In the epidemiological survey for three years, casual plasma renin activity PRA of normotensive and hypertensive subjects older than 40 years was measured using radioimmunoassay. 617 normotensives and 379 hypertensives were measured. Mean value of PRA of normotensives was utilized as one of the three criteria for normal renin group, and the values higher or lower than mean±SD were classified as high or low renin group, respectively. In hypertensive subjects, low PRA was found in 23%, normal PRA in 64%, and high PRA in 13%. The incidence of low PRA in hypertensives was significantly higher in normotensives. PRA was inversely correlated to systolic blood pressure in normotensives and whole subjects including hypertensives throughout three year survey. There was also inverse correlation between PRA and age in normotensives and whole subjects in 1974 year survey. ST and T abnormalities in ECG were found more frequently in hypertensive-high renin group. Among all subjects, there occured 11 strokes and 2 heart attacks during two years. Their PRAs were high in seven patients, low in five and normal in only one. With age-sex matched control, inidence of stroke and heart attack was significantly higher in high and low renin groups than in normal renin group. In high renin group, incidence was also higher than in normal renin group with age-sex-blood pressure matched control. Multivariate analysis revealed that systolic blood pressure and high renin were more important risk factors for stroke and heart attack. It was concluded from this prospective study that there is a relationship between the level of PRA and the incidence of stroke and heart attack, and measurement of casual PRA in epidemiological survey is significant.
Clinical presentations of AMI were compared in two groups of autopsied aged cases. Group I included 12 cases (7 men and 5 women, mean age of 79.8 Years) with hematological evidences of DIC and Group II 41 cases (21 men and 20 women, mean age of 77.7 years) in whom no evidence of DIC was documented. Incidence of initial major symptoms of AMI in Groups I and II were as follows: Chest pain, 33% and 50%; dyspnea, 9% and 17%; hypotension or shock, 17% and 12%; disturbance of central nervous system, 8% and 5%; arrhythmia, 0% and 3%. Asymptomatic AMI was more frequently observed in Group I (33%) than in Group II (13%). Unequivocal elevation of serum enzymes was observed in 16% of Group II. Equivocal elevation or no detectable change in serum enzymes was observed in the majority of cases in Group I. Electrocardiographic changes and their sequences were characteristic for AMI in 33% of Group I and 78% of Group II, while in the majority of cases in Group I electrocardiographic changes were either atypical or not diagnostic for AMI. In Group I cardiac death was encountered in only 33% and the remainder died of renal failure, cerebrovascular accident or gastrointestinal bleeding. In Group II, cardiac death was the major cause of death (80%). Atypical clinical presentations of AMI complicating DIC may reflect the pathogenesis of myocardial lesions in DIC in aged patients.
Fructose-1, 6-diphosphate aldolase (ALD) and lactic dehydrogenase (LDH) in cerebrospinal fluid (CSF) and serum were measured during acute phase of cerebral bleeding (23 cases), cerebral infarction (16 cases) and subarachnoid hemorrhage (11 cases). The results were as follows: 1) There was a significant elevation of both ALD and LDH of CSF and serum in cerebral bleeding, serum LDH in cerebral infarction, and ALD and LDH of CSF in subarachnoid hemorrhage compared with the normal control. ALD and LDH of CSF were significantly higher in cerebral bleeding than in cerebral infarction, while no significant difference of serum enzymes was found between the two diseases. 2) The patients with cerebral bleeding were divided into two groups according to bloody or clear CSF. In the clear as well as the bloody CSF group, ALD and LDH of CSF were significantly greater than in cerebral infarction. In serum, LDH activity of the bloody group was higher than cerebral infarction. 3) In the patients with cerebral bleeding, ALD and LDF of CSF was significantly higher in the severe cases compared with mild cases, while this difference was not observed in serum enzyme. 4) Enzyme activities of CSF and serum in the patients with cerebral bleeding were increased and reached the peak value within seven days, then they decreased gradually. The duration of elevation in CSF enzymes was longer than that of serum enzymes and they remained still above normal value two weeks after the attack. 5) A positive correlation between CSF-ALD and CSF protein content or CSF-ALD and -LDH and cell counts was observed in the whole patients and in the patients. However no such correlation was seen in the patients with cerebral infarction or subarachnoid hemorrahge. 6) There was a positive correlation of both ALD and LDH between CSF and serum in the whole patients and of ALD in cerebral infarction, but not in cerebral bleeding or subarachnoid hemorrhage. These findings suggest that a measurement of ALD and LDH activity of CSF is useful for the differential diagnosis and the prediction of the prognosis of cerebrovascular accident. Further studies are necessary, however, to elucidate a mechanism of the elevation of CSF or serum enzymes.
