Summary
In order to define some of the determinants of successful thrombolysis and reocclusion
during fibrinolytic therapy for acute myocardial infarction (AMI), specific molecular
markers of fibrin metabolism were serially measured in 15 patients with AMI treated
with tissue-type plasminogen activator (t-PA). Fibrin formation was assessed by measurement
of fibrinopeptide A (FpA) and fibrinolysis by assay of B-P peptides 1—42 and 15—42
and crosslinked fibrin degradation products (XDP). At baseline, FpA levels were high
while markers of fibrinolysis were near normal. Following a 90-minute infusion of
t-PA (0.5—1.1 mg kg−1 hr−1), all markers of fibrinolysis increased. Levels of FpA remained elevated despite
heparin at the initiation of cardiac catheterization. None of these markers discriminated
between patients with successful reperfusion from those without. At 4 hours, B-β 15—42
peptide and XDP levels remained elevated suggesting persistence of fibrinolysis beyond
the short circulatory half-life of t-PA. FpA levels at 4 hours were lower in patients
who underwent acute coronary angioplasty compared to those who received additional
low dose t-PA (12.3 ± 4.5 vs. 30.4 ± 5.5 ng/ ml, p <0.05). By 48 hours, markers of
fibrinolysis had returned toward normal except in 2 patients with persistently elevated
B-P 15—42 peptide levels who suffered reocclusion on days 5 and 6 (75 and 44 vs. 29
± 3 nM, p <0.005). In conclusion, molecular markers of fibrin metabolism during fibrinolytic
therapy may provide clinically relevant data.
Keywords
Fibrinolytic therapy - Tissue - type plasminogen activator - Acute myocardial infarction
- Plasminogen activator inhibitor - Percutaneous transluminal coronary angioplasty
- Fibrin metabolism
