Biomedical subjects
Publications and source records attributed to Y Miyagi.
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The effects of intravenous urokinase administration were assessed in patients with acute myocardial infarction (AMI). Of 146 patients with AMI, 101 were admitted within 12 hours of onset of chest pain, and classified in four groups according to the method of administering urokinase. PTCR group (15 cases); PTCR was performed within six hours of onset, using less than 960,000 I.U.; Group A (20 cases); 1.5 million I.U. administered in one hour or 960,000 I.U. in 30 min; Group B (48 cases); 240,000 I.U. in two hours; and 4) Group C (18 cases); 240,000 I.U. in 12 hours. In groups A, B and C, urokinase was administered intravenously. The remaining 45 patients did not receive urokinase, and served as a control group. In the chronic stage, infarction-related coronary arteries were patent at rates of 93% in the PTCR group, 82% in group A, 76% in group B, 62% in group C, and 46% in the control group. In the PTCR group and in group A, alpha 2-plasmin inhibitor showed a steep decline to the lowest level on the day after urokinase administration, as did the summation of elevation of ST segments in conventional twelve-lead electrocardiograms. Peak CK times, which represent the duration (hours) from onset to the peak serum CK value increased in the following order: 13.3 +/- 4.8 in the PTCR group, 17.3 +/- 4.9 in group A, 17.3 +/- 6.9 in group B, 20.7 +/- 6.7 in group C and 22.5 +/- 6.4 in the control group. These data suggest early recanalization of occluded coronary arteries in the group A, and intravenous administration of high doses of urokinase in the early phase of AMI seemed to contribute to salvage the ischemic myocardium. However, assessment of ventricular wall motion by two-dimensional echocardiography failed to confirm appreciable improvement in the PTCR group and group A in comparison with the other groups.
To assess myocardial tissue changes by two-dimensional echocardiography, quantitative evaluation and color display of the echo intensity were attempted using computerized image processing. The materials consisted of 11 patients with old anteroseptal myocardial infarction one year or more after the onset (OMI), and 12 normal subjects. Two-dimensional echocardiograms in the parasternal long-axis view were obtained using a commercially-available phased-array sector scanner. Scanner receiver settings including sensitivity-time control were maintained constant in all subjects. Images were recorded on the U-matic tape using a video tape recorder, then stop-frame end-diastolic images were converted to digital images. To measure echo intensity, regions of interest (ROI) were placed in the interventricular septum (IVS), the left ventricular posterior wall (LVPW), the left ventricular cavity, and the pericardium. The mean value of the echo intensities was determined for each ROI. Then, the relative echo intensity of the IVS or LVPW was calculated using the mean value of the pericardium as the maximum echo intensity, and the mean value of the left ventricular cavity as the minimum echo intensity. In normal subjects, the relative echo intensity of the IVS was 0.40 +/- 0.05 (mean +/- SE) and that of the LVPW was 0.31 +/- 0.02. By contrast, in patients with OMI, there was a significant increase (p less than 0.001) in the relative echo intensity of the IVS (0.71 +/- 0.06). The relative echo intensity of the LVPW was less than normal, but the difference was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
Two Japanese boys, 6 and 10 years old, required operation for severe Kawasaki heart disease. Both had multiple coronary arterial aneurysms and stenoses, and one had mitral regurgitation as well. The operations consisted of anastomosis between the left internal mammary artery and the left anterior descending artery and insertion of an autologous saphenous vein between the aorta and the posterior descending artery in both patients. The mitral valve was replaced in the one with mitral regurgitation. Angina pectoris has been completely relieved as confirmed by postoperative angiocardiography. Late results of coronary bypass grafting with the saphenous vein in pediatric patients with Kawasaki disease have been less than satisfactory because of the high occlusion rate of the graft. The internal mammary artery may be superior, at least theoretically, to the saphenous vein graft because it is a "living graft" with a high possibility of growing and with less susceptibility to degeneration. This is the first report of successful operation utilizing an internal mammary artery graft in coronary bypass for Kawasaki disease.
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A new method of closing a perimembranous malalignment ventricular septal defect (VSD) in corrected transposition of the great arteries (TGA) of the [S,L,L] type is presented. The method consists of combined approaches to the VSD through both a right atriotomy and an aortotomy without a ventriculotomy. The VSD is patched obliquely from the morphological right ventricular side of the septum, cranially through the aortic valve to the left ventricular side of the septum, caudally through the mitral valve. Although this method has been successfully applied in only one adult patient, some advantages may be expected: (1) prevention of trauma to the His bundle, which runs along the anterosuperior rim of the VSD on the left ventricular side; and (2) prevention of trauma to the tricuspid, mitral, and aortic valves without having to open the ventricles. We believe that this new method warrants a further trial as possibly better for closure of the VSD in corrected TGA of the [S,L,L] type.
