Thallium-201 and gallium 67 single photon emission computed tomographic imaging in cardiac sarcoidosis.
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Biomedical subjects
Publications and source records attributed to C Kurata.
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To elucidate the circadian variation of fibrinolytic components in vasospastic angina, plasma levels of tissue plasminogen activator antigen (t-PA), free plasminogen activator inhibitor antigen (free PAI-1), t-PA/PAI-1 complex, and total PAI-1 were measured in venous plasma samples. Samples were taken every 6 hours (6:00 AM, noon, 6:00 PM, and midnight) for 24 hours in 14 patients with vasospastic angina, in 9 patients with exertional angina, and in 19 normal subjects. Twenty-four-hour Holter monitoring (Holter monitor, Del Mar Avionics, Irvine, Calif.) was also carried out in all subjects. All of the fibrinolytic components showed circadian variation, with a peak level at 6:00 AM in every study group except for the t-PA/PAI-1 complex in the group of patients with exertional angina. The values for all or the fibrinolytic components at each sampling time were higher in patients with coronary artery disease than in normal subjects. In particular, the mean value of free PAI-1 at 6:00 AM in patients with vasospastic angina was significantly higher than that in normal subjects and that in patients with exertional angina. This value of free PAI-1 in patients with vasospastic angina was closely associated with the duration of ischemic attacks. These results suggested that the circadian fluctuation of fibrinolytic components may be an important factor that leads to coronary thrombosis at the time of coronary spasm, especially in the early morning.
OBJECTIVE: The aim was to characterise the transmural distribution of beta adrenergic receptors in failing myocardium in cardiomyopathy. METHODS: Using a quantitative autoradiographic technique with 125I-cyanopindolol (ICYP), the density and transmural distribution of beta adrenergic receptors were compared between eight cardiomyopathic BIO 14.6 Syrian hamsters with heart failure and six normal age matched controls (BIO 14.6HAM). RESULTS: Binding of ICYP to transmural slices of hamster myocardium was rapid, saturable, stereoselective, and displaceable by antagonists. The binding isotherm showed a significant increase in the total tissue content of beta adrenergic receptors in the failing myocardium of cardiomyopathic hamsters: 15.3(SEM 1.6) fmol.mg-1 protein v 9.4(1.2) fmol.mg-1 protein in normal myocardium of control hamsters (p < 0.05). There was no difference in receptor affinity. Quantitative autoradiography showed regional heterogeneity of beta adrenergic receptors in cardiomyopathic hamsters, with an increase of beta adrenergic receptor density in the septal and subendocardial regions. In addition, the regions with increased interstitial fibrosis corresponded to the sites of increased beta adrenergic receptor density. CONCLUSIONS: The transmural distribution of beta adrenergic receptor is heterogeneous in the failing myocardium of cardiomyopathic hamsters and an increased beta adrenergic receptor density may be associated with the development of cardiomyopathy.
This study was undertaken to determine whether the site of ST depression on 12-lead exercise electrocardiography can identify the ischemic site assessed by myocardial Tl-201 emission computed tomography in 409 patients with transient defects. ST depression in some leads was more frequent in those with inferior or lateral ischemia than in those with anterior ischemia. In 214 patients with ST depression and no ST elevation, however, the frequency of ST depression in each lead was similar between those with and without anterior ischemia. In 63 patients with ST depression, single vessel disease and no infarction, the frequency of ST depression in each lead was similar among those with anterior, inferior and lateral ischemia. Moreover, in patients with abnormal Q waves, the site of ST depression was not related to the location of ischemia. In conclusion, the site of exercise-induced ST depression could not be used to determine an ischemic region.
Routine coronary angiography was performed in order to determine the incidence and clinical condition of coronary artery disease in 37 patients with arteriosclerosis obliterans or aortic aneurysm. Coronary angiography demonstrated significant stenosis in 12 (57%) of 21 patients with arteriosclerosis obliterans and in 7 (44%) of 16 patients with aortic aneurysm. The prevalence of risk factors for arteriosclerosis was similar for patients with arteriosclerosis obliterans and those with aortic aneurysm, and similar for patients with and without coronary artery stenosis. But coronary artery disease is often silent in patients with arteriosclerosis obliterans.
To evaluate the relationship between regional wall motion and 99mTc-methoxy-isobutyl-isonitrile (MIBI) uptake, ECG-gated single-photon emission computed tomography (SPECT) with 99mTc-MIBI was performed in 20 patients with prior myocardial infarction. The left ventricular images at end-diastole (ED) and end-systole (ES) were divided into 39 segments, respectively. Based on circumferential profile analysis, relative uptake (%EDc, %ESc), percent count increase (% delta C), and normalized percent count increase (% delta Cn) were analyzed in each segment and compared with regional wall motion indices assessed by echocardiography and left ventriculography. ECG-gated SPECT with 99mTc-MIBI provided high contrast tomograms of the left ventricular myocardium. %EDc and %ESc showed good correlations with regional wall motion indices. % delta C and % delta Cn, however, showed lower correlations compared with %EDc and %ESc. In conclusion, high-quality left ventricular images were obtained with 99mTc-MIBI ECG-gated SPECT, but quantitative analysis based on only percent count increase (% delta C) have limitations for evaluation of regional wall motion.
