Simple annealing process for producing unique one-dimensional fullerene crystal named fullerene finned-micropillar.

We propose a process for easily fabricating a unique one-dimensional fullerene crystal, i.e., a fullerene finned-micropillar (FFMP). To fabricate a one-dimensional fullerene crystal more easily than when using current processes, fullerene was first annealed at 1173 K for 1 h with an argon gas flow of 0.5 L/min. We then examined how the FFMP structure changed when the fabrication process conditions, such as temperature, annealing time, and argon gas flow rate, were varied. FFMPs can be prepared within a short time and may have the same electrical characteristics as other one-dimensional crystals, e.g., fullerene nanowhiskers, so they are expected to be very useful for field-effect transistors, organic photovoltaics, and so on in the near future.

Myocardial beta-adrenergic receptor density assessed by 11C-CGP12177 PET predicts improvement of cardiac function after carvedilol treatment in patients with idiopathic dilated cardiomyopathy.

UNLABELLED: We evaluated whether myocardial beta-adrenergic receptor (beta-AR) density, as determined by 11C-CGP12177 PET, could predict improvement of cardiac function by beta-blocker carvedilol treatment in patients with idiopathic dilated cardiomyopathy (IDC). METHODS: Ten patients with IDC (left ventricular ejection fraction [LVEF]<45%) were studied. Myocardial beta-AR density was estimated using 11C-CGP12177 PET before treatment with carvedilol. Changes of LVEF in response to dobutamine infusion (DeltaLVEF-dobutamine) were also measured by echocardiography. Changes of LVEF (DeltaLVEF-carvedilol) were evaluated after 20 mo of carvedilol treatment. RESULTS: Baseline myocardial beta-AR density significantly correlated with DeltaLVEF-carvedilol (r=-0.88, P<0.001). In contrast, DeltaLVEF-dobutamine did not correlate with DeltaLVEF-carvedilol (P=0.65). Myocardial beta-AR density was the significant multivariate independent predictor of DeltaLVEF-carvedilol (beta=-0.88, P<0.001) among univariate predictors, including functional class (r=0.76, P<0.05), plasma norepinephrine (r=0.85, P<0.01), LVEF (r=-0.64, P<0.05), and age as confounding factors. Furthermore, myocardial beta-AR density was significantly correlated with plasma norepinephrine (r=-0.79, P<0.01) and LVEF (r=0.70, P<0.05). CONCLUSION: Myocardial beta-AR density is more tightly related to improvement of LVEF-carvedilol than is cardiac contractile reserve in patients with IDC. Patients with decreased myocardial beta-AR have higher resting adrenergic drive, as reflected by plasma norepinephrine, and may receive greater benefit from being treated by antiadrenergic drugs.

Heterogeneous reduction of myocardial oxidative metabolism in patients with ischemic and dilated cardiomyopathy using C-11 acetate PET.

BACKGROUND: The 11C-acetate positron emission tomography can estimate myocardial oxidative metabolism, but previous studies have only evaluated small populations and the difference between ischemic (ICM) and idiopathic dilated cardiomyopathy (DCM) has not been fully investigated. The present aims were to evaluate global and regional myocardial oxidative metabolism in a well-characterized, large population with left ventricular (LV) dysfunction in order to clarify the metabolic differences between ICM and DCM. METHODS AND RESULTS: Seventy-eight patients with ejection fraction (EF) < or =50% (33 ICM; 45 DCM) were compared with 14 healthy controls. Myocardial oxidative metabolism was estimated with a clearance rate constant (K(mono)) and the coefficient of variation (CV) of regional K(mono). Patients with LV dysfunction had reduced K(mono) and higher CV (p<0.05). In the comparison of oxidative alterations with clinical variables there was a weak correlation between K(mono) and LVEF (r=0.27). Although K(mono) was reduced in both ICM and DCM, CV was more pronouncedly increased in ICM (p=0.001). In multivariate analysis, the presence of left bundle branch block (LBBB) was an independent predictor of heterogeneous oxidative metabolism in DCM (R2=0.30, p<0.0001). CONCLUSIONS: Global reduction of myocardial oxidative metabolism occurred in both ICM and DCM. Heterogeneous oxidative metabolism was observed in these patients, especially those with ICM. Furthermore, LBBB was the independent predictor of heterogeneous oxidative metabolism in patients with DCM.

