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 gated myocardial perfusion single photon emission computed tomography improves the prediction of regional functional recovery in akinetic areas after coronary bypass surgery: useful tool for evaluation of myocardial viability.

OBJECTIVE: Assessment of myocardial viability in akinetic areas is essential in surgery for ischemic heart disease, including coronary artery bypass grafting and left ventriculoplasty. The aim of this study is to evaluate the utility of quantitative indices of perfusion uptake, wall motion, and wall thickening of each region calculated by quantitative electrocardiogram-gated single photon emission computed tomography (SPECT) for prediction of functional recovery after coronary artery bypass grafting. METHODS: Forty patients scheduled for coronary artery bypass grafting were prospectively included. Electrocardiogram-gated SPECT was performed before and 1 week and 3 months after operation, and coronary angiography was performed before and after operation. The myocardium was divided into 9 segments and myocardial viability, assessed by improvement of the wall motion score using a cine mode display, and evaluated by radionuclide criteria (perfusion uptake, wall motion, wall thickening). Twenty-four segments with moderate hypokinesis and 14 segments with akinesis with patent grafts were assessed. RESULTS: All segments with moderate hypokinesis except 1 (96%) had improved wall motion scores postoperatively, whereas of 14 segments with akinesis only 7 segments (50%) had improved wall motion scores. The preoperative perfusion uptake in the improved segments was significantly higher than in the nonimproved segments (62.7% +/- 15.6% vs 46.4% +/- 24.5%, P =.01). There was a significant difference in wall motion between the improved and nonimproved segments (3.8 +/- 2.2 mm vs 1.4 +/- 1.4 mm, P =.001), and the preoperative wall thickening of the improved segments was significantly higher than in the nonimproved segments (27.2% +/- 14.1% vs 8.2% +/- 10.3%, P <.0001). The optimal cutoff level of perfusion uptake was 50%, with the highest accuracy of 72%, and the optimal cutoff levels of wall thickening and wall motion were 10% and 1.5 mm, with the highest accuracies of 76% and 85%, respectively. CONCLUSION: The regional functional index calculated by electrocardiogram-gated SPECT indicated that wall thickening was well correlated with functional recovery compared with wall motion or perfusion uptake. This suggests that the wall thickening calculated by electrocardiogram-gated SPECT may be more useful to predict functional recovery than regional myocardial perfusion. Or, it could suggest that in addition to perfusion uptake, wall thickening could enhance the objective assessment of myocardial viability.

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.

Altered myocardial flow reserve and endothelial function late after Kawasaki disease.

OBJECTIVES: Coronary arterial lesions after Kawasaki disease (KD) may cause coronary endothelial dysfunction as the result of intimal hypertrophy. Our purpose was to assess myocardial flow reserve (MFR) and endothelial function in various myocardial regions after KD by using positron emission tomography. STUDY DESIGN: Twenty-seven patients, 17.2 +/- 3.2 years of age, who had KD at 1.9 +/- 1.4 years, and 12 normal healthy subjects, 26.5 +/- 3.4 years of age, were evaluated by means of myocardial blood flow (MBF) with (15)O-water positron emission tomography. MFR was estimated by MBF changes under adenosine triphosphate infusion and endothelial function by MBF changes under cold pressor testing. The left ventricle was divided into three coronary territories. Ten stenotic regions, 20 aneurysmal regions, 30 regressed aneurysmal regions, and 21 regions without coronary arterial lesions were compared with 36 control regions of the normal volunteers. RESULTS: MBF at rest was similar in each region. Hyperemic blood flow and MFR in each region after KD was significantly lower than those in the regions of normal volunteers. MBF during cold pressor testing was significantly reduced in each region after KD, as compared with no change in the control regions. CONCLUSIONS: Our study indicates impaired MFR and endothelial function regardless of coronary artery status after KD.

Assessment of coronary function in children with a history of Kawasaki disease using (15)O-water positron emission tomography.

BACKGROUND: Coronary abnormalities after Kawasaki disease (KD) may be associated with endothelial dysfunction due to intimal hypertrophy. The purpose of this study was to evaluate myocardial flow reserve (MFR) and endothelial function in regressed aneurysmal regions after KD. Methods and Results- Subjects were 12 patients aged 16.0+/-2.6 years who suffered from KD at 1.7+/-1.5 years and 12 normal subjects aged 26.5+/-3.4 years. MFR and endothelial function were estimated, respectively, by changes in myocardial blood flow (MBF) during ATP infusion and by that during cold pressor test using (15)O-water positron emission tomography. Data from 24 regressed aneurysmal regions were compared with those from the corresponding regions (n=36) in the control group. Although the MBF at rest in the regressed aneurysmal regions was similar to that in controls, the MBF at a hyperemic state induced by ATP infusion in the regressed aneurysmal regions was significantly lower than that in the control regions. Therefore, the MFR in regressed aneurysmal regions was significantly lower than that in controls (3.53+/-0.95 versus 4.60+/-1.14; P<0.05). MBF at rest and during the cold pressor test did not change in the control regions, but it was significantly reduced in regressed aneurysmal regions. The ratio of MBF during the cold pressor test to MBF at rest was significantly lower in regressed aneurysmal regions than in control regions (0.67+/-0.15 versus 1.00+/-0.15; P<0.05). CONCLUSIONS: MFR and endothelial function are often impaired in regressed aneurysmal regions after KD, and tomography enables the noninvasive evaluation of coronary function.