Evaluation of profilin 1 as a biomarker in myocardial infarction.

OBJECTIVE: Profilin 1 (Pfn1) is likely to be involved in atherogenesis and myocardial infarction (MI). Clinical data on this subject are very limited. The aim of this study was to search for associations between serum Pfn1 and a number of parameters in MI patients: symptom onset to PCI time (OPT), myocardial necrosis markers, thrombolysis in myocardial infarction (TIMI) flow, antiplatelet drugs, heparin administration and typical atherosclerosis risk factors. PATIENTS AND METHODS: We included patients with type 1 MI (according to the Third Universal Definition of Myocardial Infarction) who were able to precisely determine the time of symptom onset. Exclusion criteria involved conditions potentially altering platelet function. We screened 114 patients and included 65. We assessed serum Pfn1 in three time points: on admission (Pfn1_0), 24 hours post PCI (Pfn1_24) and 48 hours post PCI (Pfn1_48) and correlated it with OPT, cardiac necrosis markers (troponin T, CK, CKMB), TIMI flow in the infarct-related artery, pre-hospital P2Y12-antagonist and heparin administration and known atherosclerosis risk factors. RESULTS: Patients with a shorter OPT had higher Pfn1_0 (838.5 vs. 687.1 pg/ml, p=0.007). Patients with impaired coronary flow post PCI had lower Pfn1_24 (748.2 vs. 925.2 pg/ml, p=0.017) and Pfn1_48 (744.5 vs. 879.8, p=0.031. Pfn1_24 and Pfn1_48 were lower in patients who received a P2Y12 antagonist prior to hospital admission. Diabetic patients presented with lower Pfn1_0 concentrations. CONCLUSIONS: This is the first study assessing Pfn1 in type 1 MI patients in relation to the chosen parameters. Pfn1 may be a biochemical tool to objectify information on OPT in MI patients. We found an association between Pfn1 and post-PCI TIMI flow, antiplatelet drug administration and diabetes mellitus.

Reduced plasma fibrin clot permeability and susceptibility to lysis are associated with increased risk of postthrombotic syndrome.

BACKGROUND: The postthrombotic syndrome (PTS) is a severe complication of deep vein thrombosis (DVT). Reduced plasma clot permeability and lysability have been linked to DVT and residual vein obstruction. OBJECTIVES We investigated whether altered fibrin clot properties are associated with the occurrence of PTS. PATIENTS AND METHODS: Plasma fibrin clot permeability (Ks ) and lysability were investigated in a cohort of 197 consecutive patients aged 18 to 65 years recruited 3 months following the first-ever DVT. Patients with severe thrombophilia or comorbidities known to adversely affect clot phenotype were ineligible. RESULTS: During a 1-year follow-up PTS developed in 48 (24%) patients, who were characterized by lower Ks , prolonged fibrin clot lysis time (CLT) and slower release of D-dimer from clots (D-Drate ), together with higher plasma D-dimer, C-reactive protein and thrombin-activatable fibrinolysis inhibitor (TAFI). No PTS-associated differences in fibrinogen, thrombin generation, factor VIII, other fibrinolysis proteins and the quality of anticoagulation were observed. Ks (r = -0.71), CLT (r = 0.45), D-Drate (r = -0.30) and TAFI activity (r = 0.38) were associated with the Villalta scale (all P < 0.05). Recurrent VTE occurred also more commonly in PTS patients during follow-up and the 26 (13.2%) patients had lower Ks , longer CLT and lower D-Drate (all P < 0.05). A multivariate model adjusted for age, body mass index, fibrinogen and glucose showed that independent predictors of PTS were idiopathic DVT, plasma D-dimer, Ks , D-Drate , tissue plasminogen activator and TAFI activity. CONCLUSIONS: This study demonstrates that formation of more compact fibrin clots displaying impaired susceptibility to lysis predisposes to PTS.