[The dual energy myocardial SPECT of 99mTc-PYP and 201TlCl for diagnosis of acute myocardial infarction].
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Biomedical subjects
Publications and source records attributed to Y Ikuno.
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Two novel acute lymphoblastic leukemia (ALL) cell lines, HOON and HYON, have been established from patients with non-T, non-B ALL. The cell lines have been characterized and shown to express phenotypic markers on non-T, non-B ALL. By indirect immunofluorescence and flow cytometry they express Ia and common ALL (CALLA) antigens and are reactive with monoclonal antibodies BA-1, BA-2 and OKT-9. However, the cells do not express detectable amounts of B1 antigen or of cytoplasmic mu chain, which are markers of pre-B cells. Quantitation of Ia and CALLA antigens on HOON and HYON cell lines using a cellular radioimmunoassay revealed that both cells bind high levels of anti-Ia antibodies, 110 X 10(4) molecules per cell, and low levels of anti-CALLA antibodies, 7 X 10(4) molecules per cell. Although both HOON and HYON carry equivalent amounts of Ia on their surface, only the former is a good stimulator of the one-way mixed lymphocyte reaction.
Serial non-invasive studies including echocardiography were performed for the evaluation and follow-up of the cardiac lesions in six cases with genetic mucopolysaccharidoses. These cases were classified by the enzyme assay into one case of Scheie syndrome, three of Hunter syndrome, one of Sanfilippo syndrome and one of Maroteaux-Lamy syndrome. The echocardiographic examination revealed the most striking change in the mitral valve, which was progressive with increase of the age in most cases. The mitral valve echo was dense and multilayered with a decreased diastolic descent rate (DDR) in the M-mode echocardiogram, and its thick leaflets showed diminished opening on the two-dimensional echocardiogram. The aortic valve echo was also dense in three cases inducing one case with the prolapse of the non-coronary cusp into the left ventricular (LV) cavity. The pulmonary and tricuspid valves showed an unremarkable change, although the echocardiographic signs of pulmonary hypertension was observed in two cases. Diffuse hypertrophy of the interventricular septum and LV posterior wall was observed in five cases and apical hypertrophy was found in a case of Hunter syndrome (Case 2). Parameters of the LV contractility showed almost normal values but the distensibility of the LV posterior wall was impaired in two cases, suggesting stiffness of the cardiac muscle. Although no ischemic change was observed on the electrocardiogram, the echo density of coronary artery wall was not uniform on the two-dimensional echocardiogram and dilated coronary artery was found in two cases. Phonocardiograms disclosed an aortic regurgitant murmur in one case and an apical mitral regurgitant murmur in two cases. In one case of Scheie syndrome, a pansystolic murmur (Levine 3/6) and a mid-diastolic rumble (Levine 2/6) were present at the age of 15 and 16, but after the transient increase in the loudness these disappeared at the age of 18 and only an ejection systolic murmur is audible at the present time, while the mitral valve showed a progressive limitation of the movement on the two-dimensional echocardiogram. Contrary to the reduced DDR and diminished opening of the mitral valve in 3 cases, neither diastolic rumble nor opening snap was recognized in the phonocardiogram. The echocardiographic findings seemed to reflect the patho-anatomical manifestation of this disease, and thus, the periodical echocardiographic evaluation is rewarding to assess the cardiac lesions and their progression in mucopolysaccharidoses.
Some of cases of congestive heart failure (CHF) are intractable or refractory and respond poorly to conventional treatment. We have examined factors which may influence the clinical course and prognosis. The subjects were 114 hospitalized patients with CHF. Of these, 77 had a good response to treatment and were classified as the curative group (Group C) while the remaining 37 who were difficult to treat, including those with poor prognosis, were designated the refractory group (Group R). Of the various clinical background factors including the findings of laboratory and other examinations, the following 8 variables made a significant contribution to differentiation between the 2 groups: 1) heart rate (X1), 2) hemoglobin content (X2), 3) serum K (X3), 4) serum total protein (X4), 5) A/G (X5), 6) BUN (X6), 7) grade of hepatomegaly (X7), and 8) number of previous CHF episodes (X8). The linear discriminant function represented by the following equation using these 8 variables showed an excellent result in differentiating the 2 groups. Y = - 9.64 - 0.0686X1 + 0.345X2 + 1.351X3 + 1.513X4 + + 1.988X5 - 0.0876X6 - 0.792X7 - 0.737X8. When Y value is over 0, Group C is judged. When Y value is under 0, group R is judged. We concluded that the discriminant equation covering these 8 factors is a useful means of predicting the prognosis in CHF and the response to treatment.
