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13.2 Can MIBG and BMIPP scintigraphy at 2 weeks after acute myocardial infarction predict LV remodeling at 6 months after infarction?
Poster Display V Saturday, May 5, 2001 10:00
- 12:00
13.1
13.3
Can radionuclide angiography offer a coherent interpretation of various entities included in restrictive cardiomyopathy? C Ginghina, E Apetrei, A Jovin, D Stanescu, M Marinescu, D Dragomir.
I8F-FDG pet imaging in experimental murine myocarditis W Okumura, T Iwasaki, T Toyama, R Seki, S Kasama, H Seki, M Kurabayashi, T Suzuki, T Inoue, K Endo Gtmma Univ. School of Medicine, Maebashi, Japan
Background. Restrictive cardiomyopathy (RC) is defined by abnormal myocardial stiffness. Under this single haemodynamic restrictive profile were included different diseases with various signs at radionuclide angiography (RNA). Purpose. The assessment of classification based on RNA data according to the site of restriction to patients (pts.) with RC confu'med by cardiac catherisation (cath.); the correlation of the RNA with other noninvasive methods: echocardiography (echo), computerised tomography (CT) and magnetic resonance imaging (MRI), Methods. We studied RNA data (filing fraction, time to peak filling rate, first 1/3 diastolic filling fraction, atrial contribution to ventricular filling) of 19pts./mean 41_+5 years; I l males with RC, all confirmed by cath. RNA data were compared with: ECHO data (TM, 2D, Doppler), CT(8pts), MRI (5pts). Endomyocardial biopsy were performed in 7 pts. Results. Three types of RC were indentified based on RNA data according to the site of restriction: type A-symmetric RC (10pts) with restrictive RNA pattern (decreased filling fraction, increased time to peak filling rate>200 msec, decreased peak filling rate in stroke volume/sac, decreased first 1/3 diastolic filling fraction, atrial contribution to veutricular f'ding >30%) affects both ventricles; type B-left asymmetric RC (5pts) involves selectively the left ventricle and type C-right asymetric RC(4pts) affects only the right ventricle. Echo, CT and MRI offered additional arguments for type of restriction.
Ojective. 18F-FDG (fluorodeoxyglucose) PET is a useful detecting agent not only for neoplastic tumor but also for inflammatory tissue. To examine the feasibility of 18F-FDG PET for imaging of inflammatory reaction in myocarditis, we performed PET imaging, biodstribusiton study, and micro autoradiography using 18F-FDG in experimental murine viral myocardotis. Methods. Intraperitoneal inoculation of EMC (encepalomyocarditis) virus were performed to C3H female mice to produce experimental myocarditis. A timecourse study was performed from 1 to 8 weeks after inoculation. 18F-FDG PET imaging were carried out in the fasting mice and myocardial uptake of FDG was studied using SUV (standardized uptake value). Radioactivity of the heart and the other organs were counted and percent injection dose per gram of tissue (% ID/g) was calculated to analyze tissue distribution of FDG. Furthermore, microautoradiography of the myocardium was performed to study the cellular distribution of FDG. Results. In the early phase of myocarditis, high accumulations of FDG were found in the hearts on PET imagings and high density os silver grains were observed at the areas of inflammatory cellular unfiltration in microautoradiographic study. In late phase when inflammatory cellular infiltration were not found, myocardial uptake of FDG still remained higher than that of the control mice and silver grains were mainly distributed on myocytes.
Conclusion. The application of a classification of RC based on RNA data according to the site of myocardial restriction, may offer a coherent pathophysiotogical interpretation of various entities included in RC Associated noninvasive methods can increase the accuracy of diagnosis by "morphological"(CT,MRl) or "'functional" data (ECHO).
Conclusion. 18F-FDG PET is a useful method for the detection of inflammatory reaction in the early phase of myocarditis.
13.2
13.4
Can MIBG and BMIPP scintigraphy at 2 weeks after acute myocardial infarction predict LV remodeling at 6 months after infarction? T Hata, H Tamai, S Takeda, T Tsuji, H Komori, T. Nakamura, M Okada, K Kosuga, Y Hsu, S Motohara, H Uehata. Shiga medical center for adult diseases, Moriyama, Japan
Interstitial and cellular kinetics of TI-201 and MIBI inside myocardiym submitted to low-flow ischemia and to post-ischemic stunning A Ayalew, P-Y Marie, P-M Mertes, P Menu, N Hassan, O Claudon, Polivier, N Danchin, G Karcher, A Bertrant. CHU Nancy, France
Following AMI there is evidence of sustained sympathetic overactivity which has been shown to contribute to LV remodeling in animal model. Chronic poor blood flow to rescued infarct area has been also reported to induce LV remodeling. At 2 weeks after the first onset on anterior AMI, we evaluated myocardial sympathetic nervous function, perfusion and fatty acid metabolism using MIBG, thallium and BMIPP with 41 patients on which the successful angioplasty was performed to elucidate whether myocardial scintigraphy predict LV remodeling. LV function and LV end-systolic (ESV) and enddiastolic volumes (EDV) were assessed at 3 weeks, 3 and 6 months (M) after AMI by LVG. Significant deterioration of EF with increased EDV defined LV remodeling. Scintigraphy interpreted using a 20-segment and 5-point scoring system. The precent myocardial MIBG washout from 15 min to 4 hours after injection and that heart-mediastinum activity ratio were calculated at 2 weeks after AMI. Irrespective of thallium uptake at anteroseptal wall, both defect of BMIPP at the infarct area and rapid clearance of myocardial MIBG after 2 weeks of AMI are closely related to LV remodeling at 6M after infarction. Thus, LV remodeling at 6M after infarction is predicted by MIBG and BMIPP myocardial scintigraphy at 2 weeks after the first onset of AMI.
