(Circulation. 2007;116:e390.)
© 2007 American Heart Association, Inc.
Correspondence |
University of Geneva, Geneva, Switzerland
Groupe Hospitalier Bichat-Claude-Bernard, Paris, France
Cardiovascular Center, OLV Hospital, Aalst, Belgium
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
We are grateful for the thorough comments by Agostoni et al and Kereiakes et al, which give us the opportunity to clarify our position. As Agostoni et al point out, important limitations exist in the measurements of luminal dimensions that may be magnified when the change in those dimensions are assessed by measurement of late loss (LL). Furthermore, there is variation in absolute quantitative coronary angiography (QCA) values according to core laboratories, which makes comparison of QCA data problematic.1 Regardless of these facts, QCA of lumen dimensions has long been the backbone of clinical studies in the field of restenosis.2 It has now become crucial to go beyond luminal measurements and to focus on both events that matter to the patient and their pathogenesis. For the patient, the clinical consequences of late stent thrombosis often are nonfatal myocardial infarction and death.3 Recently, late stent thrombosis and its consequences have become more the topic of committees dealing with the redefinition of end points and readjudication of events. Efforts by the Academic Research Consortium have indeed led to the introduction of new definitions and hence new analyses of pooled data by selected investigators and/or clinical research organizations. Although these efforts are valuable, they should not obscure the fact that the entire data set remains largely underpowered, so a robust answer to the raised concerns is simply not available yet. In addition, these efforts should not distract from necessary attempts to understand the biology of these late side effects, which seem to be
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