Impairment of early fibrinolytic activation after PTCA: a mechanism for restenosis-related clinical recurrence?

Citation
M. Capanni et al., Impairment of early fibrinolytic activation after PTCA: a mechanism for restenosis-related clinical recurrence?, FIBRINOL PR, 13(1), 1999, pp. 8-14
Citations number
30
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
FIBRINOLYSIS & PROTEOLYSIS
ISSN journal
13690191 → ACNP
Volume
13
Issue
1
Year of publication
1999
Pages
8 - 14
Database
ISI
SICI code
1369-0191(199901)13:1<8:IOEFAA>2.0.ZU;2-O
Abstract
Objective: This study was aimed to investigate the acute effect of PTCA on clotting activation and fibrinolytic system and the possible role of modifi cations of haemostasis in relation to restenosis-related clinical recurrenc e after PTCA. Setting: Istituto di Clinica Medica Generale e Cardiologia, University of F lorence, Florence, Italy. Material and methods: In 83 unselected patients (70 men and 13 women) under going PTCA, blood clotting (fibrinogen, F1+2, TAT) and fibrinolytic activat ion (D-dimer, ELT, PAI-1, t-PA) were assayed before and immediately after P TCA. Results: At the end of the procedure there was a significant decrease in pl asma levels of fibrinogen (P < 0.0001), F1+2 (P < 0.0001), TAT (P < 0.0001) , PAI-1 (P < 0.0001) and t-PA (P < 0.001), a shortening of ELT(P < 0.0001) and a significant increase in D-dimer concentration (P < 0.0005). Post-proc edural PAI-1 activity levels were significantly higher in patients with sub sequent clinical recurrence owing to restenosis than in those without (P < 0.0005); similarly, patients with restenosis showed lower t-PA levels (P < 0.0005) and longer ELT (P < 0.05) after PTCA than those without. An earlier occurrence of clinical recurrence owing to restenosis was observed in pati ents with an increase or no variation of PAI-1 levels at the end of the pro cedure. Conclusion: These results suggest that the early fibrinolytic response to b alloon injury is a relevant determinant of the risk of clinical recurrence owing to restenosis after PTCA, possibly by determining 'per se' a longer l ocal persistence of thrombus and by triggering a release of mediators invol ved in the proliferation of smooth muscle cells.