Decreased myocardial beta-adrenergic receptor density in relation to increased sympathetic tone in patients with nonischemic cardiomyopathy.

UNLABELLED: Cardiac sympathetic function plays an important role in the regulation of left ventricular (LV) function and the pathophysiology of LV dysfunction. (11)C-CGP-12177 ((11)C-CGP) has been used to assess myocardial beta-adrenergic receptor (beta-AR) density in vivo using PET. The aim of this study is to measure myocardial beta-AR density in patients with nonischemic cardiomyopathy and to compare the measurements with various standard parameters of heart failure (HF), particularly with presynaptic function assessed by (123)I- metaiodobenzylguanidine ((123)I-MIBG) imaging. METHODS: (11)C-CGP PET was performed on 16 patients with nonischemic cardiomyopathy and 8 age-matched healthy volunteers using a double injection method. A (11)C-CGP dynamic scan for 75 min was performed after the injection of (11)C-CGP with a high specific activity. After 30 min, (11)C-CGP with a low specific activity was injected. The beta-AR density of the whole LV was calculated on the basis of the graphical analysis method. Additionally, beta-AR density was compared with LV ejection fraction (LVEF), sympathetic presynaptic function assessed using (123)I-MIBG kinetics, and neurohormonal parameters. RESULTS: The beta-AR density of patients was significantly lower than that of healthy volunteers (3.80 +/- 0.96 vs. 7.70 +/- 1.92 pmol/mL; P < 0.0001). In the patients, beta-AR density correlated significantly with LVEF (r = 0.62, P < 0.05). Furthermore, beta-AR density correlated significantly with the (123)I-MIBG washout rate (r = -0.68, P < 0.01) and delayed heart-to-mediastinum ratio (H/M ratio) (r = 0.61, P < 0.05). On the other hand, the correlation between beta-AR density and early H/M ratio was not significant (r = 0.40, P = 0.13). The beta-AR density of patients with severe HF (New York Heart Association functional [NYHA] class III) was significantly lower than that of those with NYHA functional class I or class II HF (3.24 +/- 0.96 vs. 4.24 +/- 0.73 pmol/mL; P < 0.05). CONCLUSION: A reduction in beta-AR density measured by (11)C-CGP PET was observed in patients with nonischemic cardiomyopathy. This downregulation may be due to the increased presynaptic sympathetic tone as assessed by (123)I-MIBG imaging.

Olmesartan, but not amlodipine, improves endothelium-dependent coronary dilation in hypertensive patients.

OBJECTIVES: We aimed to compare the effects of the angiotensin II receptor blocker (ARB) olmesartan versus the calcium channel blocker (CCB) amlodipine on coronary endothelial dysfunction in patients with hypertension. BACKGROUND: Angiotensin II receptor blockers are thought to have greater beneficial effects than CCBs on coronary vasomotion by directly blocking action of angiotensin II. METHODS: Twenty-six patients with untreated essential hypertension were prospectively assigned to treatment with either olmesartan (27.7 +/- 12.4 mg/day, n = 13) or amlodipine (5.6 +/- 1.5 mg/day, n = 13) for 12 weeks. Changes of corrected myocardial blood flow (DeltaMBF) and coronary vascular resistance (DeltaCVR) from rest to cold pressor were measured by using 15O-water and positron emission tomography before and after treatment. Blood biomarkers including lipids, glucose, insulin, high-sensitivity C-reactive protein, interleukin-6, tumor necrosis factor-alpha, and superoxide dismutase (SOD) were also measured. RESULTS: Olmesartan and amlodipine reduced blood pressure (BP) to the same extent (-28.7 +/- 16.2 mm Hg vs. -26.7 +/- 10.8 mm Hg). In the olmesartan group, DeltaMBF tended to be greater (-0.15 +/- 0.19 ml/g/min vs. 0.03 +/- 0.17 ml/g/min, p = 0.09 by 2-way analysis of variance), and DeltaCVR was significantly decreased (7.9 +/- 23.5 mm Hg/[ml/g/min] vs. -16.6 +/- 18.0 mm Hg/[ml/g/min], p < 0.05) after treatment, whereas these parameters did not change in the amlodipine group (DeltaMBF: -0.15 +/- 0.12 ml/g/min vs. -0.12 +/- 0.20 ml/g/min; DeltaCVR: 6.5 +/- 18.2 mm Hg/[ml/g/min] vs. 4.8 +/- 23.4 mm Hg/[ml/g/min]). Serum SOD activity tended to increase (4.74 +/- 4.77 U/ml vs. 5.57 +/- 4.74 U/ml, p = 0.07 by 2-way analysis of variance) only in the olmesartan group. CONCLUSIONS: Olmesartan, but not amlodipine, improved endothelium-dependent coronary dilation in hypertensive patients independent of BP reduction. These beneficial effects on coronary vasomotion might be via an antioxidant property of ARBs.

