title: Subacute stent thrombosis in the era of intravascular ultrasound-guided coronary stenting without anticoagulation: frequency, predictors and clinical outcome.
abstract: OBJECTIVE
  This study was performed to determine predictors of subacute stent thrombosis (SST) in the era of intravascular ultrasound (IVUS)-guided coronary stenting without anticoagulation.
  
  
  BACKGROUND
  The incidence of stent thrombosis has declined with the application of high pressure stent deployment with only antiplatelet therapy. However, no data are available on predictors of stent thrombosis in this era.
  
  
  METHODS
  Between March 30, 1993 and July 31, 1995, 1,042 consecutive patients underwent coronary stenting without anticoagulation. For this analysis, we excluded patients who underwent coronary artery bypass surgery, died or had acute stent thrombosis within the 1st 24 h after stenting (41 patients). A total of 1,001 patients (1,334 lesions) were included; 982 patients (1,315 lesions) without SST and 19 patients (19 lesions) with SST.
  
  
  RESULTS
  The rate of SST was 1.9% (per patient). There was no difference between the SST and No SST groups in rescue stenting (12% vs. 13.5%, p = 1.0) or mean +/- SD reference diameter (3.11 +/- 0.58 vs. 3.19 +/- 0.53 mm, p = 0.54). A preexisting thrombus was present in 12% of the SST group and in 4.5% of the No SST group (p = 0.19). Predictors of SST by univariate analysis were low ejection fraction (p = 0.004), more stents per lesion (p = 0.049), use of combination of different stents (p = 0.012), smaller balloon size (p = 0.012) and suboptimal result in terms of smaller lumen dimensions by angiography (p = 0.016) and IVUS (p = 0.004), residual dissections (p = 0.027) and slow flow (p = 0.0001). In stepwise logistic regression analysis, ejection fraction (p = 0.019), use of a combination of different stents (p = 0.013) and postprocedure dissections (p = 0.014) and slow flow (p = 0.0001) were predictive of SST.
  
  
  CONCLUSIONS
  In the present era of stent implantation, factors that may predispose to SST are low ejection fraction, intraprocedural complications leading to utilization of more stents, particularly with different stent designs, and suboptimal final result in terms of smaller lumen dimensions and persistent slow flow and dissections.
authors.affiliation: Lenox Hill Hospital, New York, New York, USA.
authors.forename: I
authors.initials: I
authors.lastname: Moussa
authors.forename: C
authors.initials: C
authors.lastname: Di Mario
authors.forename: B
authors.initials: B
authors.lastname: Reimers
authors.forename: T
authors.initials: T
authors.lastname: Akiyama
authors.forename: J
authors.initials: J
authors.lastname: Tobis
authors.forename: A
authors.initials: A
authors.lastname: Colombo
mesh_terms: D000925:Anticoagulants / Q000627:therapeutic use*; D001241:Aspirin / Q000627:therapeutic use; D016022:Case-Control Studies; D015984:Causality; D017023:Coronary Angiography; D003327:Coronary Disease / Q000628:therapy*; D003328:Coronary Thrombosis / Q000175:diagnosis / Q000188:drug therapy / Q000453:epidemiology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D015994:Incidence; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D012189:Retrospective Studies; D015607:Stents; D013988:Ticlopidine / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
chemical_list: D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D013988:Ticlopidine; D001241:Aspirin