BackgroundPrimary percutaneous coronary intervention (PCI) has improved outcomes greatly in patients with ST-elevation myocardial acute infarction (STEMI). However, the no-reflow phenomenon significantly reduces its efficacy.Material/MethodsIn this study, we investigated the value of combining plasma D-dimer level on admission and pre-infarction angina (PIA) in predicting no-reflow phenomenon in STEMI patients after primary PCI. A total of 926 STEMI patients who underwent primary PCI were included.ResultsThe average age was 52.6 years, 617 (66.6%) of them had experienced a PIA, and 435 (47.9%) showed no-reflow phenomenon after primary PCI. Both PIA and plasma D-dimer on admission were independent predictors of no-reflow, with a risk of 0.516 (95% CI: 0.380 to 0.701) and 2.563 (95% CI: 1.910 to 3.439), respectively. Plasma D-dimer level had an area under curve (AUC) of 0.604 (95% CI: 0.568~0.641) in predicting no-reflow phenomenon, and PIA had an AUC of 0.574 (95% CI: 0.537 to 0.611). Importantly, the new signature combining D-dimer level on admission and PIA showed an increased AUC (0.637, 95%CI: 0.601 to 0.673) in predicting the no-reflow phenomenon. Moreover, the patients with high D-dimer level on admission but without PIA had significantly increased ratio of no-reflow phenomenon and in-hospital mortality compared to the other patients (P<0.001 and P=0.041, respectively).ConclusionsBased on these solid results, we conclude that combining plasma D-dimer level on admission and PIA might create a good signature for use in predicting the no-reflow phenomenon after primary PCI in STEMI patients.

Thrombotic disease is a serious threat to human health.

BACKGROUND Reversal of antiplatelet therapy is desirable in patients presenting with life‐threatening bleeding or requiring urgent surgery. This study aimed to examine ticagrelor reversal using donor platelets and to explore the effects of residual ticagrelor on donor platelets. STUDY DESIGN AND METHODS In Cohort 1, 16 healthy subjects were treated with ticagrelor 90 mg twice daily alone or in combination with aspirin 100 mg once daily for 7 days followed by single blood sampling for preparation of platelet‐rich plasma. An additional 16 healthy subjects served as controls. In Cohort 2, 16 healthy subjects were treated with ticagrelor 90 mg twice daily or clopidogrel 75 mg once daily for 7 days followed by serial blood samplings for preparation of platelet‐poor plasma (PPP). An additional 16 healthy subjects served as controls. RESULTS In Cohort 1, inhibition of adenosine diphosphate–induced platelet aggregation (PLADP) by ticagrelor could not be fully reversed by mixing with up to 90% control platelets, whereas inhibition of arachidonic acid–induced platelet aggregation by aspirin was fully reversed with the addition of 60% control platelets. In Cohort 2, 10% PPP obtained from ticagrelor‐treated subjects reduced PLADP from 74% to 40% at 2 hours, 72% to 58% at 6 hours, and 73% to 59% at 10 hours, while 10% or 20% PPP obtained from clopidogrel‐treated subjects did not inhibit PLADP. CONCLUSION The antiplatelet effect of ticagrelor cannot be fully reversed by donor platelets, which could be explained by the presence of active drug. The effect of residual drug on donor platelets appears to be evident for at least 10 hours after ticagrelor ingestion.