(Circulation. 2000;101:e95.)
© 2000 American Heart Association, Inc.
Circulation Electronic Pages |
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, the methodological approach used deserves comment. First, the investigators based the sample size and the clinical event rates 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 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 its 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 trial, stating that we randomized patients with a poor
characterization. At the present time, the only study conducted in
uniformly unstable patients is ROXIS, in which we clearly defined the
entry criteria to select a standard population with acute
coronary events, as shown in the original
article.4 In the final report of the study,5
we showed
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