(Circulation. 2000;101:e118.)
© 2000 American Heart Association, Inc.
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Coronary Care Unit, Favaloro Foundation, Buenos Aires, Argentina
| Introduction |
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In a recent issue of Circulation, Anderson et al1 reported the 6-month results of the ACADEMIC trial. In this interesting study, the authors intended to answer the question whether Chlamydia pneumoniae plays a critical role in coronary artery disease, in order to justify antibiotic therapy.
Beyond the final results of this work, it seems to us that the methodological approach used deserves some comment. First, the investigators based the sample size and the clinical event rate estimates on prior data from a small study that used the same compound.2 For this purpose, the authors did not include unstable or subacute cases but rather included only stable coronary patients. Similarly, the British study selected postmyocardial infarction patients in the quiescent phase, thus making the present study statistically underpowered, as stated in the editorial comment by Dr Grayston.3
Second, the authors analyzed some particular and common markers
of inflammation, because infection increases their plasmatic levels.
These markers decreased at 6 months but interestingly not at 3 months.
It is hard to explain why these markers were practically neutral at 90
days, when 39 patients experienced new clinical infections over the
3-month treatment period. Furthermore, the authors compared their study
with our ROXIS (Roxithromycin Ischemic Syndromes) trial,
stating that we randomized patients with a poor characterization. At
the present time, the only study conducted in uniformly unstable
patients is the ROXIS, in which we clearly defined the entry criteria
to select a standard population with acute coronary events, as
shown
Department of Medicine, Division of Cardiology, University of Utah, LDS Hospital, Salt Lake City, Utah
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