Plasma interleukin-6 and tumor necrosis factor-alpha can predict coronary endothelial dysfunction in hypertensive patients.

Coronary endothelial function is impaired in hypertension; however, the severity of this impairment varies among patients. We aimed to identify the predictors of coronary endothelial dysfunction among clinical variables related to hypertension and atherosclerosis. Twenty-seven untreated, uncomplicated essential hypertensive patients and 10 age-matched healthy controls were studied prospectively. Myocardial blood flow (MBF) was measured by using (15)O-water positron emission tomography (PET) at rest and during a cold pressor test (CPT). Coronary vascular resistance (CVR) during CPT was used as a marker of coronary endothelial function. Serum low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, triglycerides, malondialdehyde-LDL, homeostasis model assessment, high-sensitivity C-reactive protein (hs-CRP), and plasma interleukin-6 (IL-6) and tumor necrosis factor (TNF)-alpha were also measured. CVR during CPT was significantly higher in hypertensive patients than in healthy controls (114+/-26 vs. 94+/-12 mmHg/[mL/g/min]; p<0.05). By univariate analysis, CVR during CPT was correlated with LDL cholesterol (r=0.38, p<0.05), IL-6 (r=0.46, p<0.02), and TNF-alpha (r=0.39, p<0.05) in hypertensive patients. By multivariate analysis, IL-6 and TNF-alpha were significant independent predictors of CVR during CPT. Elevated plasma IL-6 and TNF-alpha levels were independent predictors of coronary endothelial dysfunction in hypertensive patients. These results suggest that plasma IL-6 and TNF-alpha might be useful for identifying the high risk subgroup of hypertensive patients with coronary endothelial dysfunction and provide an important clue to link systemic inflammation to the development of coronary atherosclerosis.

[Cardiac receptor imaging].

Molecular imaging has been focused in the field of cardiovascular medicine. With use of suitable radiopharmaceuticals, neuronal function in the cardiovascular system has been assessed in vivo. Of particular, positron emission tomography(PET) plays an important role for in vivo quantification of various neurotransmitter and receptor functions. We have recently developed 11C-labeled CGP12177, hydrophilic beta-adrenoreceptor antagonist, to measure myocardial beta-receptor density(Bmax) in vivo. The basic study showed high uptake in the lung and myocardium which was significantly suppressed by propranolol pretreatment in the rat model, suggesting specific binding of this ligand in the beta-receptors. Bmax was significantly reduced in patients with congestive heart failure. In addition, Bmax was inversely correlated with washout rate of 123I-MIBG from the myocardium in these patients. These new imaging technique has a potential role for assessing severity of heart failure and providing appropriate treatment strategy.

Elevated plasma plasminogen activator inhibitor type-1 is an independent predictor of coronary microvascular dysfunction in hypertension.

