Dap. Figal et al., Subacute stent thrombosis in a nonselected population using antiplatelet therapy: Frequency and predictors, REV ESP CAR, 53(6), 2000, pp. 791-796
Introduction. After coronary stenting, the incidence of subacute stent thro
mbosis have been reduced to 0% using aspirin and ticlopidine, in studies wi
th selected populations and intracoronary ultrasounds.
Objective. To evaluate the incidence and predictors of subacute stent throm
bosis in a nonselected population, using antithrombotic therapy.
Methods. We studied 285 stents, consecutively and successfully implanted in
268 lesions of 226 patients. We used high pressure balloon inflation witho
ut intracoronary ultrasound. Post-stenting protocol included aspirin and ti
clopidine during four weeks with no anticoagulation. We defined subacute st
ent thrombosis as death, acute myocardial infarction myocardial infarction
or angiographic occlusion of stent, with TIMI flow 0-1, after the first 24
hours and during the first month.
Results. Four patients presented events (1.7%): Three nonfatal myocardial i
nfarction after discharge, with documented angiographic thrombosis of stent
, and one death due to in-hospital myocardial infarction. All three non-fat
al AMI, occurred in vessels less than 3 mm (p = 0.07) and in patients takin
g aspirin without ticlopidine (p < 0.001). After discharge, three (17%) of
18 patients with inadvertent discontinuation of ticlopidine presented subac
ute stent thrombosis, in contrast to none of 25 patients taking ticlopidine
without aspirin. Excluded patients with discontinuation of ticlopidine, th
e incidence of subacute stent thrombosis was 0.5%.
Conclusion. After intracoronary stenting in a nonselected population, using
antithrombotic treatment with aspirin and ticlopidine, we may expect a rat
e of subacute stent thrombosis about 1%. Ticlopidine seems to have the main
role in preventing subacute stent thrombosis, above all in predisposing ci
rcumstances as small vessels.