This paper described the Guideline for Diagnosis and Management of Hyperlipidemias for Prevention of Atherosclerosis proposed by The Japan Atherosclerosis Society (JAS) Guideline Investigating Committee (1,995-2,000) under the auspices of the JAS Board of Directors. 1) The guideline defines the diagnostic criteria for serum total cholesterol (Table 1), LDL-cholesterol (Table 1), triglycerides (Table 4) and HDL-cholesterol (Table 7). It also indicates the desirable range (Table 1), the initiation levels of management (Table 2) and the target levels of treatment (Table 2) for total and LDL-cholesterol. 2) Though both total and LDL-cholesterol are shown as atherogenic parameter in the guideline, the use of LDL-cholesterol, rather than total cholesterol, is encouraged in daily medical practice and lipid-related studies, because LDL-cholesterol is more closely related to atherosclerosis. 3) Elevated triglycerides and low HDL-cholesterol are included in the risk factors, since no sufficient data have been accumulated to formulate the guideline for these two lipid disorders. 4) Emphasis is laid on evaluation of risk factors of each subject before starting any kind of treatment (Table 2). 5) This guideline is applied solely for adults (age 20-64). Lipid abnormalities in children or the youth under age 19, and the elderly with an age over 65 have to be evaluated by their own standard. 6) This part of the guideline gives only the diagnostic aspects of hyperlipidemias. The part of management and treatment will follow in the second section of the guideline that will be published in future.

SummaryPlatelet activation induced by shear forces occurring in a stenosed coronary artery is one of the mechanisms of coronary thrombosis. We evaluated the shear-induced platelet aggregation (SIPA) dynamics in patients with effort angina during treadmill exercise. SIPA was measured by a rotational cone-plate aggregometer. SIPA was markedly increased by exercise from 71.2 ± 8.9% to 81.9 ± 7.6% (p <0.01) in the patient group. Although epinephrine concentrations were elevated, its rate of increase was not correlated with that of SIPA. Yohimbine partially inhibited the exercise-induced increase in SIPA. In contrast, a significant correlation between the changing rate of plasma von Willebrand factor (vWF) larger multimers and that of SIPA (r = 0.74, p <0.05) was observed. Exercise-augmented SIPA is probably dependent on an increase in vWF larger multimers rather than platelet alpha2-receptor activation. Prevention of the interaction between vWF and its platelet receptors may play some role in decreasing the risk of coronary thrombosis during exercise.

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