Investigation of the effect of platelet function evaluated in patients with ST-elevation myocardial infarction on six-month mortality and morbidity

Introduction and objective: STEMI remains the most common cause of death in the hospital setting despite developments in commencement of treatment before admission to the hospital, quicker onset of treatment and compherensive treatment guidelines. In this study, we examined the effects of reperfusion strategy, different loading doses of clopidogrel and adjuvant treatment on platelet aggregation. Method: Fiftyeight patients between the ages of 18-80 that were admitted to Ege University School of Medicine, Cardiology Clinic from April 2015 to July 2016 with the diagnosis of STEMI were included in the study. Blood samples were drawn on 2nd 4th and 24th hours after the onset of antiplatelet treatment and platelet function was studied using Multiplate analyzer. Subjects were allocated to two groups according to their 4" hour residual platelet aggregation measurements with a cutoff value of 47U, higher levels suggesting a higher risk of thrombosis.Subjects with 4* hour platelet aggregation measurements higher than 47U formed group A (n:28) while the remaining subjects formed group B (n: 30). It was shown that the most common reason for high platelet reactivity was the administration of morphine, therefore subgroup analyses were carried out for presence of morphine treatment. The effects of high platelet reactivity, morphine administration and reperfusion strategy on the clinical end points were assessed. Results: In this study, we found that subjects with higher 4th hour platelet aggregation measurements were those that had received 300 mg clopidogrel loading in addition to fibrinolytic therapy and also received morphine for prolonged pain (p:0.003, p:0.036, p<0.001). In hospital events were found to increase 6.637 times in patients that received fibrinolytic therapy compared to those who did not [OR (%95 GA): 6.637 (1.391, 31.658), p:0.018]. This result implies the insufficiency of medical reperfusion instead of primary PCI. When we examine the standalone effect of morphine on platelet aggregation, there is a correlation with higher residual platelet aggregation in 2nd and 4t* hours but this correlation decreases in 24th hour, which suggests that morphine delays the action of clopidogrel (p<0.001, p: 0.070). Morphine administration was found to correlate with increased morbidity in the first month (p:0.03) but did not show a direct correlation with increased morbidity. Higher platelet reactivity did not correlate significantly with the clinical end points. Conclusion: Our findings imply that medical reperfusion strategy is insufficient and morphine administration delays the action of clopidogrel. This delay was not found to be clinically significant, however there was an increase in hospital admissions for chest pain and the need for revascularization in this patient group. There is need for longer term follow-up results.