(Circulation. 2000;102:e110-a.)
© 2000 American Heart Association, Inc.
Correspondence |
Acute Platelet Inhibition With Abciximab Does Not Reduce In-Stent Restenosis
BHF Cardiovascular Medicine Unit NHLI at Hammersmith Hospital, Imperial College School of Medicine, Du Cane Road, London W12 0NN, England, i.malik@ic.ac.uk
Department of Cardiothoracic Surgery, National Heart and Lung Institute, Imperial College of Science, Technology, and Medicine, Hammersmith Hospital, London, England
To The Editor:
Restenosis after coronary stenting may be initiated by thrombus formation followed by inflammation and smooth muscle cell infiltration.1 The Evaluation of ReoPro and Stenting to Eliminate Restenosis (ERASER) Investigators evaluate this hypothesis by using abciximab (ReoPro) to reduce thrombus formation after stent implantation and, thus, possibly reduce restenosis.2 However, 3 confounding factors must be clarified.
First, it has become standard practice to give powerful antiplatelet agents, such as ticlopidine and clopidogrel, to patients after stent insertion to reduce acute thrombosis rates.3 These agents act to prevent the ADP-mediated propagation of platelet activation. Platelet activation causes the release of mediators such as platelet-derived growth factor, which encourage smooth muscle proliferation (a major contributor to intimal hyperplasia). Abciximab, acting via the glycoprotein IIb/IIIa receptor, reduces platelet aggregation; it reduces activation by binding to the fibrinogen receptor. It is not necessarily true that the use of one therapy removes the need for the other. Leaving ticlopidine use to the discretion of the operator may have introduced a bias in the results, because operators might have been reluctant to use the 2 agents together. This may have had an effect on restenosis rates.
Second, infarct-related arteries have higher restenosis rates than others after percutaneous coronary transluminal angioplasty.4 Excluding patients with an infarct <3 days before randomisation may not have reduced this bias. Was there a difference in the number of patients randomized to each arm within 6 weeks of myocardial infarction? Were the results different for patients in this subgroup versus those who had a "cold" procedure?
Finally, the number of stents per lesion are mentioned descriptively as being equal between groups; however, the results presented are for the groups as a whole. Multiple stenting is associated with higher restenosis rates.5 The higher rate of multiple stents in one of the abciximab groups, although not significant, may have skewed the data against abciximab. Did a difference exist between the placebo and abciximab arms after excluding all multiple stenting procedures?
References
1. Schwartz RS, Edwards WD, Huber KC, et al. Coronary restenosis: prospects for solution and new perspectives from a porcine model. Mayo Clin Proc. 1993;68:54–62.
2.
The ERASER Investigators. Acute platelet
inhibition with abciximab does not reduce In-stent restenosis.
Circulation. 1999;100:799–806.
3.
Moussa I, Oetgen M, Roubin G, et al. Effectiveness of
clopidogrel and aspirin versus ticlopidine and aspirin in preventing
stent thrombosis after coronary stent implantation.
Circulation. 1999;99:2364–2366.
4.
Bauters C, Khanoyan P, McFadden EP, et al.
Restenosis after delayed coronary angioplasty of the
culprit vessel in patients with a recent myocardial infarction treated
by thrombolysis. Circulation. 1995;91:1410–1418.
5. Kastrati A, Elezi S, Dirschinger J, et al. Influence of lesion length on restenosis after coronary stent placement. Am J Cardiol. 1999;83:1617–1622.[Medline] [Order article via Infotrieve]
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