Platelet aggregation ratio in myocardial infarction.
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Biomedical subjects
Publications and source records attributed to T F Rohrer.
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Quantitative determinations of platelet aggregation were made by a modified version of the Wu-Hoak-method in venous blood samples from ten healthy volunteers. It was demonstrated that the extent to which aggregates are formed depends on the rate of flow in the needle and on other methodical influences as well as on the platelet count. Accordingly, no definite conclusions concerning aggregation conditions in vivo can be drawn from the results obtained with venous blood samples.
Quantitative measurements of platelet aggregation in samples of venous blood were made in altogether 66 healthy volunteers by a modified version of the method of Wu and Hoak. The formation of aggregates was found to be unaffected or at the most barely affected by such factors as sex, age, smoking, fatty food, physical exertion and medication with isoprenaline or ovulation inhibitors. No difference in the number of aggregates formed was noted between 12 control patients and 16 patients with myocardial infarcts or 14 with other conditions predisposing to arterial thrombosis. Anticoagulant therapy had no effect on aggregation. It is suspected that aggregation in vitro due to methodological factors may obscure any quantitative alterations in the formation of aggregation present in vivo.
The influence of acetylsalicylic acid (ASA) on alterations of the platelets resulting from physical exertion was studied in 10 healthy volunteers. Before and 2 h after the administration of placebo or 1 g ASA, venous blood samples were taken for platelet counts, thrombelastography (TEG) and tests of ADP- and epinephrine-induced platelet aggregation. The blood in which the 2-h values were determined was sampled at the highest work-load during sub-maximum exercise on a bicycle ergometer (5 min each at 50, 100 and 150 watts). ASA had no effect on the alterations of the platelets due to physical effort: the increase in the first phase of epinephrine-induced aggregation, the elevation of the platelet count and the hypercoagulability demonstrable by TEG still persisted after the administration of ASA. Some effects were noted, however, that are also observed after the administration of ASA at rest: the second phase of epinephrine-induced aggregation was suppressed and disaggregation after induction with ADP was accelerated.
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