Background & Objective: A pro-thrombotic state may contribute to on-going vascular occlusion in AMI, but there are few evidences that hemostatic measurements can influence on TIMI flow following primary PCI in STEMI patients.
Methods: We prospectively enrolled STEMI patients who underwent primary PCI (n = 334) and assessed TIMI flow grade post-PCI. Before angiography, laboratory measurements including biochemical and hemostatic parameters were performed. Hemostatic components were evaluated with VerifyNow and thromboelastography (TEG®). Slow coronary flow was defined as a final TIMI flow grade < 3 post-PCI. A major adverse cardiovascular event (MACE) was a composite of cardiovascular death, myocardial infarction, revascularization, and heart failure during the follow-up of 19.0 ± 11.8 months.
Results: The thirty-seven patients (11.1%) showed slow flow after PPCI. Before procedure, platelet reactivity was not different between the groups (p = 0.218), but “Platelet-Fibrin Clot Strength” (TEG®-MAthrombin: maximal amplitude stimulated by thrombin) was higher in the slow- vs. normal-flow group (71.1 ± 4.9 vs. 67.4 ± 8.3 mm; p = 0.010). Prevalence of slow flow was increased proportionally according to TEG®-MAthrombin quartile (3.7% vs. 9.5% vs. 15.3% vs. 15.6%; p for trend = 0.044). In multivariate analysis, the TEG®-MAthrombin (> 66.4 mm) was an independent predictor for slow flow occurrence post-PCI (OR: 4.150; 95% CI: 1.477 to 11.665; p = 0.007) (Table). MACE occurred more frequently in the slow-flow group compared with the normal-flow group (24.7% vs. 11.7%, p = 0.048).
Conclusion: This study is the first analysis to show the close relationship between pre-procedural “Platelet-Fibrin Clot Strength” and coronary flow post-PCI in STEMI patients, which may implicate clinical benefit of optimal anticoagulant therapy on coronary flow recovery following PCI.