tomographic image revealed an average infarct size of 100.1 +/- 36.0 ml (ranged 45 to 198). The calculated infarct volume correlated significantly with sigma CPK (p less than 0.01) and with left ventricular ejection fraction (p less than 0.01), but not with the peak CPK. In patients with acute inferior myocardial infarction, the mean infarct volume was 78.4 +/- 29.1 ml in the coronary thrombolysis group, and 105.1 +/- 33.7 ml in the conventional bypass graft treatment group (p less than 0.05). We concluded that successful intracoronary thrombolysis may reduce infarct size. ECT imaging with 99mTc-PYP to determine infarct size may be clinically applicable in patients with acute myocardial infarction.