[Infected Thoracic Aortic Aneurysm Secondary to the Purulent Pericarditis;Report of a Case].

A 69-year-old man was hospitalized urgently to the department of cardiology, with the progressive general malaise. On admission, his blood pressure was 80/42 mmHg, his white cell count 13,700/µl, and C-reactive protein 25.55 mg/dl suggesting existence of aggressive infection with impaired circulation. Massive pericardial effusion was detected in echocardiography. Pericardial drainage was undergone promptly. There was drainage of 700 ml and the property was purulent. Pneumococcus was detected by the culture test of the pericardial fluid. Antibiotic administration was started by a diagnosis of the purulent pericarditis. His general condition was improved. However, a rapidly expanding saccular aneurysm was found in a descending thoracic aorta by computed tomography( CT). As an infected thoracic aortic aneurysm secondary to the purulent pericarditis, we performed thoracic endovascular aneurysm repair (TEVAR). The intravenous administration of antibiotics was continued for 2 weeks after TEVAR, which was followed by oral antibiotic administration for 1 year. The aneurysm completely disappeared by CT, 10 months after TEVAR. In case with an infected thoracic aortic aneurysm, TEVAR can be a 1st choice of treatment, depending on a causative organism and the morphology of the aneurysm.

Identification of a novel GLA mutation (F69 L) in a Japanese patient with late-onset Fabry disease.

Fabry disease is an X-linked recessive inborn error of glycosphingolipid catabolism caused by a mutation in the GLA gene. We sequenced the α-galactosidase A gene (GLA) of a patient who had been clinically diagnosed with late-onset Fabry disease. Abundant globotriaosylceramide was present in his urine, which indicated typical Fabry disease. Here, we report a novel hemizygous mutation, c.207C>A (Phe69 Leu), which caused a mild/late-onset form of Fabry disease.

Isolated cardiac sarcoidosis requiring open-chest myocardial biopsy for differentiation from malignant lymphoma.

A 68-year-old woman with a history of hypertension was admitted to our hospital because of dyspnea during physical exertion. Echocardiography demonstrated impaired left ventricular systolic function, and her ejection fraction was reduced to 30%. Coronary angiography did not show significant stenosis. Endomyocardial biopsy showed only nonspecific findings without noncaseating granulomas. Cardiac magnetic resonance (CMR) imaging showed transmural late gadolinium enhancement on the basal part of the left ventricle. 18F-Fluorodeoxyglucose positron emission tomography (18F-FDG PET) showed abnormal focal uptake specific to the left ventricle; no abnormal manifestations in other organs were observed. The CMR and 18F-FDG PET features could not rule out either sarcoidosis or malignant lymphoma. Therefore, we conducted open-chest myocardial biopsy to differentiate between the two possible diseases. Histopathological findings showed noncaseating epithelioid cell granuloma, confirming isolated cardiac sarcoidosis. This is an example of a challenging case of diagnosing isolated cardiac sarcoidosis. .

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.

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.

Sensitive detection of myocardial viability in chronic coronary artery disease by ultrasonic integrated backscatter analysis.

BACKGROUND: Myocardial viability is not synonymous with contractile reserve and identifiable in a significant percentage of dysfunctional myocardial segments without contractile reserve. The usefulness of ultrasonic tissue characterization by the phase-corrected magnitude of cyclic variation of integrated backscatter (MVIB) in chronic coronary artery disease is not fully validated. Thus, whether MVIB predominantly reflects the contractile reserve or myocardial viability of chronically dysfunctional myocardium was determined. METHODS: The MVIB of severely dysfunctional interventricular septum or posterior wall was measured in 34 consecutive patients with previous myocardial infarction. Dobutamine stress echocardiography and fluorine-18 fluorodeoxyglucose positron emission tomography were used as the standards of contractile reserve and myocardial viability, respectively. RESULTS: Among 44 dysfunctional segments, only 15 were judged as having contractile reserve and 29 were judged as not by dobutamine stress echocardiography, whereas 26 segments showed myocardial viability using fluorine-18 fluorodeoxyglucose positron emission tomography and 18 did not. MVIB was greater in segments with than in those without contractile reserve (4.7 +/- 2.2 vs -1.4 +/- 4.9 dB, P < .0001), but there was considerable overlap between the groups. On the other hand, MVIB of segments with and without myocardial viability (4.1 +/- 2.6 vs -4.3 +/- 3.3 dB, P < .0001) was distinctly different and predicted myocardial viability with a sensitivity of 92% and a specificity of 94%. CONCLUSIONS: For patients with chronic coronary artery disease, MVIB better reflects myocardial viability than it does contractile reserve. Ultrasonic tissue characterization, in concordance with fluorine-18 fluorodeoxyglucose positron emission tomography, is a sensitive method for detecting myocardial viability.

Reduced oxidative metabolic response in dysfunctional myocardium with preserved glucose metabolism but with impaired contractile reserve.

