Changes regarding age and correlations between serum lipids and body mass index in humankind.

OBJECTIVES: To improve insight into age and gender related distributions of serum lipids and their correlation with body mass index (BMI). METHODS: Serum lipids embracing atherogenic index (AI) and BMI were analyzed from the results obtained in 19,823 men and 14,788 women undergoing a health examination between 1986 and 1996. RESULTS: The changes in total cholesterol (TC), triglyceride (TG), AI and BMI differed regarding gender. Although high-density lipoprotein-cholesterol (HDL-C) showed a flat pattern for all ages in both genders, its level in women was higher than in men. The ratio of the number in the unsuitable range to those in the suitable range increased with age as to TC in both sexes, then more than half of the population have an unsuitable level in the sixth decade. As for the correlation between serum lipids and BMI: TC, TG and AI correlated positively, but HDL-C correlated negatively. There were significant gaps between both age and gender. CONCLUSIONS: We suggest that the normal range of values of serum lipids needs to be revised according to gender and age to evaluate the risk status for a cardio-cerebrovascular disease more precisely in the field of preventive medicine. Simpler guidelines are preferable in specialized care as well as in general practice, particularly since computer technology is not yet universally adapted. In the near future, when computed information technology will be as common as the electricity and the telephone are current on the whole earth, all guidelines will have to be computed on the spot and personally.

Spontaneous reduction of leukemic lymphoma cells possibly by anti-tumor antibody-mediated phagocytosis; a kappa lambda-dual-positive B cell lymphoma.

We have investigated the possible role of anti-tumor antibody detected in a case of follicular lymphoma which demonstrated the spontaneous reduction of leukemic tumor cells. The tumor cells genotypically had monoclonal rearrangements of the immunoglobulin J H and C kappa genes, but phenotypically exhibited surface IgG, A, kappa and lambda (kappa lambda dual positivity). The culture study revealed that IgGlambda, at least, was derived from the serum, and IgAkappa was expressed intrinsically. Furthermore, the positive correlation between the densities of both surface light chains on two-color flow cytometry, the rosette formation study and its inhibition test by the Fcgamma fragment suggested that the serum IgGlambda combined with some antigens on the tumor-cell surface via its Fab portion and with the Fcgamma receptor of macrophages via its Fc portion. From these findings, we regarded the present case as an anti-tumor antibody-coated lymphoma. In addition, the phagocytic study disclosed that the serum-derived IgGlambda, at least, might have induced the phagocytosis of circulating lymphoma cells by macrophages. In conclusion, the existence of the anti-tumor antibody-coated lymphoma may be helpful in clarifying the immunological mechanism of the spontaneous regression occasionally seen in lymphomas.

Role of MB isoforms (isomers) in the early diagnosis of acute myocardial infarction.

In addition to electrocardiogram (ECG), analysis of creatinine phosphokinase (CPK), lactate dehydrogenase (LDH) and their isoenzymes is commonly employed to diagnose acute myocardial infarction (AMI). The aim of this study was to observe the efficiency of isomers of CPK for early diagnosis of AMI. ECG, though useful in many ways, is not 100% sensitive. The drawback involved with CPK and LDH isoenzymes is the time lag factor in diagnosing AMI early enough for interventional therapy. Recently the subunits of these isoenzymes, namely MM and now the MB isomers are being tested for their effectiveness in the early diagnosis of AMI. In our experience MB isomers were found to be accurate markers in the early diagnosis of AMI. They were especially valuable in diagnosing myocardial infarction not detectable by ECG in cases such as non-Q AMI, cardiomyopathy, and bundle branch block among other such cases.

A case of creatine kinase isomer anomaly in relation to the diagnosis of acute myocardial infarction.

Creatine kinase (CK) isomers have recently been suggested to be of value in the diagnosis of acute myocardial infarction (AMI). The aim of this report was to determine whether measurement of CK isomers, especially the MM isomer and the cardio-specific marker MB isomer, is practical in the diagnosis of AMI. A 64-year-old female with consistently high values for total CK showed an electrophoretic pattern which suggested AMI. We ruled out all possible causes of increased CK, and its MB isomer, including IgGBB, beta-LP (lipoprotein) and mitochondrial complexes as well as myocarditis, muscular disorders, and myoglobinuria. Regardless of the source of the anomaly, the fact remains that CK macroanomaly cases can be an obstacle in the diagnosis of AMI. CK isomers have proven to be accurate markers in AMI and valuable in doubtful cases, such as non Q-AMI. However, in light of this particular case of CK macroanomaly, isomers are not 100% accurate (specific) in the diagnosis of AMI.

Electrocardiographic surveys with respect to high voltage of the left ventricle.

A total of 1012 persons were divided into the following four groups according to the values of both SV1 + RV5 by the criterion of Sokolow and Lyon and cardio-thoracic ratio (CTR). In all cases the blood pressure, chest X-ray, body surface area, degree of obesity, and chest PA length were measured. From the above data, it was concluded that cases in GII had fat physiques and those in GIII were slender. It is widely known that there are many factors which produce a high voltage in the left ventricle on ECG. This study suggests that the physique is one of many important factors which cause a high voltage in the left ventricule on ECG.

[Evaluation of latent cardiac disease in diabetic patients with Tl-201 exercise myocardial scintigram and blood pool scintigram].

