CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 5, September/October 2016
AFRICA
305
In our study, although LV function in the anterior MI group
was significantly worse than that in the posterior/inferior MI
group, only adrenomedullin level in the plasma and levels of
IL-6 and IL-1
β
in pericardial fluid in the anterior MI group
were significantly higher than those in the posterior/inferior MI
group. Reviewing these findings, one may consider that there
was a weak correlation between enhanced cytokine levels and
depressed LV function. We believe these findings suggest that
cytokine levels in the pericardial fluid may be superior to plasma
levels as a molecular marker of LV dysfunction in the setting of
MI. In addition, the number of patients included in our study
may have been insufficient to observe a statistically significant
difference in the levels of cytokines between the MI groups.
Limitations
Our study was subject to certain limitations. First, we did not
measure the extent of infarcted myocardial tissue by means of
myocardial perfusion imaging techniques. Since the magnitude
of MI may affect cytokine levels, one may consider that
changes in cytokine levels may be partly attributed to the area
of non-contractile myocardial tissue. However, we believe that
a detailed assessment of LV function by echocardiography is
sufficient to clarify the effect of MI on contractile myocardial
tissue of the left ventricle. In addition, the aim of this study was
to examine the relationship between MI site, cytokine levels and
LV function. Therefore the relationship between the magnitude
of MI and cytokine levels was beyond the scope of this study.
Second, in our study, the elapsed time between MI and
CABG was three weeks or longer. This interval may be sufficient
for an increase in certain cytokines, such as adrenomedullin
and angiotensin-II, but too long for other cytokines, such
as IL-6 or IL-1
β
, to remain high in the systemic circulation.
The time points at which cytokines peak and the intervals in
which cytokines remain high in the plasma differ. As Tashiro
et al
.
35
stated, concentrations of monocyte-related cytokines
dynamically change during the course of acute MI, suggesting
that they may contribute to the inflammatory and subsequent
proliferative responses in acute MI. Therefore levels in the
pericardial fluid appear to be more reliable and superior to levels
in the plasma as a molecular marker in the early stages of MI
and LV dysfunction.
Third, the absence of a control group in our study is
another limitation but pericardial fluid samples are obtained by
pericardiocentesis or during cardiac surgery. Therefore obtaining
pericardial fluid samples from healthy individuals was not
possible, for ethical reasons.
Conclusions
We found that (1) patients with anterior MI had worse LV
function than both patients with no previous MI and those with
posterior/inferior MI, and (2) the levels of pro-inflammatory
cytokines in plasma and pericardial fluid in patients with anterior
MI were increased compared to patients with no previous MI.
The finding of elevated pro-inflammatory cytokine levels in
patients with anterior MI could be interpreted as reflecting both
the magnitude of MI and/or LV dysfunction and the site of MI.
Our results also suggest that cytokine levels in pericardial
fluid were superior to plasma levels as a molecular marker of
LV dysfunction in the setting of MI. However, further clinical
studies with larger patient numbers are required to clarify the
prognostic or biomarker role of cytokines in pericardial fluid
related to LV dysfunction or remodelling after acute MI.
The abstract of this study was presented in 57th International Congress of
the European Society for Cardiovascular Surgery, Barcelona, Spain, 24–27
April 2008.
The study was financially supported by the Department of Scientific
Research Projects, Suleyman Demirel University (project no: 1389-M-06).
None of the authors has financial or other relationships that would influence
assessment of the data or that would constitute a conflict of interest.
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