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RESEARCH PRODUCT

Platelet Function Changes In Acute Myocardial Infarction

subject

description

Whether the thrombotic component of myocardial infarction is primary or secondary in a given patient, platelet function alterations can influence many mechanism from which depends if the thrombotic lesion grows or sends platelet emboli to the smaller myocardial vessels. Recently in some cases of infarction, coronary artery spasm has been demonstrated angiographically; thromboxanes, vasoconstrictive and platelet-aggregating substances, are released by platelets during myocardial ischemia. The local release of these substances may modify the myocardial cell viability and regional blood flow.The aim of the present study was to investigate changes in platelet function in relation to the time interval after the beginning of the chest pain in 8 patients suffering from acu te myocardial infarction.The following parameters were estimated: plasmatic PF4 and BTG levels, thromboxane B2 formation by platelets stimulated with thrombin, plasmatic levels of thromboxane B2 MDA formation by platelets stimulated with thrombin, platelet sensi tivity to exogenous prostacyclin; factor XIII activity was also determined.The tests showed, in the first three days, an augmented re lease of platelet constituents together with a “platelet exhaustion”, demonstrated by a reduced formation of MDA and thromboxane B2; in the following days the platelets changed to a state of hyperactivity. The platelet sensitivity to pro stacyclin was reduced during the whole period after the onset of the acute myocardial infarction; this provides an additional mechanism involved in increased platelet aggregation.