Serum glycosaminoglycans (GAG) were measured by a modified method of Emura et al in 552 persons (male 180, female 372) at the annual health examination in Fukuoka City. Serum GAG concentration of various disease groups was compared with that of healthy group. 1) The mean concentration of GAG in the serum of healthy males (n=50) was 0.80±0.16 and in females (n=108) 0.79±0.16mg per 100ml of serum. There was no significant sex or age variations in serum GAG concentration (Table 2). 2) In the disease groups, significantly high concentration of serum GAG was observed in groups of hypertensive (n=175), atherosclerosis (n=133), hypercholesterolemia (n=87), hyper-beta-lipoproteinemia (n=67), and hyperlipidemia (n=87) (p<0.005∼0.001). Liver disease group showed significantly reduced serum GAG concentration (p<0.001) (Fig. 4). 3) In atherosclerosis-group, serum GAG concentration was compared with serum cholesterol, beta-lipoprotein and total lipid concentrations. There were, however, no significant correlations between these values.
In order to estimate“normal values”or“normal ranges”for serum chemical constitutents in the aged subjects, the statistical approaches of consecutive patient data were carried out according to Hoffmann's method. The subjects were classified by sex and age into eight groups, consisting of approximately 1500 patients in each group. The data of medical examinations of the subjects over 65 years old, living in the Tokyo Metropolitan Homes for the Aged, new participants of the Homes and young healthy adults were compared with data of the hospital patients. The results were as follows: 1. As for electrolytes, there were sex differences in potassium, chloride and inorganic phosphorus and the values of sodium and calcium decreased with aging in both sexes. 2. In the analyses of nonprotein nitrogenous constituents, the mean values of bilirubin, urea nitrogen, creatinine and uric acid in males were significantly higher than those in females. Age was accompanied by increases in estimated normal limits of urea nitrogen and creatinine for both sexes. The present data suggested that a trend towards lower uric acid levels with aging for males, whereas higher for females. 3. There was either no or only a slight difference in serum total protein between sexes. On the other hand, a significant decrease with age and significant differences with groups were observed. 4. As for serum cholesterol level, the present results were in substantial agreement with previously published reports. 5. The present results suggested that there were trends to increase the standard deviations of various chemical constituents with aging, and that the normal values and ranges were valid only for the laboratory testing of the specimens and for the group tested.