BACKGROUND: Elevated plasma plasminogen activator inhibitor-1 (PAI-1) is related to cardiovascular events, but its role in subclinical coronary microvascular dysfunction remains unknown. Thus, in the present study it was investigated whether elevated plasma PAI-1 activity is associated with coronary microvascular dysfunction in hypertensive patients. METHODS AND RESULTS: Thirty patients with untreated essential hypertension and 10 age-matched healthy controls were studied prospectively. Myocardial blood flow (MBF) was measured by using (15)O-water positron emission tomography. Clinical variables associated with atherosclerosis (low-density lipoprotein-cholesterol, high-density lipoprotein (HDL)-cholesterol, triglyceride, homeostasis model assessment (HOMA-IR), and PAI-1 activity) were assessed to determine their involvement in coronary microvascular dysfunction. Adenosine triphosphate (ATP)-induced hyperemic MBF and coronary flow reserve (CFR) were significantly lower in hypertensive patients than in healthy controls (ATP-induced MBF: 2.77+/-0.82 vs 3.49+/-0.71 ml x g(-1) x min(-1); p<0.02 and CFR: 2.95 +/-1.06 vs 4.25+/-0.69; p<0.001). By univariate analysis, CFR was positively correlated with HDL-cholesterol (r=0.46, p<0.02), and inversely with HOMA-IR (r=-0.39, p<0.05) and PAI-1 activity (r=-0.61, p<0.001). By multivariate analysis, elevated PAI-1 activity remained a significant independent determinant of diminished CFR. CONCLUSIONS: Elevated plasma PAI-1 activity was independently associated with coronary microvascular dysfunction, which suggests that plasma PAI-1 activity is an important clue linking hypofibrinolysis to the development of atherosclerosis.

Smoking cessation normalizes coronary endothelial vasomotor response assessed with 15O-water and PET in healthy young smokers.

UNLABELLED: Cigarette smoking is one of the risk factors of cardiovascular diseases and is related to abnormal peripheral and coronary vascular vasomotion. Coronary vascular endothelial dysfunction is caused by chronic smoking in smokers without epicardial coronary artery stenosis. The coronary endothelial vasomotion abnormality is restored by interventions such as l-arginine or vitamin C infusion. However, to our knowledge, the effect of smoking cessation on coronary vasomotor response has not been elucidated. Therefore, the aim of this study was to assess the effect of smoking cessation on coronary vasomotor response by quantitative myocardial blood flow (MBF) measurement using (15)O-water and PET. METHODS: Fifteen young smokers (Brinkman index > 100; mean age +/- SD, 26 +/- 4 y) with no evidence of heart disease or cardiovascular risk factors, except for smoking, and age-matched nonsmokers (n = 12) were enrolled in this study. MBF was measured at rest, during the cold pressor test (CPT), before and at 1 and 6 mo after smoking cessation. In addition, MBF measurement during adenosine triphosphate (ATP) infusion was performed before and at 6 mo after smoking cessation. In nonsmokers, MBF was measured at rest, during ATP infusion, and during the CPT. RESULTS: MBF at rest and during ATP infusion did not differ between smokers and nonsmokers (0.73 +/- 0.12 vs. 0.80 +/- 0.15 mL/g/min and 3.15 +/- 1.43 vs. 3.69 +/- 0.76 mL/g/min, respectively; P = not significant). In contrast, MBF during the CPT in smokers was lower than that in nonsmokers (0.90 +/- 0.19 vs. 1.12 +/- 0.28 mL/g/min; P < 0.05). There was no significant difference in MBF either at rest or during ATP infusion between before and after smoking cessation, but MBF during the CPT increased at 1 mo in comparison with before cessation of smoking (0.90 +/- 0.19 vs. 1.02 +/- 0.22 mL/g/min; P < 0.01). An improvement of MBF response to the CPT was preserved at 6 mo after smoking cessation. CONCLUSION: Coronary vasomotor abnormality assessed by MBF response to the CPT was improved at 1 mo after smoking cessation. These findings indicate that coronary endothelial dysfunction may be reversible within 1 mo after smoking cessation in healthy young smokers.

Myocardial flow reserve is influenced by both coronary artery stenosis severity and coronary risk factors in patients with suspected coronary artery disease.

