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Volume 153, Issue 1, Pages 66.e1-66.e8 (January 2007)


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Antiplatelet therapy and progression of coronary artery disease: a placebo-controlled trial with angiographic and clinical follow-up after myocardial infarction

Hendrik-Jan Dieker, MDa, John K. French, MB, ChB, PhD, FACCbcCorresponding Author Informationemail address, Irene C. Joziasse, MDa, Marc A. Brouwer, MD, PhDa, John Elliott, MB, ChB, PhDd, Teena M. West, BScb, Bruce J. Webber, MH Scb, Freek W.A. Verheugt, MD, PhD, FACCa, Harvey D. White, MB, ChB, DSc, FACCb

Received 16 February 2006; accepted 8 October 2006.

Introduction

In patients after ST-elevation myocardial infarction (STEMI), antiplatelet therapy reduces subsequent cardiac events, which are often attributed to recurrent thrombosis with (sub)total occlusion in the infarct-related artery. Whether antiplatelet therapy influences the often subclinical process of coronary disease progression in noninfarct arteries has not been reported.

Methods

Quantitative coronary angiography of noninfarct arteries was performed on paired cine-angiograms of 149 patients from fibrinolytic trials who had a patent infarct-related artery 3 to 4 weeks following STEMI and who were randomized to either continue the daily combination of 50-mg aspirin and 400-mg dipyridamole or to matching placebo. Follow-up angiography was scheduled at 1 year.

Results

On a per-patient basis, the change in minimal luminal diameter (MLD) was 0.00 mm in the aspirin/dipyridamole group (n = 76) and was 0.01 mm in the placebo group (n = 73). There was no difference between these groups in the changes in MLD (−0.02 mm; 95% CI −0.09 to 0.05), neither were there significant differences in mean luminal diameter and diameter stenosis. Progression (1 segment/patient with ≥0.40 mm decrease in MLD) was seen in two thirds of patients and did not independently predict long-term death and/or reinfarction.

Conclusion

In this placebo-controlled trial after STEMI, the combination of aspirin and dipyridamole did not affect noninfarct artery disease progression. Progression did not predict long-term clinical outcome.

a Department of Cardiology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

b Department of Cardiology, Green Lane Cardiovascular Research Unit, Green Lane Cardiovascular Service Auckland City Hospital, Auckland, New Zealand

c Department of Cardiology, Liverpool Hospital, Sydney, Australia

d Department of Medicine, Christchurch School of Medicine, Christchurch Hospital, Christchurch, New Zealand

Corresponding Author InformationReprint requests: John K. French, MB, ChB, PhD, FACC, Cardiology Department, Liverpool Hospital, Locked Bag 7103, Liverpool BC1871 NSW, Australia.

 None of the authors have any conflict of interest in connection with this work.

PII: S0002-8703(06)00894-5

doi:10.1016/j.ahj.2006.10.006


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