UNLABELLED: The recovery of function in myocardium defined as viable by (18)F-FDG PET may differ from that defined by dobutamine stress echocardiography (DSE). The aim of this study was to investigate the difference in the oxidative metabolic response between myocardial segments with preserved contractile reserve (CR) and those without CR, in segments with and without preserved glucose metabolism (GM), using (11)C-acetate PET. METHODS: Twenty patients with previous myocardial infarction (left ventricular ejection fraction, 37.1% +/- 16.5%) underwent dynamic (11)C-acetate PET at rest and during dobutamine (7.5 microg/kg/min) infusion. GM was evaluated using (18)F-FDG PET and CR was evaluated using DSE. Dysfunctional segments were divided into 3 groups: group A (n = 26) with preserved CR and GM, group B (n = 15) without CR but with preserved GM, and group C (n = 41) without CR and without preserved GM. RESULTS: Resting oxidative metabolism (k mono = monoexponential clearance rate) was preserved in group A and group B (0.052 +/- 0.011/min vs. 0.051 +/- 0.012/min, P = not significant) but was reduced in group C (0.040 +/- 0.015/min) (P < 0.03 vs. group A and group B). The change in k mono, as a measure of the metabolic response to low-dose dobutamine, was significantly higher in group A (0.018 +/- 0.012) than that in group B (0.0075 +/- 0.0096, P < 0.03) and group C (0.0080 +/- 0.012, P < 0.005). CONCLUSION: Viable segments based on (18)F-FDG PET have preserved resting oxidative metabolism. However, segments without CR but with preserved GM show a reduction in the oxidative metabolic response to low-dose dobutamine infusion. The decrease in CR may be related to the reduction in the metabolic response to inotropic stimulation despite preservation of tissue viability on (18)F-FDG PET.

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.

Reduction of coronary flow reserve in areas with and without ischemia on stress perfusion imaging in patients with coronary artery disease: a study using oxygen 15-labeled water PET.

BACKGROUND: Myocardial perfusion single photon emission computed tomography (SPECT) occasionally fails to detect coronary stenosis in patients with coronary artery disease (CAD). We evaluated coronary flow reserve (CFR) using oxygen 15-labeled water in areas with and without ischemia on technetium 99m tetrofosmin stress perfusion SPECT in patients with angiographically documented CAD. METHODS AND RESULTS: Twenty-seven patients with CAD and eleven age-matched normal subjects were studied. Baseline myocardial blood flow (MBF) and MBF during hyperemia induced by intravenous adenosine triphosphate infusion (0.16 mg. kg(-1). min(-1)) were determined with the use of O-15-labeled water positron emission tomography, and the CFR was calculated. Tc-99m tetrofosmin stress/rest SPECT was performed for comparison. On the basis of the results of coronary angiography and SPECT, coronary segments were divided into 3 types: segments with coronary stenosis and a perfusion abnormality on stress SPECT imaging (group A, n = 16), segments with coronary stenosis without a perfusion abnormality (group B, n = 42), and remote segments with no coronary stenosis or perfusion abnormality (group C, n = 18). Baseline MBF values were similar among the 3 groups. CFR in group A was lower (1.82 +/- 0.54) than in group B (2.22 +/- 0.87, P <.05), in group C (2.92 +/- 1.21, P <.01), and in normal segments (3.86 +/- 1.24, P <.001). CFR in group B was lower than in group C (P <.02) and in normal segments (P <.001). CFR in group C was lower than in normal segments (P <.02). CONCLUSIONS: Areas with a perfusion abnormality on stress SPECT had reduced CFR. In the areas without a perfusion abnormality and with coronary stenosis, lowering of CFR was intermediate between the areas with a perfusion abnormality and remote segments. Moreover, CFR was slightly, but significantly, lower in remote segments in patients with CAD compared with normal segments.

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.

Estimation of myocardial blood flow and myocardial flow reserve by 99mTc-sestamibi imaging: comparison with the results of [15O]H2O PET.

We developed a noninvasive method to quantitatively estimate the myocardial blood flow (MBF) index and flow reserve (MFR) using dynamic and static data obtained with technetium-99m sestamibi, and compared the results with MBF and MFR measured by oxygen-15-labeled water ([(15)O]H(2)O) PET. Twenty patients with coronary artery disease (CAD) and nine normal subjects underwent both (99m)Tc-sestamibi and PET studies within 2 weeks. From the anterior view, dynamic data were acquired for 2 min immediately after the injection of (99m)Tc-sestamibi, and planar static images were also obtained after 5 min at rest and during ATP stress (0.16 mg kg(-1) min(-1) for 5 min) on another day. The area under the time-activity curve on the aortic arch (Aorta ACU), myocardial weight with the SPET image (M), and the myocardial count on the planar image for 1 min (C(m)) were obtained. The MBF index (MBFI) was calculated as follows: MBFI=Cm/Aorta ACU x 100M. MFR was measured by dividing the MBFI at ATP stress by MBFI at rest. The MBFI measured by (99m)Tc-sestamibi was significantly correlated with MBF obtained using [(15)O]H(2)O PET (MBFI=13.174+11.732 x MBF, r=0.821, P<0.001). Furthermore, MFR measured by (99m)Tc-sestamibi was well correlated with that obtained using [(15)O]H(2)O PET, with some underestimation (r=0.845, P<0.001). MFR using (99m)Tc-sestamibi in patients with CAD was significantly lower than that in normal subjects (CAD: 1.484+/-0.256 vs normal: 2.127+/-0.308, P<0.001). These data suggest that the MBFI and MFR can be measured with (99m)Tc-sestamibi. This may be useful for the quantitative assessment of CAD, especially in those patients with diffuse coronary disease.