Pre- and postoperative hemodynamics were assessed in 14 consecutive patients who developed ventricular septal perforation (VSP) following acute myocardial infarction (AMI). Results were correlated with the surgical outcome and with postoperative clinical improvements. The patients were divided into 3 groups according to the time intervals between the onset of AMI and the operation; acute (within 2 weeks after AMI), subacute (between 2 and 4 weeks) and chronic (after 4 weeks). In the above groups, 6, 2 and 6 patients were included, respectively. Eleven patients had anteroseptal infarction and 3 patients sustained inferior infarction. The survival rates were 33, 50 and 100% in the acute, subacute and chronic groups, respectively with an overall survival rate of 64%. Hemodynamic comparisons between survivors and non-survivors revealed that the systolic aortic pressure and left ventricular stroke volume index were significantly higher and the right ventricular end-diastolic pressure was significantly lower in survivors than in non-survivors (p less than 0.05). Although no statistical significance was obtained, left ventricular end-diastolic volumes and ejection fractions were higher in survivors. No difference was present between survivors and non-survivors in either Qp/Qs, Pp/Ps, Rp/Rs, systolic pulmonary pressure, left ventricular end-diastolic pressure or cardiac index. Patients with low arterial pressure and high right ventricular end-diastolic pressure under intensive medical regimens, indicating the presence of cardiogenic shock and/or associated right ventricular infarction or severe failure, had a high mortality and should be considered for emergency operation. Postoperative hemodynamics improved significantly in all variables measured (p less than 0.05-0.01). Patients with a VSP should all be considered for surgery unless a definite contraindication exists.
The computed tomography (CT) number within the region of interest (ROI) was used as a parameter to assess lung density in patients with congestive heart failure. Thirty-eight patients with valvular heart disease (VHD) and 34 patients with ischemic heart disease (IHD) were studied. Based on the New York Heart Association (NYHA) classification, 24 VHD patients were in class I or II (VHD I-II) and the other 14 were in NYHA class III or IV (VHD III-IV). Eighteen patients with IHD were in NYHA class I or II (IHD I-II) and 16 were in class III or IV (IHD III-IV). The CT number was measured bilaterally at the upper, middle and lower levels of the chest and compared with the corresponding values in 21 normal subjects (Group N). In a preliminary study on Group N, the CT numbers were insensitive to the size of the ROI, but were closely related to its location. In clinical applications, the mean values of the CT numbers in all six lung fields increased in the order of IHD I-II, to VHD I-II, IHD III-IV and VHD III-IV. Except for patients in IHD I-II, they were significantly larger than in Group N. The relationship between the CT number and the systolic and mean pulmonary arterial pressures and the pulmonary capillary wedge pressure were evaluated in 36 patients. Significant correlations were obtained in all six lung fields (r = 0.65-0.78, p less than 0.001). The results suggest that measurement of lung density by CT is useful for the quantitative evaluation of the severity of disease in patients with congestive heart failure.
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We evaluated clinically the infarct size in addition to left ventricular end-diastolic and end-systolic volumes (EDV, ESV) and ejection fraction (EF) using two-dimensional echocardiography (2-D) and algorithms based on the modified Simpson's rule. EDV, ESV and EF obtained by 2-D and three algorithms were compared with those obtained by left ventriculography in 23 patients with various heart diseases. Correlation coefficients obtained by our and other two algorithms were 0.88, 0.88 and 0.90, respectively, for EDV and ESV (p less than 0.01), and 0.71, 0.60 and 0.84 for EF (p less than 0.01). Myocardial mass of the region showing asynergy (asynergic size) was calculated by the above-mentioned three methods and compared with peak serum CK values in 14 patients with acute myocardial infarction. The correlation coefficient between both values was 0.76 (p less than 0.01) by our algorithm and it was higher than by other two algorithms (0.37 and 0.70). The time course of changes in asynergic size in acute myocardial infarction was studied by the use of 2-D and our algorithm. Asynergic size was significantly larger on the day of the onset (24.9 +/- 2.9 ml, mean +/- SE) than the third (21.5 +/- 2.7 ml) and seventh day (20.7 +/- 3.0 ml) after the onset (p less than 0.01). These results suggest that one can make a quantitative and serial estimation of infarct size as well as left ventricular volume by 2-D and our modified model, and that our algorithm is suitable for the purpose.
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