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Blood platelet activity and levels of proteinase inhibitors and proteolytic components were assessed in patients with progressive angina of effort, spontaneous angina and acute myocardial infarction. alpha 1-antitrypsin and alpha 2-macroglobulin were shown to be involved in fibrinolysis regulation and kininogenesis. In acute myocardial infarction, there was a close inverse correlation between platelet release and blood kallikrein levels.

In patients with coronary heart disease and in healthy individuals, the characteristics of platelet aggregation were compared to those of circulating immune complexes. Platelet aggregation and the level of immune complexes were found to be significantly increased as compared with healthy donors. No correlation was revealed between platelet aggregation parameters and the concentration of immune complexes in the serum treated with 3.5% polyethylene glycol. A significant reverse correlation was revealed upon comparing the results of platelet aggregation with the level of small immune complexes detectable in 7% polyethylene glycol. A mechanism is suggested by which platelet aggregation is suppressed by small immune complexes.

A study was made of the effect of burn injury on aggregation properties of the vascular wall and platelet aggregation capacity. Maximal accumulation of malonic dialdehyde during thrombin-induced aggregation, maximal rise of the spontaneous intravascular platelet aggregation index, and the most remarkable functional lesions of the vascular wall were observed in the early period (within the first hours), at the disease height (day 7), and during the recovery (day 30). Variation of the homestatic balance between the prostacycline- and thromboxane-generating systems of the blood vessels and platelets in the disease early period is linked with stress reaction and release of biologically active substances (adrenaline, cortisone) to the circulation, whereas at the disease height with marked inflammation and emergence in the blood of endotoxin and break down products of cell membrane phospholipids.

Circulating platelet morphology (using scanning electron microscopy), platelet adhesion and flattening on silicone slides (interference contrast microscopy), and spontaneous platelet aggregation were investigated. Platelet status was thus assessed in patients with acute myocardial infarction (AMI), chronic coronary disease (CCD) and normal subjects (controls). In AMI patients, the majority of circulating platelets were inactivated: 70% and more were of smooth discoid shape, a finding similar to that of the controls. On the contrary, platelet flattening, adhesion and spontaneous aggregation were changed in AMI patients, and also, though on a smaller scale, in CCD patients. Changes in platelet flattening ability were most pronounced, the latter parameter being sharply increased in 73% of AMI patients.