Safety and efficacy of low-dose unfractionated heparin during percutaneous coronary revascularisation and the relationship between activated clotting time and haemorrhagic or ischaemic complications: our results.

OBJECTIVE: An inverse relation between the degree of heparin anticoagulation and the subsequent risk of postprocedural thrombotic complications was observed in the era of conventional balloon angioplasty, but the optimal dose of heparin during percutaneous coronary intervention (PCI) using newer interventional equipment and glycoprotein IIb/IIIa receptor inhibition has not been clearly defined. Previous studies did not assess the increased risk of adverse cardiac events with an activated clotting time of <200 s using strategies of routine stent placement and glycoprotein IIb/IIIa receptor inhibition. We hypothesised that the efficacy and safety of PCI would be maintained, if not improved, especially when performed in conjunction with glycoprotein IIb/IIIa receptor inhibitors (abciximab, tirofiban or eptifibatide as a bolus plus infusion for 12-18 h) and oral antiplatelet therapy (clopidogrel 75 mg plus aspirin 325 mg/day) associated with low doses (5000-10 000 U) of unfractionated heparin using a target activated clotting time of </=200 s during PCI. In this way, the sheath could be immediately removed at the end of the procedure.

METHODS: We evaluated the outcome at 30 days and at one year of 2552 consecutive patients who underwent PCI and stenting; most of them were treated with PCI and selective administration of glycoprotein IIb/IIIa inhibitors in high-risk cases (61%).

RESULTS: By design, the activated clotting time was 184 +/- 39 s. The incidence of access site complications and of in-hospital major adverse cardiac events during the first 48 h following PCI was 3.7% and 3.3%, respectively. The incidence of major adverse cardiac events was 4.5% at 30 days and 7.6% at one year.

CONCLUSIONS: This study shows the safety and efficacy of this therapeutic strategy in the era of frequent stent implantation and aggressive intravenous and oral platelet inhibition. Additional research is warranted to determine whether these results can be extrapolated routinely to patients with acute myocardial infarction or undergoing PCI without stent implantation.