Circulation. 2000;101:e95
(Circulation. 2000;101:e95.)
© 2000 American Heart Association, Inc.
Circulation Electronic Pages |
Chlamydia pneumoniae in Coronary Artery Disease
Enrique Gurfinkel, MD, PhD;
Gerardo Bozovich, MD;
Branco Mautner, MD
Coronary Care Unit,
Favaloro Foundation,
Buenos Aires, Argentina
 |
Introduction
|
|---|
To the Editor:
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 that the beneficial effect was sustained until 90 days.
Beyond this point, the P value is no longer statistically
significant. The potential reasons were presented in March 1998
(at the meeting of the American College of Cardiology)
and published elsewhere.5
Finally, the authors speculate in their conclusion that the ACADEMIC
trial tested C pneumoniae as an additional risk factor. The
authors should clarify how a marker of chronic infection may be
regarded as a risk factor, in light of the sample size, the clinical
event rates estimated, the serology cutoff point at 1:16, and the
immunological basis of this and other infective
hypotheses.6
 |
References
|
|---|
-
Anderson JL, Muhlestein JB, Carlquist J, Allen A,
Trehan S, Nielson C, Hall S, Brady J, Egger M, Horne B, Lim T.
Randomized secondary prevention trial of azithromycin in patients with
coronary artery disease and serological evidence for
Chlamydia pneumoniae infection: the Azithromycin in
Coronary Artery Disease: Elimination of Myocardial Infection
with Chlamydia (ACADEMIC) Study. Circulation. 1999;99:15401547.[Abstract/Free Full Text]
-
Gupta S, Leatham EW, Carrington D, Mendall MA, Kaski
JC, Camm AJ. Elevated Chlamydia pneumoniae antibodies,
cardiovascular events and azithromycin in male
survivors of myocardial infarction. Circulation. 1997;96:404407.[Abstract/Free Full Text]
-
Grayston JT. Antibiotic treatment trials for secondary
prevention of coronary artery disease events.
Circulation. 1999;99:15381539.[Free Full Text]
-
Gurfinkel E, Bozovich G, Daroca A, Beck E, Mautner B.
Randomised trial of roxithromycin in non-Q-wave coronary
syndromes: ROXIS Pilot Study: ROXIS Study Group. Lancet. 1997;350:404407.[Medline]
[Order article via Infotrieve]
-
Gurfinkel E, Bozovich G, Livellara S, Testa E, Beck E,
Mautner B. Antibiotic effects on unstable angina: the final report of
the ROXIS trial. Eur Heart J. 1999;20:121127.[Abstract/Free Full Text]
-
Buchmaier K, Neu N, de la Mata LM, Pal S, Hessel A,
Penninger JM. Chlamydia infections and heart disease linked
through antigenic mimicry. Science. 1999;2838:13351339.