$78
The impact of ischemia on the myocardial kinetics of :°lTl and MIBI remains controversial. The f'trst-pass kinetics of 2°tTl and MIBI were determined in an isolated heart model under normoxia (N; n-16), low-flow ischemia (I; n=15) and post-ischemic stunning (S; n-15). Activities from interstitial space (Ce) were determined with microdialysis and expressed as ratios with activities from cellular space (Ci). Ischemia, but not post-ischeimc stunning, led to an increase of the average values of Ce/Ci for both 2°~TI (I: 0.011±0.007 vs N: 0.006~0.005, p<0.05; S: 0.007±0.004 vs N, NS) and M1BI (I: 0.011±0.009 vs N: 0.005±0.003, p<0.05; S: 0.005±0.003 vs N, NS). However, both ischemia and post-ischeimc stunning led to an increase of the extraction of the tracers and to a decrease of their clearance rates through the capillary membrane, resulting in an enhanced averaged myocardial retention fraction for ~°~Tl (I: 0.63±0.09 vs N: 0.50~0.14, p<0.05; S: 0.59±0.10 vs N, p<0.05) and MIBI (I: 0.45±0.10 vs N: 0.31±0.09, p<0.05; S: 0.41~0.14 vs N, p<0.05). Ischeima, but not post-ischemic stunning, slows down the transit of 2°lTl and MIBI through the plasmic membrane of myocytes. However, predominant changes in tracers kinetics occur through the capillary membrane and these changes cause an increase of the myocardial retention of Z°lTl and MIBI during both ischeima and post-ischemic stunning.
Journal of Nuclear Cardiology January/February 2001
- 12:00
13.1
13.3
Can radionuclide angiography offer a coherent interpretation of various entities included in restrictive cardiomyopathy? C Ginghina, E Apetrei, A Jovin, D Stanescu, M Marinescu, D Dragomir.
I8F-FDG pet imaging in experimental murine myocarditis W Okumura, T Iwasaki, T Toyama, R Seki, S Kasama, H Seki, M Kurabayashi, T Suzuki, T Inoue, K Endo Gtmma Univ. School of Medicine, Maebashi, Japan
Background. Restrictive cardiomyopathy (RC) is defined by abnormal myocardial stiffness. Under this single haemodynamic restrictive profile were included different diseases with various signs at radionuclide angiography (RNA). Purpose. The assessment of classification based on RNA data according to the site of restriction to patients (pts.) with RC confu'med by cardiac catherisation (cath.); the correlation of the RNA with other noninvasive methods: echocardiography (echo), computerised tomography (CT) and magnetic resonance imaging (MRI), Methods. We studied RNA data (filing fraction, time to peak filling rate, first 1/3 diastolic filling fraction, atrial contribution to ventricular filling) of 19pts./mean 41_+5 years; I l males with RC, all confirmed by cath. RNA data were compared with: ECHO data (TM, 2D, Doppler), CT(8pts), MRI (5pts). Endomyocardial biopsy were performed in 7 pts. Results. Three types of RC were indentified based on RNA data according to the site of restriction: type A-symmetric RC (10pts) with restrictive RNA pattern (decreased filling fraction, increased time to peak filling rate>200 msec, decreased peak filling rate in stroke volume/sac, decreased first 1/3 diastolic filling fraction, atrial contribution to veutricular f'ding >30%) affects both ventricles; type B-left asymmetric RC (5pts) involves selectively the left ventricle and type C-right asymetric RC(4pts) affects only the right ventricle. Echo, CT and MRI offered additional arguments for type of restriction.