We studied whether emission computed tomography (ECT) with 123I-labeled 15-(p-iodophenyl)-3R,S-methylpentadecanoic acid (BMIPP) shows myocardial distribution different from 201Tl in hypertrophic cardiomyopathy. In 10 patients with asymmetric septal hypertrophy (ASH), 5 with diffuse hypertrophy and 2 with apical hypertrophy, ECT was acquired 30 min (early) and 4 hr (late) after injection of 123I-BMIPP at rest and was compared with ECT with 201Tl. In 10 patients with ASH, the relative regional uptake (RRU) of the septum was lower in the early 123I-BMIPP study than in the 201Tl study, although that of the posterior wall was similar. In the early and late 123I-BMIPP studies, the RRU of the septum was lower in 10 patients with ASH than in 7 without ASH, although that of the posterior wall was similar. In the 201Tl study, however, the RRU of both the septum and posterior wall was similar in those with and without ASH. Moreover, in 16 patients, the apparent left ventricular size was larger in the early 123I-BMIPP study than in the 201Tl study, which suggested reduced 123I-BMIPP uptake in the subendocardium. In patients with hypertrophic cardiomyopathy, thus, 123I-BMIPP imaging may reveal impaired regional fatty acid utilization, which is independent of regional perfusion.
To assess the role of fibrinolytic system, 19 patients with rest angina and insignificant coronary artery stenosis and 23 controls performed symptom-limited multistage exercise. Vasospasm was angiographically demonstrated in 12 patients. Pre- and peak exercise blood samples from each patient were assayed to determine the fibrinolytic components. The patients displayed significantly increased PAI activity both under the basal conditions (p less than 0.01) and at peak exercise (p less than 0.01) as compared with the controls. However, the values of other fibrinolytic components, such as t-PA antigen, t-PA/PAI-1 complex and free PAI-1 antigen, in the controls and patients were similar. Nineteen patients were divided into two groups according to PAI activity levels under basal conditions. Nine patients displayed high PAI activity (more than the mean + 1 SD of the control value) under the basal conditions. When compared to the remaining 10 patients, the high PAI activity group had both a significantly short time interval from the last attack to the time of getting the blood sample (p less than 0.05), and a worse short-term prognosis (p less than 0.05). Thus, the level of PAI activity under basal conditions reflected the extent of disease activity, suggesting that PAI activity may be a useful clinical indicator of the severity of rest angina in patients without significant coronary stenosis.
A-59-year old woman died from heart failure associated with tricuspid regurgitation and pulmonary hypertension. Necropsy revealed that her tricuspid valve was composed of six leaflets. We found no previous report of this type of tricuspid valve abnormality.
Certain patients with coronary artery disease (CAD) may have neither ST depression nor chest pain during exercise despite the presence of myocardial ischemia. The frequency and characteristics of such electrocardiographically and symptomatically silent ischemia were studied in 171 patients with both angiographically documented CAD and scintigraphically documented ischemia. Fifty-six (33%) of 171 patients had neither ST depression nor chest pain (Group N), and 115 (67%) had ST depression and/or chest pain (Group P). The two groups were similar with respect to age, gender, the prevalence of prior infarction, and peak systolic blood pressure. Group N patients, however, had a higher mean peak heart rate and rate-pressure product, less severe scintigraphic ischemia, a lower lung thallium-201 uptake, and a smaller number of diseased vessels. Stepwise discriminant analysis showed a history of effort angina, lung thallium-201 uptake, and scintigraphic severity of ischemia to be significant discriminators between Groups N and P. In conclusion, electrocardiographically and symptomatically silent ischemia may be common during exercise in patients with CAD, and less severe ischemia may be one of important determinants.
To test whether the analysis of lung uptake is worth adding to the interpretation of exercise thallium-201 (201TI) emission computed tomography (ECT), a lung/heart ratio of 201TI uptake was measured from an anterior image during ECT in 25 clinically normal (Group 1), 91 angiographically normal (Group 2), and 265 subjects with coronary artery disease (Group 3). The mean +2 s.d. of ratios in Groups 1 and 2 were the same (0.37). In Group 3, 80 subjects (30%) with increased ratios (greater than 0.37) had higher frequencies of prior infarction and multi-vessel disease, more severe left ventricular dysfunction, and 201TI defects than 185 subjects with normal ratios. Subjects with markedly increased ratios (greater than 0.45) had three-vessel disease more frequently than those with slightly or moderately increased ratios (67% versus 14% or 35%). Thus the measurement of lung/heart ratios may provide information regarding the severity of coronary artery disease and should be added to the routine interpretation of exercise ECT.