An 18-yr-old male developed Mycoplasma pneumoniae pneumonia associated with IgA nephropathy. In the biopsied renal tissue, immunofluorescence showed striking deposits of IgA, C3 and C3 activator in the mesangium, and electron microscopic examination showed electron-dense deposits in the mesangial region. When the patient's serum was preincubated with rabbit antiserum to human IgA, the passive hemagglutination titer for M. pneumoniae was much decreased. We suggest that in some cases, IgA nephropathy may follow infection by an organism which stimulates in IgA antibody response, leading to the formation of IgA antigen antibody immune complex deposits in the glomerular mesangium.
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The applicability of ECG gated cardiac computed tomography (CT) in 12 patients with hypertrophic cardiomyopathy was examined. Six of the 12 patients had hypertrophic obstructive cardiomyopathy, including one patient with mid-ventricular obstruction. Three of the 12 patients had hypertrophic non-obstructive cardiomyopathy, and three had apical hypertrophic cardiomyopathy. The diagnosis of hypertrophic cardiomyopathy was confirmed by the angiocardiogram in all patients. Cardiac CT was performed after intravenous administration of contrast media usually given as a bolus injection. The gantry was set with positive 20 degree tilt angle. In all patients with hypertrophic obstructive cardiomyopathy except for mid-ventricular obstruction, the hypertrophied interventricular septum in the basal and mid portions was observed, and the left ventricular cavity was narrowed in systole. In a patient with mid-ventricular obstruction, the marked hypertrophied interventricular septum and antero-lateral papillary muscle were observed. In diastole, the left ventricular cavity was narrow and divided into two parts. The apical cavity was completely disappeared in systole. In all patients with hypertrophic non-obstructive cardiomyopathy, the diffuse hypertrophied interventricular septum was observed in diastole. In systole, the apical portion of the left ventricular cavity was markedly narrow and anterio-lateral papillary muscle was hypertrophic. In all patients with apical hypertrophic cardiomyopathy, the marked apical hypertrophy of the left ventricular wall was observed in diastole. It is concluded that ECG gated cardiac CT could estimate myocardial wall motion and thickness and differentiate the types of hypertrophic cardiomyopathy each other.
In 19 patients with anteroseptal myocardial infarction, the wall motion of interventricular septum was analyzed by RI angiography using the amplitude image and the phase image. Both images were obtained from ECG gated blood pool data by Fourier analysis. Namely, from the first harmonic in the Fourier series, the heart motion was detected as the amplitude and phase of time-activity curve in each pixel. The distribution of the amplitudes and phases were displayed in color scale, and then both the amplitude and phase images were acquired. Those images allowed us visualization of the ischemic area, even if the scar was parallel to the detector. Moreover, we were able to assess the wall motion of the entire interventricular septum and to distinguish hypokinetic region and dyskinetic region from the hypokinetic region with shift of phase estimated by conventional method. Abnormal region detected by those images closely corresponded with the region of decreased radioisotope concentration in thallium-201 myocardial scintigram.
ECG gated cardiac computed tomography (cardiac (T) was performed in 9 cases with old myocardial infarction. Seven of these had anterio-septal infarction, one had inferior wall infarction and the remaining one had posterior wall infarction. All were investigated by left ventriculography and coronary arteriography. Cardiac CT was performed after intravenous administration of contrast medium usually given as a bolus injection. The infarcted myocardium was thin and showed abnormal wall motion in cardiac CT, but the motion did not always coincide with left ventricular cineangiographic findings. In 3 cases, mural thrombi at the left ventricular apex were observed by cardiac CT, and in 2 of which the thrombi were confirmed by left ventriculography. In 2 cases, cardiac CT showed stasis of contrast medium and aneurysmal formation in the left ventricular cavity and the aneurysms were confirmed by left ventriculography. Sequential 8 mm thick non-ECG gated cardiac CT scans from the cardiac apex to the base were performed in 7 cases with anterio-septal infarction, and the infarcted area were observed in the anterior interventricular septum in 6 cases. We concluded that cardiac CT was a useful noninvasive method to detect abnormal wall motion, abnormally thin wall, mural thrombus and left ventricular aneurysm in old myocardial infarction.
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Right heart pressure tracings were studied in 5 cases with constrictive pericarditis. The pressure of the A-wave in the right atrium of these cases was higher than the pulmonary arterial diastolic pressure. In addition, a presystolic wave appeared in the pulmonary arterial and the right ventricular pressure tracings, in coincidence with atrial systole. The pressure of this presystolic wave was similar to that of the right atrial A-wave. This suggests that the pulmonary valve opens following atrial systole, and then the blood flows into the pulmonary artery in the presystolic phase in patients with constrictive pericarditis. In 2 cases, pulmonary valve echograms were recorded. The a-dip in these 2 cases was as deep as 8.4 mm and 9.6 mm (1.8-4.1 mm with a mean of 2.80 mm for normal men), and its duration was prolonged to 0.17 sec and 0.18 sec (0.10-0.13 sec with a mean of 0.115 sec for normal men). In conclusion, such a deep and prolonged a-dip on pulmonary valve echogram is presumably a sign of presystolic pulmonary valve opening.
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