To find latent heart disease in diabetic patients, 142 diabetic patients were divided into 4 groups: 1) No hypertension and normal ECG (DM group); 2) Hypertension recognized clinically (HT group); 3) Myocardial damage on ECG (MD group) 4) group associated with the previous 2 (HT + MD group). In all groups Tl-201 exercise myocardial scintigrams and blood pool scintigrams were taken for comparative analysis. Positive rates of SPECT were 27.7% (23/83) in the DM group, 30.0% (9/30) in the HT group, 50.0% (6/12) in MD group, and 70.6% (12/17) in the HT + MD group. The rate in the HT + MD group was significantly higher than in that of the DM and HT groups (p less than 0.001, p less than 0.01). Blood pool scintigrams revealed that in the HT + MD group, as compared with the normal control group, both 1/3 FF and PFR were significantly depressed, in addition to significant TPF prolongation in the former (p less than 0.001, p less than 0.05, p less than 0.05). These findings suggest that in diabetic patients hypertension and myocardial damage would lead to a high incidence of abnormality in SPECT and left ventricular rapid filling dysfunction. This indicate a high incidence of latent cardiac disease which can be recognized in diabetic patients by stress myocardial and blood pool scintigrams.

Four brief periods of myocardial ischemia cause no cumulative ATP loss or necrosis.

The effect of repetitive periods of coronary occlusion on myocardial adenine nucleotides, lactate, and infarct size was studied. In one series of dogs, the circumflex artery was occluded for one, two, or four 10-min episodes, each separated by 20 min of reperfusion. Hearts were excised and sampled for metabolic assays after one or more periods of ischemia before or after reperfusion. One 10-min period of ischemia caused a 61% loss of ATP and 41% loss of adenine nucleotides from the most severely ischemic subendocardial zone. Reperfusion resulted in rapid restoration of the adenylate charge but in only slight repletion of the adenine nucleotide pool. However, two or even four 10-min periods of ischemia caused no further adenine nucleotide loss. In contrast, 40 min of continuous coronary occlusion caused an 87% depletion of ATP and 67% of the adenine nucleotide pool from the same subendocardial region. Collateral blood flow was similar during all occlusions, but lactate accumulation was less during later occlusions. In a second series of experiments, myocardial necrosis was quantitated 4 days after four 10-min periods of ischemia. Necrosis was observed in only one of six dogs and, in this dog, was only 1.5% of the anatomic area at risk. Thus intermittent reperfusion prevents cumulative metabolic deficits and myocardial ischemic cell death, perhaps by restoring the capacity for high-energy phosphate (HEP) production and/or washing out deleterious catabolites. A first episode of ischemia also slows HEP utilization in subsequent episodes.

Protection of the ischemic myocardium with calcium antagonistic drugs.

Ligation of the coronary artery to produce myocardial infarction experimentally was performed in 41 mongrel dogs. The dogs were then treated with niludipine or nifedipine. Niludipine in doses of 0.05 mg/kg/day (niludipine A group) and 0.1 mg/kg/day (niludipine B group) or nifedipine 0.05 mg/kg/day (nifedipine group) was administered for 7 postoperative days. The animals were sacrificed, their hearts removed and extent of myocardial damage studied. 1. The size of infarctions measured by 99mTc-PYP myocardial scintigrams of the isolated heart was significantly smaller in the niludipine A group. 2. The degree of ischemia indicated by LDH isoenzyme patterns was lowest in the niludipine A group followed by nifedipine and niludipine B group in this order. The value for H subunits of LDH isoenzymes on the subepicardial side was higher in the nifedipine group. 3. Histopathological findings varied from specimen to specimen, but in general the niludipine A group showed best improvement. Our results suggest that the calcium antagonistic drugs, niludipine and nifedipine, seem to have myocardium protective properties in dogs. To what degree these findings can be applied clinically needs further studies.

A-V block and A-V dissociation in electrocardiographic surveys of middle school students.

(1) ECG surveys were performed on 12,523 middle school students. The incidence of A-V block was 0.04% (0.37% in males and 0.43% in females). The incidence of A-V dissociation was 0.11% (0.09% in males and0.13% in females). (2) There was no case of Mobitz type II or complete A-V block in this survey. (3) Sixty-four school students were picked at random from the students with A-V block who had been diagnosed by ECG surveys during the last there years and were given the Master's two-step test. The following four types of response were recognized; Type 1, Type 2, Type 3A, B, C, and Type 4. (4) Elevation of ASLO and antistreptkinase (ASK) were found in 6.4% and 13.5%, respectively. The serum cold agglutinin titer was elevated in four of the 12 students tested. (5) Most students with A-V block or A-V dissociation had no past history of severe disease or no major complaints.

Experimental study on enzyme distribution and its relation to myocardial ischemic changes following coronary circulatory disturbances.

Coronary artery ligation of canine heart was performed to investigate the relationship between the lactate dehydrogenase (LDH) pattern in myocardium and the distribution of coronary flow, especially in the early stage of ligation and after reperfusion. In the myocardium of normal dogs, the LDH pattern was similar in the left ventricle, the interventricular septum, and the right ventricle; the average LD5:LD4 ratio was 1.1, 1.2, and 1.2, respectively, and consisted mainly of heart type. In the left and right auricles, however, the ratios were 0.3 and 0.2, respectively, lacking heart type. In the left ventricle, LD5:LD4 ratio in the subendocardium was different from that in the subepicardial layer. Blood flow distribution in canine myocardium was investigated by the fluorescent pattern on the cut surface of heart, in which 10% fluorescein sodium was injected into the cavity. By this method the evolution of the ischemic area from the endocardial layer to the epicardial side following coronary artery ligation and the effect of reperfusion on the ischemic area were clarified. Electron microscopic studies indicated that loss of mitochondrial function may account for the irreversibility of myocardial cell alteration. A new method for studying enzyme localization in tissues was introduced for studying LDH isoenzyme distribution in normal and injured myocardium.