UNCORRECTED PROOF
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The Role of Platelets in ST-Segment
Elevation Myocardial Infarction
We read with great interest the report
of Ly et al
1
on the relation of platelet
counts with presentation and clinical
outcomes in patients with ST-elevation
myocardial infarction (STEMI) on the
basis of the combined data of several
Thrombolysis In Myocardial Infarction
trials. Such large set of data (10,793
patients) enabled the investigators to
find eventually that the higher platelet
counts were associated with higher rates
of adverse clinical outcomes at 30 days.
We may assume that this observation
was possible mainly because of this
large cohort of patients. In clinical prac-
tice, other platelet indexes seem to offer
prognostic value much more useful in
smaller patient groups and are possibly
more attractive from a pathophysiologic
point of view. One of these is mean
platelet volume (MPV), routinely and
automatically measured at many cen-
ters, including ours. It has been shown
that platelets, especially activated plate-
lets (which are larger and denser), play
an important role in the pathogenesis of
the no-reflow phenomenon during the
occlusion and reperfusion period of
myocardial infarction.
2
Platelets’ size,
expressed as MPV, is correlated with
their reactivity.
3
Higher MPVs charac-
terize patients with myocardial infarction
and unstable angina compared with
those with stable angina or noncardiac
chest pain, and elevated MPV has been
recognized as an independent risk factor
for myocardial infarction and stroke.
4–7
In addition, elevated MPV is associated
with poor clinical outcomes in survivors
of myocardial infarctions.
8,9
In 1 of our
studies, MPV was a strong and indepen-
dent predictor of impaired angiographic
reperfusion and 6-month mortality in
patients with STEMI treated with pri-
mary angioplasty, when blood samples
for MPV estimation were obtained on
admission in 398 consecutive patients.
No predictive value was recognized for
admission platelet count in that study.
10
Therefore, if possible, it would be of
special interest to look at MPV values
in the combined data of several Throm-
bolysis In Myocardial Infarction trials.
It would be interesting to compare the
prognostic value of MPV and platelet
counts reported by Ly et al
1
in patients
with STEMI.
We also wish to comment on the
investigators’ discussion of the second
conclusion of their study, namely, the
observation that a greater decrease in
follow-up platelet counts (relative to
baseline values) was independently as-
sociated with an increased risk for rein-
farction at 30 days. Ly et al
1
suggested
a “smoldering autoimmune process
similar to that leading to heparin-in-
duced thrombytopenia” or “activation
of the coagulation cascade” as the pos-
sible mechanism. We agree that the
mechanism could be explained by sev-
eral hypotheses and is probably multi-
factorial. However, we believe that the
mechanism of platelet count decrease
could instead be compared with dissem-
inated intravascular coagulation syn-
drome. Disseminated intravascular co-
agulation is defined as a disorder of
diffuse activation of the clotting cas-
cade that results in the depletion of clot-
ting factors in the blood, whereas a
platelet count decrease observed about
3 days after STEMI admission could be
referred to as an episode of platelet hy-
peractivation resulting in the depletion
of platelets in the blood. In our study of
398 STEMI patients,
10
there was a
weak, although significant, negative
correlation between MPV and platelet
count. A slight, but significant, positive
correlation was also observed between
MPV and leukocyte count. It has been
reported that larger MPVs may corre-
spond to the increased numbers of
platelet–leukocyte and platelet–platelet
aggregates.
11
The correlations between
MPV and platelet count as well as be-
tween MPV and leukocyte count ob-
served in our study support this hypoth-
esis. Following such argumentation, the
increased number of platelet–leukocyte
and platelet–platelet aggregates could
be another mechanism responsible for
the platelet count decreases observed by
Ly et al
1
2.69 1.2 days after admis-
sion for STEMI.
Zenon Huczek
Krzysztof J. Filipiak
Grzegorz Opolski
Warsaw, Poland
9 August 2006
1. Ly HQ, Kirtane AJ, Murphy SA, Buros J,
Cannon CP, Braunwald E, Gibson CM, TIMI
Study Group. Association of platelet counts
on presentation and clinical outcomes in ST-
elevation myocardial infarction (from TIMI
trials). Am J Cardiol 2006;98:1–5.
2. Rezkalla SH, Kloner RA. No-reflow phenom-
enon. Circulation 2002;105:656 – 662.
3. Van der Loo B, Martin JF. A role for changes
in platelet production in the cause of acute
coronary syndromes. Arterioscler Thromb Vasc
Biol 1999;19:672– 679.
4. Cameron HP, Ibbotson RM, Carson PHM.
Platelet size in myocardial infarction. BMJ
1983;287:449 – 451.
5. Pizzuli L, Yang A, Martin JF, Luderitz B.
Changes in platelet size and count in unstable
angina compared to stable or non-cardiac
chest pain. Eur Heart J 1998;19:80 – 84.
6. Endler G, Klimesch A, Sunder-Plassmann H,
Schillinger M, Exner M, Mannhalter C, Jor-
danova N, Christ G, Thalhammer R, Huber
K, Sunder-Plassmann R. Mean platelet vol-
ume is an independent risk factor for myo-
cardial infarction but not for coronary artery
disease. Br J Haematol 2002;117:399 – 404.
7. Bath P, Algert C, Chapman N, Neal B,
PROGRESS Collaborative Group. Associa-
tion of mean platelet volume with risk of
stroke among 3134 individuals with history
of cerebrovascular disease. Stroke 2004;35:
622– 626.
8. Martin J, Bath PM, Burr ML. Increased plate-
let size following myocardial infarction is
associated with subsequent death and nonfa-
tal reinfarction. Lancet 1991;338:1409 –1411.
9. Pabon Osuna P, Nieto Ballesteros F,
Morinigo Munoz JL, Sanchez Fernandez PL,
Arribas Jimenez A, Diego Dominguez M,
Martin Luengo C. The effect of mean platelet
volume on the short-term prognosis of acute
myocardial infarction. Rev Esp Cardiol 1998;
51:816 – 822.
10. Huczek Z, Kochman J, Filipiak KJ, Horszc-
zaruk GJ, Grabowski M, Piatkowski R, Wil-
czynska J, Zielinski A, Meier B, Opolski G.
Mean platelet volume on admission predicts
impaired reperfusion and long-term mortality
in acute myocardial infarction treated with
primary percutaneous coronary intervention.
J Am Coll Cardiol 2005;46:284 –290.
11. Tsiara S, Elisaf M, Jagroop IA, Mikhailidis
DP. Platelets as predictors of vascular risk: is
there a practical index of platelet activity?
Clin Appl Thromb Hemost 2003;9:177–190.
doi:10.1016/j.amjcard.2006.08.008
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