Decreased endothelium-dependent coronary vasomotion in healthy young smokers.

Chronic cigarette smoking alters coronary vascular endothelial response. To determine whether altered response also occurs in young individuals without manifest coronary disease we quantified coronary blood flow at rest, following adenosine vasodilator stress and during the cold pressor test in healthy young smokers. Myocardial blood flow (MBF) was quantified by oxygen-15 labelled water positron emission tomography in 30 healthy men aged from 20 to 35 years (18 smokers and 12 non-smokers, aged 27.4 +/- 4.4 vs 26.3 +/- 3.3). The smokers had been smoking cigarettes for 9.4 +/- 4.9 pack-years. MBF was measured at rest, during intravenous adenosine triphosphate (ATP: 0.16 mg kg(-1) min(-1)) infusion (hyperaemic response), and during cold pressor test (CPT) (endothelial vasodilator response). Rest MBF and hyperaemic MBF did not differ significantly between the smokers and the non-smokers (rest: 0.86 +/- 0.11 vs 0.92 +/- 0.14 and ATP: 3.20 +/- 1.12 vs 3.69 +/- 0.76 ml g(-1) min(-1); P = NS). Coronary flow reserve was similar between the two groups (smokers: 3.78 +/- 1.83; non-smokers: 4.03 +/- 0.68; P = NS). Although CPT induced a similar increase in rate-pressure product (RPP) in the smokers and the non-smokers (10,430 +/- 1,820 vs 9,236 +/- 1,356 beats min(-1) mmHg(-1)), CPT MBF corrected by RPP was significantly decreased in the smokers (0.65 +/- 0.12 ml g(-1) min(-1)) compared with the non-smokers (0.87 +/- 0.12 ml g(-1) min(-1)) ( P < 0.05). In addition, the ratio of CPT MBF to resting MBF was inversely correlated with pack-years ( r = -0.57, P = 0.014). Endothelium-dependent coronary artery vasodilator function is impaired in apparently healthy young smokers.

Low-dose dobutamine stress gated SPET for identification of viable myocardium: comparison with stress-rest perfusion SPET and PET.

The detection of viable myocardium is important for the prediction of functional recovery after revascularisation. However, a fixed perfusion defect often includes viable myocardium, and perfusion imaging then underestimates myocardial viability. We previously reported that low-dose dobutamine stress gated single-photon emission tomography (SPET) provides similar findings to dobutamine stress echocardiography in the assessment of myocardial viability. The present study investigated whether low-dose dobutamine stress gated SPET is of additional value as compared with stress-rest technetium-99m tetrofosmin SPET for the detection of myocardial viability. Standard stress-rest perfusion SPET, low-dose dobutamine stress gated SPET and fluorine-18 fluorodeoxyglucose positron emission tomography (FDG PET) were studied in 23 patients (mean age 67+/-7.6 years) with previous myocardial infarction. Twenty-one of them were successfully studied with each technique. FDG PET viability (FDG uptake >/=50%) was employed as the gold standard. One-day stress-rest (99m)Tc-tetrofosmin myocardial SPET was performed. After the resting study, gated SPET was acquired following infusion of 7.5 microg kg(-1) min(-1) of dobutamine. Left ventricular wall motion in 16 segments was assessed by cine mode display using a four-point scale. Myocardial viability was considered present when there was improvement by one point. Of a total of 336 segments analysed, 53 had persistent defects on stress-rest perfusion SPET. FDG viability was seen in 16 of 17 dobutamine-responsive segments, but in only 11 of 36 dobutamine non-responsive segments ( P<0.01). Thus, in the segments with persistent defects, viability findings on low-dose dobutamine stress gated SPET were concordant with those on FDG PET in 77% of segments (kappa value =0.55). For the detection of FDG-viable myocardium, the combination of stress-rest perfusion SPET and low-dose dobutamine stress gated SPET achieved a better sensitivity than stress-rest perfusion SPET alone (35/46, 76% vs 19/46, 41.3%, P<0.001), with a similar specificity (25/29, 86% vs 26/29, 90%, P=NS). We conclude that in the identification of viable myocardium, low-dose dobutamine stress gated SPET may provide additional information missed on a routine stress-rest perfusion scan. Dobutamine stress gated SPET may provide new insights into myocardial viability on the basis of ischaemia and contractile reserve.

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.