Relationship of plasminogen activator inhibitor-1 levels following thrombolytic therapy with rt-PA as compared to streptokinase and patency of infarct related coronary artery
F. Paganelli et al., Relationship of plasminogen activator inhibitor-1 levels following thrombolytic therapy with rt-PA as compared to streptokinase and patency of infarct related coronary artery, THROMB HAEM, 82(1), 1999, pp. 104-108
Background Type 1 plasminogen activator inhibitor (PAI-1) is considered to
be risk factor for acute myocardial infarction (AMI). A rebound of circulat
ing PAI-1 has been reported after rt-PA administration. We investigated the
relationships between PAI-1 levels before and after thrombolytic therapy w
ith streptokinase (SK) as compared to rt-PA and the patency of infarct-rela
ted arteries. Methods and Results: Fifty five consecutive patients with acu
te MI were randomized to streptokinase or rt-PA. The plasma PAI-1 levels we
re studied before and serially within 24 h after thrombolytic administratio
n. Vessel patency was assessed by an angiogram at 5 +/- 1 days. The PAI-1 l
evels increased significantly with both rt-PA and SK as shown by the levels
obtained from a control group of 10 patients treated with coronary angiopl
asty alone. However, the area under the PAI-1 curve was significantly highe
r with SK than with rt-PA (p < 0.01) and the plasma PAI-1 levels peaked lat
er with SK than with rt-PA (18 h versus 3 h respectively). Conversely to PA
I-1 levels on admission, the PAI-1 levels after thrombolysis were related t
o vessel patency. Plasma PAI-1 levels 6 and 18 h after SK therapy and the a
rea under the PAI-1 curve were significantly higher in patients with occlud
ed arteries (p < 0.002, p < 0.04 and p < 0.05 respectively). The same tende
ncy was observed in the t-PA group without reaching significance. Conclusio
ns: This study showed that the PAI-1 level increase is more pronounced afte
r SK treatment than after t-PA treatment. There is a relationship between i
ncreased PAI-1 levels after thrombolytic therapy and poor patency. Therapeu
tic approaches aimed at quenching PAI-1 activity after thrombolysis might b
e of interest to improve the efficacy of thrombolytic therapy for acute myo
cardial infarction.