Lipid status and apolipoprotein E phenotypes were tested in 1000 patients who underwent coronary angiography. The same number of factory employees was chosen as a control group. We distinguished between six different apolipoprotein E phenotypes and determined their frequencies in all groups. For the three homozygous phenotypes E3/3, E4/4, and E2/2, the percentage distribution in the group of factory employees was 62.7%, 2.3%, and 0.8%, respectively; for the three heterozygous phenotypes E4/3, E3/2, and E4/2, we determined frequencies of 20.3%, 11.0%, and 3.0%, respectively. In the group of patients with and without signs of coronary atherosclerosis, we observed almost the same frequencies except that heterozygotes (E3/2) occurred significantly more frequently in the group of coronary angiography patients unaffected by coronary sclerosis. Cholesterol and triglyceride values were significantly elevated in patients with coronary artery disease, whereas high density lipoprotein cholesterol levels were not significantly different. The data further suggest that apolipoprotein E2/2 homozygosity, despite the presence of B-very low density lipoproteins in the plasma of these patients, cannot be considered a biochemical indicator of an increased risk of coronary atherosclerosis. On the other hand, apolipoprotein E3/2 heterozygosity may have a protective effect on the development of early atherosclerosis. (Arteriosclerosis 3:310-315, July/August 1983)

SUMMARY The etiology of cerebrovascular disease (CVD) in young patients is difficult to establish if the common causes of a focal neurological deficit are excluded by appropriate investigations. Since in some observations prolapse of the mitral-valve (MVP), alterations of platelet function, or both have been linked with cerebral ischemic events, we studied the in vivo platelet release reaction and the incidence of MVP in 47 patients (12 males, 35 females) under 45 years of age with TIA or stroke of unknown cause and in an ageand sex-matched control group. The mean plasma beta-thromboglobulin (/3-TG) level of the patients (mean = 54.9 ± 31.4 ng/ml) was significantly higher than that of the controls (mean = 20.6 ± 6.9 ng/ml, p < 0.001). MVP was demonstrated in 13 of 47 patients in contrast to 4 of the controls (p < 0.01). However, the 0-TG levels of patients with MVP (n = 13,52.9 ± 25.5 ng/ml) did not differ from those of patients without MVP (n = 34, 55.7 ± 33.7 ng/ml) significantly (p < 0.4). Our results confirm that the incidence of MVP is higher in young patients with cerebral ischemia of unknown cause than in asymptomatic controls. The significantly elevated plasma /3-TG concentrations in the patient's group indicate an increased platelet activity in vivo. Since there was no significant difference between /3-TG levels of patients with and without MVP, the mitral-valve abnormality can not be the cause for the altered platelet activity.Stroke, Vol 13, No 4, 1982

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A randomly chosen population in the area of Westphalia (West Germany) was screened for apolipoprotein A-I mutants. About 5000 individuals were investigated and compared with a group of 1300 patients who had undergone coronary angiography. Four electrophoretically different apolipoprotein A-Imutants (named Münster-1 to 4) were discovered. Five non-related probands were observed in the group of the unselected patients and three non-related probands in the group of coronary angiography patients. In most cases the familial nature of the abnormality was confirmed by pedigree analysis.