951-69 Serial Angioscopic Assessment of Coronary Stent Lining with Antiplatelet or Anticoagulant Therapy

Abstract

The most effective pharmacologic regimen to inhibit subacute coronary stent thrombosis has yet to be defined with certainty. To assess the effects of different antithrombotic therapies on thrombus deposition and early tissue reaction in stented coronary arteries we performed serial angioscopy in 20 consecutive pts who received Palmaz-Schatz coronary stent. Pts were randomized in a 3:1 ratio to receive either ticlopidine (250 mg t.i.d.1 and aspirin (325 mg day) (Group 1, 15 pts) or continuous i.v. heparin (titrated to APTI of 60–100 seconds) combined with aspirin (325 mg day) and dipyridamole 175 mg t.i.d.1 (Group 2, 5 pts), until the day 7th. Long term treatment was only with ticlopidine and aspirin. Coronary angioscopy was performed pre stenting, immediately post implant (Imm), on day 7th (Wk) and 2 months later (Mth). All indications for stenting were included; 7 pts (35%) had multiple stents placed. High pressure low compliant balloons were chosen for complete stent expansion. Angioscopic images were categorised unaware of therapeutic treatment. Appearance Covering pattern Thrombus shiny dim full absent smooth rough patchy covered red Group 1 1 mm 15 - – 15 – – – – n = 15 1 Wk 6 9 – 4 3 3 5 1 2 Mth 2 3 10 – 12 2 1 – Group 2 1 mm 5 – – 5 – – – – n = 5 lWk 3 2 – 3 1 1 – – 2 Mth – 1 4 – 5 – – – No pts suffered subacute stent thrombosis. The angioscopic features of covering reactions in stented coronary arteries are time dependent and not completely similar in the two tested antithrombotic regimens. 1) Coverage was absent or very thin and focally distributed on day 7th. 2) Completion of the neointimallining was obtained in 2 months in the majority of patients. 3) Early intense patchy red reaction was only seen in the antiplatelet treated group. 4) Thrombus deposition was rare, without evidence of occlusive thrombus. Ticlopidin + aspirin may promote an early angioscopic tissue reaction similar but not equal to that induced by standard anticoagulation.