PURPOSE: Myocardial flow reserve (MFR) measurement has an important role in assessing the functional severity of coronary artery stenosis. However, a discrepancy between the anatomical severity of coronary artery stenosis and MFR is often observed. Such a discrepancy may be explained by coronary risk factors. In this study, we aimed to investigate the influence of coronary artery stenosis severity and risk factors on MFR. METHODS: Seventy-four patients suspected to have coronary artery disease and seven age-matched healthy volunteers were enrolled. Myocardial blood flow (MBF) and MFR were measured using 15O-labelled water PET. Regional MFR was calculated in regions with significant coronary artery stenosis (stenotic regions) and in regions without significant stenosis (remote regions). The contributions of coronary artery stenosis severity and coronary risk factors were assessed using univariate and multivariate analyses. RESULTS: In stenotic regions, MFR correlated inversely with coronary artery stenosis severity (r=-0.50, p<0.01). Univariate analysis did not show any significant difference in MFR between the patients with and the patients without each risk factor. In remote regions, however, MFR was significantly decreased in the diabetes and smoking groups (each p<0.05). By multivariate analysis, diabetes and smoking were independent predictors of MFR (each p<0.05). In the group with more than one risk factor, MFR was significantly lower (2.78+/-0.79) than in the other group (3.40+/-1.22, p<0.05). CONCLUSION: MFR is influenced not only by coronary stenosis severity but also by coronary risk factors. In particular, the influence of risk factors should be considered in regions without severe coronary stenosis.

Reduced 123I-BMIPP uptake implies decreased myocardial flow reserve in patients with chronic stable angina.

PURPOSE: Long-chain fatty acid (LCFA) is the main energy source for normal myocardium at rest, but in ischemic myocardium, the main energy substrate shifts from LCFA to glucose. 123I-BMIPP is a radiolabeled LCFA analog. In chronic stable angina without previous infarction, we suppose that reduced 123I-BMIPP uptake is related to the substrate shift in myocardium with decreased myocardial flow reserve (MFR). The purpose of this study was to relate 123I-BMIPP uptake to rest myocardial blood flow (MBF), hyperemic MBF, and MFR assessed with 15O-water positron emission tomography (PET). METHODS: We enrolled 21 patients with chronic stable angina without previous infarction, all of whom underwent 123I-BMIPP single-photon emission computed tomography (SPECT) and 15O-water PET. The left ventricle was divided into 13 segments. In each segment, rest MBF and hyperemic MBF were measured by PET. 123I-BMIPP uptake was evaluated as follows: score 0=normal, 1=slightly decreased uptake, 2=moderately decreased uptake, 3=severely decreased uptake, and 4=complete defect. 123I-BMIPP uptake was compared with rest MBF, hyperemic MBF, and MFR. RESULTS: The numbers of segments with 123I-BMIPP scores 0, 1, 2, 3, and 4 were 178, 40, 25, 24, and 0, respectively. The rest MBFs for scores 0, 1, 2, and 3 were 0.93+/-0.25, 0.86+/-0.21, 0.97+/-0.30, and 0.99+/-0.37 ml/min/g, respectively. The hyperemic MBFs for scores 0, 1, 2, and 3 were 2.76+/-1.29, 1.84+/-0.74, 1.37+/-0.39, and 1.08+/-0.40 ml/min/g, respectively. The MFRs for scores 0, 1, 2, and 3 were 3.01+/-1.38, 2.20+/-0.95, 1.44+/-0.22, and 1.10+/-0.26, respectively. As 123I-BMIPP uptake declined, hyperemic MBF and MFR decreased. CONCLUSION: In chronic stable angina without previous infarction, reduced 123I-BMIPP uptake implies decreased MFR.

Sympathetic denervation and reinnervation after the maze procedure.