Ojective. 18F-FDG (fluorodeoxyglucose) PET is a useful detecting agent not only for neoplastic tumor but also for inflammatory tissue. To examine the feasibility of 18F-FDG PET for imaging of inflammatory reaction in myocarditis, we performed PET imaging, biodstribusiton study, and micro autoradiography using 18F-FDG in experimental murine viral myocardotis. Methods. Intraperitoneal inoculation of EMC (encepalomyocarditis) virus were performed to C3H female mice to produce experimental myocarditis. A timecourse study was performed from 1 to 8 weeks after inoculation. 18F-FDG PET imaging were carried out in the fasting mice and myocardial uptake of FDG was studied using SUV (standardized uptake value). Radioactivity of the heart and the other organs were counted and percent injection dose per gram of tissue (% ID/g) was calculated to analyze tissue distribution of FDG. Furthermore, microautoradiography of the myocardium was performed to study the cellular distribution of FDG. Results. In the early phase of myocarditis, high accumulations of FDG were found in the hearts on PET imagings and high density os silver grains were observed at the areas of inflammatory cellular unfiltration in microautoradiographic study. In late phase when inflammatory cellular infiltration were not found, myocardial uptake of FDG still remained higher than that of the control mice and silver grains were mainly distributed on myocytes.
Conclusion. The application of a classification of RC based on RNA data according to the site of myocardial restriction, may offer a coherent pathophysiotogical interpretation of various entities included in RC Associated noninvasive methods can increase the accuracy of diagnosis by "morphological"(CT,MRl) or "'functional" data (ECHO).
Conclusion. 18F-FDG PET is a useful method for the detection of inflammatory reaction in the early phase of myocarditis.
13.2
13.4
Can MIBG and BMIPP scintigraphy at 2 weeks after acute myocardial infarction predict LV remodeling at 6 months after infarction? T Hata, H Tamai, S Takeda, T Tsuji, H Komori, T. Nakamura, M Okada, K Kosuga, Y Hsu, S Motohara, H Uehata. Shiga medical center for adult diseases, Moriyama, Japan
Interstitial and cellular kinetics of TI-201 and MIBI inside myocardiym submitted to low-flow ischemia and to post-ischemic stunning A Ayalew, P-Y Marie, P-M Mertes, P Menu, N Hassan, O Claudon, Polivier, N Danchin, G Karcher, A Bertrant. CHU Nancy, France
Following AMI there is evidence of sustained sympathetic overactivity which has been shown to contribute to LV remodeling in animal model. Chronic poor blood flow to rescued infarct area has been also reported to induce LV remodeling. At 2 weeks after the first onset on anterior AMI, we evaluated myocardial sympathetic nervous function, perfusion and fatty acid metabolism using MIBG, thallium and BMIPP with 41 patients on which the successful angioplasty was performed to elucidate whether myocardial scintigraphy predict LV remodeling. LV function and LV end-systolic (ESV) and enddiastolic volumes (EDV) were assessed at 3 weeks, 3 and 6 months (M) after AMI by LVG. Significant deterioration of EF with increased EDV defined LV remodeling. Scintigraphy interpreted using a 20-segment and 5-point scoring system. The precent myocardial MIBG washout from 15 min to 4 hours after injection and that heart-mediastinum activity ratio were calculated at 2 weeks after AMI. Irrespective of thallium uptake at anteroseptal wall, both defect of BMIPP at the infarct area and rapid clearance of myocardial MIBG after 2 weeks of AMI are closely related to LV remodeling at 6M after infarction. Thus, LV remodeling at 6M after infarction is predicted by MIBG and BMIPP myocardial scintigraphy at 2 weeks after the first onset of AMI.
$78
The impact of ischemia on the myocardial kinetics of :°lTl and MIBI remains controversial. The f'trst-pass kinetics of 2°tTl and MIBI were determined in an isolated heart model under normoxia (N; n-16), low-flow ischemia (I; n=15) and post-ischemic stunning (S; n-15). Activities from interstitial space (Ce) were determined with microdialysis and expressed as ratios with activities from cellular space (Ci). Ischemia, but not post-ischeimc stunning, led to an increase of the average values of Ce/Ci for both 2°~TI (I: 0.011±0.007 vs N: 0.006~0.005, p<0.05; S: 0.007±0.004 vs N, NS) and M1BI (I: 0.011±0.009 vs N: 0.005±0.003, p<0.05; S: 0.005±0.003 vs N, NS). However, both ischemia and post-ischeimc stunning led to an increase of the extraction of the tracers and to a decrease of their clearance rates through the capillary membrane, resulting in an enhanced averaged myocardial retention fraction for ~°~Tl (I: 0.63±0.09 vs N: 0.50~0.14, p<0.05; S: 0.59±0.10 vs N, p<0.05) and MIBI (I: 0.45±0.10 vs N: 0.31±0.09, p<0.05; S: 0.41~0.14 vs N, p<0.05). Ischeima, but not post-ischemic stunning, slows down the transit of 2°lTl and MIBI through the plasmic membrane of myocytes. However, predominant changes in tracers kinetics occur through the capillary membrane and these changes cause an increase of the myocardial retention of Z°lTl and MIBI during both ischeima and post-ischemic stunning.
Journal of Nuclear Cardiology January/February 2001