Free radicals can affect lipids of membranes by initiating peroxidation. Since alterations in membrane fluidity can modulate membrane functions including ion permeability, the effects of free radicals on the intracellular Ca2+ level ([Ca2+]i) and membrane fluidity were studied. Human erythrocytes were spin-labeled with 5-DSA and the membrane fluidity was quantified by ESR during application of oxygen-derived free radicals. The morphology was observed by the scanning electron microscopy. The effects of H2O2 on [Ca2+]i were studied using single guinea pig ventricular myocytes and fura-2 AM. Superoxide and H2O2 (10(-3) and 10(-4) M) induced a decrease in membrane fluidity and morphological changes of erythrocytes. [Ca2+]i significantly increased from the control value (53 +/- 4 nmol/litre) to 110 +/- 29 nmol/litre when the cells were shortened, and to 130 +/- 26 nmol/litre before cells became rounded. This study showed that [Ca2+]i was significantly increased by oxygen-derived free radicals, possibly by lipid peroxidation of the cell membrane. During perfusion with H2O2 however, the increase in [Ca2+]i was not pronounced. Therefore, we suspect that the mechanism of cell injury due to free radicals may be a combination of direct cell membrane injury and Ca2+ overload rather than intracellular Ca2+ overload.
To assess the fibrinolytic system in patients with exercise-induced ischemia and its relation to ischemia and severity of coronary artery disease (CAD), 47 patients with CAD confirmed by results of coronary angiography underwent symptom-limited multistage exercise thallium-201 emission computed tomography. All patients with CAD had exercise-induced ischemia as assessed from thallium-201 images. Pre- and peak exercise blood samples from each patient and preexercise blood samples from control subjects were assayed for several fibrinolytic components and were also assayed for plasma adrenaline. The extent of ischemia was defined as delta visual uptake score (total visual uptake score in delayed images minus total visual uptake score in initial images) and the severity of CAD as the number of diseased vessels. In the basal condition, plasminogen activator inhibitor (PAI) activity was significantly higher in patients with exercise-induced ischemia as compared to control subjects (p less than 0.01), although there were no significant differences in other fibrinolytic variables between the two groups. Moreover, PAI activity in the basal condition displayed a significantly positive correlation with the extent of ischemia (r = 0.47, p less than 0.01). Patients with exercise-induced ischemia were divided into two groups (24 with single-vessel disease and 23 with multivessel disease). There were no significant differences in coronary risk factors, hemodynamics, or plasma adrenaline levels during exercise between single-vessel and multivessel disease except that delta visual uptake score was significantly higher in multivessel disease (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Factors associated with silent myocardial ischemia (SMI) during exercise testing were studied by means of thallium-201 emission computed tomography (ECT) in 471 patients. Coronary angiography was done in 290, of whom 167 were found to have significant coronary artery disease (CAD). Exercise-induced ischemia and its severity were defined with ECT. During exercise 108 (62%) of 173 patients with ischemia and 57 (50%) of 115 with ischemia and angiographically documented CAD had no chest pain. One third of the patients showed an inconsistency between scintigraphic ischemia and ischemia ST depression. Age, sex, prior myocardial infarction, and diabetes mellitus were not related to SMI. Patients with SMI had less severe ischemia despite a higher peak double product compared to those with painful ischemia. Among 91 with prior myocardial infarction and exercise-induced ischemia, 51 with periinfarction ischemia had a higher frequency of SMI than did 14 with ischemia remote from the prior infarct zone despite similarities in the severity of ischemia. In conclusion, factors localized within ischemic myocardium such as less severe ischemia or adjacency to a prior infarct made SMI more prevalent.
Two patients with myocardial sarcoidosis are presented, both of whom underwent SPECT imaging with Tl-201 and Ga-67. The first had Ga-67 myocardial uptake with a Tl-201 defect, which disappeared with corticosteroid therapy. The second had multiple Tl-201 defects without Ga-67 uptake, which persisted despite corticosteroid therapy. Therefore, the combination of Tl-201 and Ga-67 imaging may be useful for recognizing myocardial sarcoidosis and for predicting the response to corticosteroid therapy.
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A 67-year-old man had an acute myocardial infarction with thrombosis in the left anterior descending artery shortly after normal exercise. We were able to measure the fibrinolytic components in this patient just prior to his developing acute myocardial infarction as well as during convalescence. In this case, marked increase in total plasminogen activator inhibitor-1 (PAI-1) antigen, mainly due to free PAI-1 antigen, was observed in basal conditions before the onset of acute myocardial infarction. On the appearance of ischaemia, plasminogen activator activity was suppressed, probably due to decreased tissue plasminogen activator antigen release and increased PAI activity, compared with that during convalescence. This suggests that some patients with coronary artery disease who have a high level of free PAI-1 antigen in basal conditions may have a strong tendency to develop acute myocardial infarction, due to further impaired fibrinolysis on the induction of ischaemia.
The case of a 20-year-old man with patent ductus arteriosus complicated with Eisenmenger's syndrome is described. Radionuclide angiocardiography characterized the abnormal pattern of blood flow through the central circulation to establish a diagnosis of patent ductus arteriosus with a significant right-to-left shunt, which had not been indicated by other clinical findings.