UNLABELLED: We evaluated serial changes in cardiac sympathetic nerve distribution using 123I-metaiodobenzylguanidine (123I-MIBG) after the Maze procedure. The Maze procedure, in which multiple incisions are made in the atrium, has been concomitantly performed with mitral valve (MV) surgery in an attempt to eliminate atrial fibrillation (AF). Although attenuation of the sinoatrial node response to exercise and a reduction of left ventricular function (left ventricular ejection fraction [LVEF]) in early stages after the Maze procedure have been suggested, factors leading to these changes have not been clarified. METHODS: Thirteen patients with MV disease were enrolled in this study. Six of them had undergone MV surgery and the Maze procedure (Maze+), and 7 had undergone MV surgery without the Maze procedure (Maze-). All patients underwent cardiac 123I-MIBG imaging preoperatively and 10 d and 1 y after surgery to assess 123I-MIBG uptake (heart-to-mediastinum count ratio of early planar images [H/M]) and the washout rate (WR). Radionuclide ventriculography was also performed to calculate LVEF 3 d after each 123I-MIBG imaging. RESULTS: The LVEF of the Maze+ group significantly decreased 10 d after surgery (44.2 +/- 4.8; mean +/- SD) compared with that before surgery (60.3 +/- 6.9; P < 0.05) and significantly increased at 1 y (65.2 +/- 2.9) compared with that at 10 d (P < 0.05). In the Maze- group, there was no significant change 10 d (53.0 +/- 12.3) and 1 y (58.6 +/- 4.8) after surgery compared with that before surgery (60.4 +/- 4.6) (P = not significant, each). In the Maze+ group, the H/M (1.51 +/- 0.18) was significantly lower at 10 d after than that at the preoperative stage (1.90 +/- 0.25; P < 0.05) but significantly recovered at 1 y (2.23 +/- 0.18; P < 0.05) with a similar transient increase in the WR (36.7% +/- 6.1% at preoperative stage; 46.9% +/- 3.4% at 10 d; 39.9% +/- 6.5% at 1 y; P < 0.05, each). On the other hand, the Maze- group did not show a significant change in the H/M (1.94 +/- 0.32, 2.06 +/- 0.18, and 2.13 +/- 0.17, respectively; P = not significant, each) but did exhibit a significant decrease in the WR (40.4% +/- 5.1%, 37.0% +/- 5.1%, and 32.9% +/- 2.5%, respectively; P < 0.05, each). Changes in the H/M of both groups significantly correlated with the change in LVEF (r = 0.82; P < 0.05), and the WR showed a significant inverse correlation with changes in the LVEF (r = -0.81; P < 0.05). CONCLUSION: Cardiac sympathetic nerves were denervated at early stage and reinnervated at late stage after the Maze procedure. Such adrenergic nerve changes may be correlated, at least in part, with changes in left ventricular function after this procedure.

Quantitative analysis of myocardial glucose utilization in patients with left ventricular dysfunction by means of 18F-FDG dynamic positron tomography and three-compartment analysis.

PURPOSE: Myocardial glucose utilization (MGU) is altered in various heart diseases. The aim of this study was to quantitatively assess regional myocardial glucose utilization in patients with left ventricular (LV) dysfunction by dynamic( 18)F-fluorodeoxyglucose positron emission tomography (FDG PET). METHODS: A total of 18 subjects were studied, including ten with LV dysfunction (seven with idiopathic dilated cardiomyopathy and three with aortic regurgitation; NYHA II in 8 and III in 2) and eight healthy normal volunteers. Patients with diabetes mellitus were excluded. A dynamic PET study was performed for 40 min following the injection of 370 MBq of FDG after 50-g glucose loading. On the basis of a three-compartment model, MGU, K1, k2, and k3 were computed on a pixel by pixel basis to generate LV myocardial parametric maps. FDG standardized uptake value (SUV) was also calculated using static images obtained 40 min after FDG injection. These metabolic values were compared with myocardial flow distribution (%Flow), LVEF, LV volumes, and LV wall thickening (WT) determined by gated myocardial single-photon emission computed tomography using QGS software in eight myocardial segments. RESULTS: MGU correlated positively with LV volumes and negatively with LVEF. K(1) was significantly higher in the segments of the patients than in those of the normal volunteers (0.082+/-0.055 vs 0.041+/-0.017 ml min(-1) g(-1), p<0.05), although there was no difference in MGU between the groups. On the other hand, SUV, k2, and k3 did not differ significantly between the groups. Among the patients, the K1 values were significantly higher in the areas with impaired WT (%WT<17%) (0.109+/-0.063 vs 0.069+/-0.062 ml min(-1) g(-1), p<0.05) and in the areas with flow reduction (%Flow<71%) (0.112+/-0.076 vs 0.071+/-0.046 ml min(-1) g(-1), p<0.05). CONCLUSION: These results indicate that glucose utilization was preserved in the patients with LV dysfunction, mainly due to an increase in glucose transport, particularly in the regions with severely impaired LV function. Thus, the quantitative assessment of myocardial glucose utilization by FDG dynamic PET may provide useful information for assessing the regional myocardial metabolic status in patients with LV dysfunction.

