Key result
Acute myocardial infarction was associated with a higher de-aggregatory effect of PGI2 and rate of spontaneous platelet aggregation compared to patient controls (p<0.01).
Why the study?
Does the de-aggregatory effect of PGI2 and rate of spontaneous platelet aggregation differ in whole blood of males with acute MI compared to patient controls?
Case-Control (n=42)
Does the de-aggregatory effect of PGI2 and rate of spontaneous platelet aggregation differ in whole blood of males with acute MI compared to patient controls?
p-value: p=<0.01
The increased rate of spontaneous platelet aggregation and formation of PGI2-sensitive platelet aggregates in vitro in whole blood of MI patients appear secondary to myocardial necrosis.
May reflect necrosis-driven platelet changes in acute MI; hypothesis-generating for PGI2 response as biomarker, pending prospective validation.
The de-aggregatory effect of prostacyclin (PGI2) and the rate of spontaneous platelet aggregation (SPA) were studied in vitro in whole blood of 24 males with acute myocardial infarction (MI) and 18 males, patient controls (PC). The de-aggregatory effect of PGI2 and the rate of SPA (measured as a percentage of changes in free platelet number in whole blood) were higher (p less than 0.01) in MI than PC. The de-aggregatory effect of PGI2 in whole blood was higher (p less than 0.05) on the first day of MI than on day 14 following MI. The highest de-aggregatory effect of PGI2 was found in whole blood of patients with MI complicated by ventricular fibrillation. In neither of the groups did the de-aggregatory effect of PGI2 correlate with patients' age, haematocrit, erythrocyte and leucocyte counts, triglycerides, HDL, LDL or total cholesterol levels. In the MI group, de-aggregatory effect of PGI2 was correlated with free platelet concentration (r = -0.59, p less than 0.05), elevation of glutamic oxalacetic transaminase (r = 0.53, p less than 0.05) and creatinine phosphokinase (r = 0.69, p less than 0.001). The de-aggregatory effect of PGI2 in blood of patients with evolving MI did not differ from that in PC. It is concluded that the increased rate of SPA and formation of PGI2-sensitive platelet aggregates in vitro in whole blood of MI patients are secondary to myocardial necrosis.
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Spławińska et al. (1987) conducted a case-control in Acute myocardial infarction (n=42). Acute myocardial infarction vs. Patient controls was evaluated on De-aggregatory effect of PGI2 and the rate of spontaneous platelet aggregation (SPA) (p=<0.01). Acute myocardial infarction was associated with a higher de-aggregatory effect of PGI2 and rate of spontaneous platelet aggregation compared to patient controls (p<0.01).
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