Impaired fibrinolysis determines the outcome of percutaneus transluminal coronary angioplasty (PTCA)

Citation
Gg. Fornitz et al., Impaired fibrinolysis determines the outcome of percutaneus transluminal coronary angioplasty (PTCA), EUR J CL IN, 31(7), 2001, pp. 586-592
Citations number
30
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Journal title
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
ISSN journal
00142972 → ACNP
Volume
31
Issue
7
Year of publication
2001
Pages
586 - 592
Database
ISI
SICI code
0014-2972(200107)31:7<586:IFDTOO>2.0.ZU;2-A
Abstract
Background Coronary artery stenosis lesions dilated by percutaneus translum inal coronary angioplasty (PTCA) show a disappointingly frequent recurrence of stenosis. We have investigated the possible role of fibrinolysis and va rious platelet-release factors - specifically in the locality of the affect ed vessel - by following 19 patients for 6 months after PTCA. Methods PTCA was performed on 19 patients with a significant primary corona ry stenosis, proven by quantitative CAAS analysis. Blood for measurement of local fibrinolysis and platelet activity was drawn from the aortic root an d the coronary sinus, at three times: just before PTCA, 10 min after it, an d 6 months later. Results The incidence of restenosis at the 6 months follow-up was 37%. PTCA almost doubled the platelet-derived growth factor level (PDGF) in coronary sinus blood in all patients. The seven restenosis patients had a substanti ally higher tissue plasminogen activator inhibitor antigen (PAI-1(ag)) leve l in the aortic root before PTCA than the 12 who remained stenosis-free (me an 62.4 +/- 31.6 ng mL (-1) compared with 33.1 + 25.3; P < 0.04) and a lowe r tissue plasminogen activator activity (t-PA(ac)) level (mean 0.32 +/- 0.1 9 IU mL(-1) compared with 0.68 +/- 0.34; P < 0.03). This was corroborated b y the levels of tissue plasminogen activator inhibitor activity (PAI-1(ac)) . At reassessment after 6 months, the restenosis patients had developed, in coronary sinus blood, a large rise of PAI-1(ac) (7.7 +/- 4.8 IU mL(-1) ris ing to 15.7 +/- 13.9, P < 0.04) and a large rise of of PAI-1(ag) (48.8 +/- 31.3 ng mL(-1) vs. 72.4 +/- 47.2; P < 0.03). But no such increase occurred in the patients who remained stenosis-free. Conclusion Our results indicate that the minor balloon injury, which is ins eparable from PCTA, stimulates the local release of PDGF. We suggest that, in those patients whose fibrinolytic activity is inherently low, this rise of PDGF could be a major causative factor in restenosis. We also discuss th e possibility that the preoperative level of PAI-1(ac) could provide a limi ted but useful prediction of the outcome of PTCA.