Quantitative assessment of regional myocardial flow reserve using tc-99m-sestamibi imaging.

BACKGROUND: The aims of this study were to develop a method for quantitative estimation of the myocardial blood flow index (MBFI) and myocardial flow reserve (MFR) of the whole left ventricle using (99m)technetium (Tc-99m)-sestamibi imaging. METHODS AND RESULTS: Twenty-two patients with suspected coronary artery disease and 7 controls underwent both Tc-99m-sestamibi imaging and O-15 water positron emission tomography (PET). The global MBFI was calculated on the basis of the microsphere model from the ratio of the myocardial count to the area under the time - activity curve on the aortic arch. The regional MBFI was calculated from the relative distributions of Tc-99m-sestamibi uptake values. The regional MBFI and MFR (Tc-MFR) obtained using single-photon emission computed tomography were compared with the myocardial blood flow (MBF) and MFR (PET-MFR) obtained using PET as the gold standard. Regional MBFI significantly correlated with the MBF obtained using PET. Regional Tc-MFR also correlated with the regional PET-MFR, with some underestimation. CONCLUSION: These results indicate that regional MBF and MFR may be estimated by dynamic Tc-99m-sestamibi imaging and can be used for the early detection and estimation of the functional severity of coronary lesions without the need for a PET camera.

Serial changes in BMIPP uptake in relation to thallium uptake in the rat myocardium after ischaemia.

Several clinical studies have shown that iodine-123 labelled 15-(p-iodophenyl)-3-(R, S)-methylpentadecanoic acid (BMIPP) uptake is often lower than the uptake of perfusion tracers in patients with ischaemic heart disease. However, BMIPP accumulation may not decrease during the acute phase of a stunned myocardium in patients with acute coronary syndrome. We evaluated serial changes in BMIPP and perfusion tracer uptake in the myocardium after ischaemia. We performed a 20-min left coronary artery occlusion followed by reperfusion in male Wistar rats. One hour after the reperfusion, echocardiography was performed. Intravenous injection of iodine-125 labelled BMIPP and thallium-201 was performed 1 day (acute group) and 5 days (subacute group) after the operation. To determine the myocardial distribution of 125I-BMIPP and 201Tl, dual-tracer autoradiography was conducted. We identified regions of interest in the anterolateral wall as an area at risk and in the inferoseptum as a remote control area. The anterolateral wall/inferoseptum ratio (A/I ratio) was calculated to compare the distributions of 125I-BMIPP and 201Tl. Coronary occlusion induced hypokinesia in the anterolateral region 1 h after the reperfusion. The A/I ratio of 125I-BMIPP was significantly higher than that of 201Tl in the acute group (1.01 +/- 0.15 vs 0.80 +/- 0.23, P<0.001). On the other hand, there was no significant difference between the A/I ratios of 125I-BMIPP and 201Tl in the subacute group (0.88 +/- 0.18 vs 0.85 +/- 0.18). Two rats showed a significantly lower A/I ratio of 125I-BMIPP than 201Tl in the subacute phase. These data suggest that BMIPP uptake is preserved despite a decrease in perfusion in the acute phase after ischaemia. In the subacute phase, on the other hand, BMIPP uptake is similar to or even lower than thallium uptake. Since BMIPP uptake may change with time after ischaemia, careful interpretation of BMIPP uptake after ischaemia is required in a clinical setting.