Sixty two brain scan cases who were pathologically confirmed as CVD were experienced in Tokyo Metropolitan Geriatric Hospital during the period from June 1972 to April 1977. They were the cases of 55 infarctions and 7 bleedings. The retrospective study were performed why the prediction of the prognosis of CVD was possible by careful analysis of brain scan data. By the difference of period before the death after the onset of CVD they were divided into 4 groups, namely 1st group (died within a month after the onset of CVD)-6 cases, 2nd group (died within 6 months)-28 cases, 3rd group (died within a year)-12 cases and 4th group (died after more than a year 16 cases. The cerebral infarction showed abnormal case 55%, hot scan 58%, mean scan time 1.5 time, mean scan grading of hot lesion 1.9±1.2 and mean length of the hot lesion 5.9±3.2cm. The cases of cerebral bleeding showed 43%, 44%, 1.3 time, 1.7±1.1 grade, 6.5±1.7cm respectively. The cases of cerebral infarction showed hot scan from the onset till 5th month after the attack with maximal grade in the 4th week. The mean grading of hot lesion were 2.3±1.1 in 1st group, 2.3±1.2 in 2nd group, 1.7±1.0 in 3rd group and 1.3±1.1 in 4th group. The incidence of abnormal scan were 75% in 1st group, 68% in 2nd group, 68% in 3rd group and 33% in 4th group. There observed some good correlation between the several parameters of brain scan and the prognosis of the cases. The cases of poor prognosis (1st & 2nd groups) were characterized to have larger lesion from the early period after the onset of the stroke. The cases of good prognosis (4th group) was characterized by the rapid decline of the grade of hot lesion. The observation of the size of hot lesion showed remarkably large standard deviation in data analysis indicating not so useful method to estimate the prognosis of CVD. The correlation of grade versus size of hot lesion was not good indicating the difference of the clinical meaning of them. Because the cases of cerebral bleeding were severe and limited in number no conclusive result was observed. Thus brain scan was considered to be as one of the useful aids for the estimation of the prognosis of cerebral infarction.
In order to clarify the pathogenesis of electrocardiographic changes in cerebrovascular accidents, the electrocardiograms and laboratory data before and after the stroke were compared in 18 autopsy proven intracranial hemorrhages and in 29 cerebral infarctions of the aged. Coronary stenosis and sites as well as sizes of cerebral lesions were also investigated in each group. The electrocardiographic changes after the stroke were observed in 88.9% of intracranial hemorrhages and 89.7% of cerebral infarctions. The ST-T changes were found in 61.0% and in 69.0% respectively, the severe ischemic changes being of high incidence in cerebral infarction. Various arrhythmias were found in 55.6% in intracranial hemorrhage and in 41.4% in cerebral infarction. Appearance of atrial fibrillation on storke was exclusively observed in cerebral infarction, in 10.3%. The extrasystoles were frequently seen in intracranial hemorrhage, supraventricular origin in 22.1%, and ventricular origin in 11.1%, while the extrasystoles were seen in cerebral infarction in 10.3% and in 3.4% respectively. Significant increase in hematocrit was observed in stroke and the elevation was more prominent in cerebral infarction; in cases with ischemic ST-T changes the increase being by 2.44±0.56% in intracranial hemorrhage and by 6.04±1.74% in cerebral infarction. This suggested that the ischemic ST-T changes were attributable to the elevation of hematocrit which induced the disturbance in coronary microcirculation. The systolic blood pressure increased by 52.5±8.9mmHg in intracranial hemorrhage, and blood pressure reached over 200mmHg regardless of the pattern of the electrocardiographic changes. The cerebral infarction revealed small increase in systolic blood pressure by 8.7±10.4mmHg, indicating that the elevation of blood pressure per se could not be the cause of the electrocardiographic changes. The severity of the coronary stenosis was similar in various types of electrocardiographic changes in both cerebral hemorrhage and infarction. This indicated that the ischemic ST-T changes were not derivied from the stenosis of the large coronary arteries. The myocardial infarction was associated in intracranial hemorrhage by 5.6%, while this association was 50.0% in cerebral infarction. The ischemic ST-T changes were relatively frequent in lateral type of cerebral hemorrhage, while the infarction of medial cerebral artery revealed various types of electrocardiographic changes. The sizes of cerebral lesions showed no relations to the ischemic ST-T changes. The ischemic ST-T changes observed in intracranial hemorrhage and infarction were probably induced by the elevation of hematocrit which led to the disturbance of coronary microcirculation. The site and size of cerebral lesions, coronary stenosis, elevation of blood pressure failed to correlated with the electrocardiographic changes.