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New antiaggregative and antianginal effects of an oral antiarrhythmic drug, lidocaine, are reported. Platelet hemostasis was investigated in 55 patients, with platelet function and morphology examined prior to and seven days after the onset of the lidocaine treatment. A significant decrease was noted in platelet aggregation with the dose of 2.5 (2.3-2.7) mg lidocaine per 1 kg of body weight taken four times daily at least. As the dosage increased, the drug antiaggregative properties were enhanced accordingly. Large doses, however, were associated with side-effects. The reported dose produced a nearly two-fold reduction in platelet aggregation rate, and anginal attacks were arrested in 80% of the patients, whereas platelet morphology was not affected.

In 78 patients with ischaemic heart disease prior to and after treatment with obsidan the authors examined relationship between the indices of activity of the sympatho-adrenal and renin systems. A correlation analysis was made between the data adrenalin excretion, noradrenalin, dopamine and DOPA in the urine and renin activity in the blood. After obsidan treatment the excretion of adrenaline and renin activity in blood plasma diminish. After obsidan treatment different links of activity of the sympato-adrenal system function more conjointly. Change in the activity of one of the links produces corresponding changes in the activity of the others. Dependence of renin activity is shown to exist on the activity of the sympatho-adrenal system after treatment as compared to their levels prior to treatment . The initial background recorded prior to treatment influences significantly the final result of treatment. A negative correlation exists between the activity of the sympatho-adrenal system and renin which is regarded as evidence of protective compensatory reaction of the body. It is suggested that the increase of noradrenalin secretion, causing rise of the blood pressure is associated with the compensatory decrease of renin activity.

Willebrand's factor is plasma protein involved in the processes of thrombo- and atherogenesis. Influencing the initial stages of platelet activation it may play a role in the pathogenesis of coronary heart disease (CHD). The content of Willebrand's factor was measured in 52 healthy subjects of different age and in 63 patients with CHD. Of these, 42 patients presented with acute myocardial infarction and 21 with angina pectoris. Use was made of a quantitative method based on ristomycin aggregation of formalin-fixed platelets from healthy subjects in the presence of Willebrand's factor of the test plasma. In angina pectoris patients, the highest content was detected if the disease took a graver course. In acute myocardial infarction, the content of Willebrand's factor was noted, in part of cases, to be high since the first hours of disease. In one of the cases the high content of the factor foretold the disease development. Myocardial infarction itself brought about another elevation of the factor content in plasma.