To elucidate the relationship between serum lipoprotein (a) [Lp(a)] and ischemic heart disease (IHD), a three-generation study was conducted in 13 families with IHD and 26 families without IHD. Serum Lp(a), Lp(a) phenotype, coronary risk factors, and the prevalence of IHD were examined. Pedigree trees revealed that a high-Lp(a) (serum Lp(a)≥30mg/dl) level might be inherited in an autosomal dominant manner. The high-Lp(a) families, included more than two members with a high serum Lp(a) level, did not show a higher prevalence of IHD than control families. The eldest generation had an elevated serum Lp(a) level compared with younger generations in the families without high-Lp(a) members, as well as in the high-Lp(a) families, even after matching Lp(a) phenotypes. The mean serum Lp(a) level of the patients with IHD was higher than that of controls (log[Lp(a) (mg/dl)]: 1.43±0.35 vs. 1.14±0.45, mean ± SD, p<0.053), while the differences were minimum in younger generations. Coronary risk factors, for example, high levels of TC, TG, apoB and high blood pressure, were seen more frequently in the families with IHD than in the control families.
These data suggest that serum Lp(a), per se, is not a risk factor for IHD, and its elevated level might be a reflection of the clinical course of IHD.

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Anti-Helicobacter pylori IgA and IgG antibody titers were measured in patients with ischemic heart diseases. Sixty healthy individuals were served as control subjects, and the subjects consisted of 21 patients with acute myocardial infarction (AMI), 34 patients with old myocardial infarction (OMI), 35 patients with effort angina (AP), and 41 patients with variant angina (VSA). In the control group, the IgA and IgG antibody titers were positively correlated with age: IgA was 2.08±1.98EV in subjects aged less than 40 years and 3.41±2.24EV in subjects aged 40 years or older, and IgG was 51.65±53.60U/ml and 89.93±83.40U/ml, respectively. There were significant positive correlations between the IgA and IgG antibody titers in the control and all the patient groups (r=0.54-0.92), presumably reflecting chronic infection with the bacteria. However, CRP, an inflammation marker, did not correlate with the antibody titer. When the IgA and IgG antibody titers were compared among patient groups, IgG did not significantly differ between each patient group and the control group, showing similar titers, whereas IgA was significantly higher in the AMI (5.10±1.25EV) than in the OMI (p<0.01), AP, and control groups (p<0.05). Moreover, the positivity rate for IgA was also higher in the AMI group (90%), with an odds ratio to the control group being 2.7, whereas the rate for IgG did not significantly differ between the groups, using either 10 or 55U/ml of the cut-off value. These results suggest that an increased IgA antibody titer, which is an index of the active phase of infection, is an etiological factor for acute myocardial infarction, instead of the IgG antibody titer, which has been frequently measured.

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The association of coronary heart disease (CHD) with a slight increase in the total level of homocysteine in plasma has been reported. Therefore, we have investigated the relation between plasma homocysteine levels and the premature and progressive atherosclerosis. The study group consisted of 166 patients (82 males and 84 femals, aged 40 to 75 years) inclusive of 51 patients with vascular disease. Thirty-two randomly selected patients were examined to determine the iratherosclerosis progression grade using the TES-100 image color analysis program on CT images of abdominal aorta. The plasma homocysteine levels were measured by high-performance liquid chromatography, and other risk factors were also analyzed in the laboratory. A positive correlation between homocysteine and VCAM-1 (r=0.33, p<0.01), ICAM-1 (r=0.29, p<0.01) and atherosclerosis indices, expressed as the wall thickening and calcification rate on the lower abdominal aorta (r=0.59, p<0.001), were observed. The plasma homocystein level in the patients of the atherosclerosis group was significantly higher than that in 111 patients without the vascular diseases (17.3±9.1vs. 13.2±4.6μ mol/l p<0.0001). The plasma homocysteine level was inversely correlated with HDL-cholesterol but not with LDL-cholesterol. We suggest fror these findings the plasma homocysteine level plays an important role in vasculardiseases and atherosclerosis.

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The Sansuiken-Lipid Intervention Trial (S-LIT) was an intervention study to assess: 1) the acceptability and long-term compliance for a management program for hypercholesterolemia (serum total cholesterol concentration, TC<220mg/dl) in Japanese male workers, ≥40 years old; and 2) the relationship between serum cholesterol (TC) levels and the onset of ischemic heart disease (IHD). This interim report compared the long-term (3 years) serum lipid profile in the three cohorts; drug (simvastatin) treatment group (DT), diet-intervention group (DI), and non-treatment group (NT), which were draum from 1, 143 workers with hypercholesterolemia, patients were assigned to groups according to their own perference, not by randomization. The DT group had the highest initial levels of TC, triglyceride (TG), and low-density lipoprotein cholesterol (LDL-c) among the 3 groups. However, The DT group demonstrated the most improvement in normalizing TC (DT=34.2%, DI=7.9%, and NT=11.4%), high density lipoprotein cholesterol (HDL-c) (DT=47.6%, DI=46.3%, and NT=23.8%) and LDL-c (DT=50.0%, DI=19.3%, and NT=13.8%). While there were no differences in normalizing serum triglyceride (TG) levels. The dietary therapy (DI group) did not Show any improvement in lipid parameters in the cases with mild hyperlipidemia; with initial values of TC>250mg/dl, TG>250mg/dl, HDL-c<35mg/dl, and LDL-c>180mg/dl. These results suggest the importance of drug treatment using simvastatin for Japanese male worker with mild hyper-cholesterolemia, accordind to their lipid profiles.

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