[Analysis of the mechanisms of thrombosis after implantation of drug-eluting stents].

OBJECTIVE

Stent thrombosis has been regarded as a severe complication of PCI therapy, therefore, analyzing the causes of thrombosis after implantation of drug-eluting stents (DES) is necessary.

METHODS

This is a single center study with no limitation of entry criteria for using DES in patients with coronary heart disease (CHD). From Dec. 2001 to Dec. 2005, 3345 consecutive patients underwent implantation with Cypher stents (eluted with sirolimus: 2165 patients, 2362 lesions, 2695 stents) or TAXUS stents (eluted with paclitaxel: 1180 patients, 1453 lesions, 1725 stents) in our hospital. 10-month follow-up was completed in 2296 patients (1455 patients with 1632 lesions using 1773 Cypher stents & 841 patients with 1032 lesions used 1182 TAXUS stents). All patients were treated with aspirin plus clopidogrel at least 9 months after PCI procedure.

RESULTS

Among 3345 patients, 9 patients had acute stent thrombosis (0.27%): 7 in the sirolimus group, 2 in the paclitaxel group (0.32% vs 0.17%, P = 0.637), 7 patients had subacute stent thrombosis (0.21%): 5 in the sirolimus group and 2 in the paclitaxel group (0.23% vs 0.17%, P = 0.526) and 13 patients had late stent thrombosis (0.57%): 5 in the sirolimus group and 8 in the paclitaxel group (0.34% vs 0.95%, P = 0.114) Among the 29 patients with DES thrombosis. 8 patients (26.7%) presented as sudden death, 13 nonfatal MI and 8 unstable angina. Stent thrombosis was demonstrated by angiography in 21 patients (72.4%). The causes of acute and subacute DES thrombosis were related to suboptimal stenting in 8 patients including 7 patients with bifurcation lesions or to uncovered injury segment of the diffuse lesions in five patients. The causes for late thrombosis were discontinuation of antiplatelet drugs in four cases and related to poor left ventricular function in 6 cases with history of old myocardial infarction.

CONCLUSIONS

Our study showed that suboptimal stenting, especially for bifurcation lesions and uncovered injury segment of diffuse lesions were the main causes of acute and subacute stent thrombosis. Left ventricular disfunction and premature discontinuation of antiplatelet therapy were the main reasons of late thrombosis.