Summary
Rationale. Reocclusion after thrombolysis diminishes the benefits of early reperfusion
after acute myocardial infarction (AMI). No clinical or laboratory variables have
been identified as predictors for reocclusion yet. Methods and results. To evaluate
hemostatic variables as potential risk determinants platelet aggregation (PA, representing
platelet activity), thrombin/antithrombin complexes (TAT, representing thrombin generation),
and plasminogen activator inhibitor type 1 (PAI-1, representing endogenous fibrinolysis)
were determined in 31 patients with AMI at 0, 1, 2, and 12 h after the start of thrombolysis
as well as at hospital discharge. Reocclusion (defined as reinfarction or angiographically
confirmed, clinically silent coronary reocclusion) occurred in 5 patients within 5-14
days and in 8 patients within 1 year. TAT plasma concentrations were lower in patients
with reocclusion than in those without (9.9 ± 5.7 vs. 22.9 ± 22.2 ng/ml at 2 h, 6.5
± 3.1 vs. 11.2 ± 6.4 ng/ml at 12 h, means ± SD, p <0.05 each). Neither concentration
nor activity of PAI-1 in plasma differed between both patient groups. However, both
slope and maximum of PA (induced by 2 μmol/l ADP) were augmented in patients with
reocclusion (slope: 39.4 ± 1.7 vs. 32.5 ± 7.4 at 2 h, p <0.001; 42.6 ± 2.6 vs. 36.6
± 8.9 at 12 h, p <0.01). Results were independent of the thrombolytic agent used (alteplase
or reteplase). A PA slope at 2 h higher than the average slope before thrombolysis
(37.2 ± 5.7) could be identified as best predictor for early (within 5-14 d, p = 0.017,
sensitivity 1.00, specificity 0.69) and late reocclusion (within 1 y, p=0.009, 0.88
and 0.74, respectively). Conclusions. Increased PA following coronary thrombolysis
appears to be associated with early and late reocclusion. This marker could be useful
in identifying patients who may benefit from more aggressive anti-platelet (such as
GP IIb/IIIa receptor antagonists), interventional, or both strategies.
