Discussion
To the best of our knowledge, this is the first study evaluating the
relationship between the ratio of CAR with patency of IRA in patients
with STEMI before the p-PCI. It revealed that CAR might be related to
the IRA patency before p-PCI (p<0.001).
p-PCI is the gold standard treatment method in patients with STEMI.
However, the duration of infarction is the most important factor
affecting the clinical results of the patients11. In
the HORIZON-AMI study, early IRA patency in patients with STEMI
undergoing primary PCI is associated with better TIMI flow and
myocardial blush post PCI and is an independent predictor of lower
one-year mortality12. Christopoulos C et al.
associated the IRA patency in patients with STEMI with increased
endogenous thrombolysis, decreased platelet activity, and resulting
decreased ischemia time13. Shortness of ischemia
duration, decreased complications such as heart failure due to
infarction, malignant arrhythmia, cardiogenic shock, mortality, and high
procedure success in patients with STEMI2. Our study,
in accordance with other studies, with statistical significance in the
TIMI 0-1 group compared to the TIMI 2-3 group; There was a decrease in
eGFR and left ventricular EF, and an increase in heart rate, which was
associated with poor cardiovascular results (Table 1).
Inflammation plays an important role in determining both pathogenesis
and prognosis in STEMI14,15. Management of the
occurring systemic inflammatory process affects the prognosis of the
disease16. Macrophage activation, free radical release
and proinflammatory cytokines secreted from inflammatory cells increase
in acute myocardial infarction17. Inflammation in
STEMI causes an increase not only in the responsible plaque region but
also in all systemic circulation and other plaques18.
Besides, thrombus load in IRA creates microvascular plugs and causes
no-reflow to increase the ischemic process and thus increases myocardial
inflammation. As a result, an increase in inflammatory cells is seen in
STEMI as an indicator of plaque inflammation as well as myocardial
tissue destruction in the coronary arteries19. In the
study by Pietila et al., it was found that the height of inflammatory
markers showed the amount of destroyed myocardial tissue in patients who
could not achieve IRA patency by giving
thrombolytics20,21. In our study, consistent with
previous studies, a decrease in the inflammatory marker albumin level
and an increase in the number of neutrophils, C-reactive protein and
lymphocytes were found (Table 1). Data investigating the relationship of
IRA patency in patients with STEMI is limited. Doganay B. et al., who
investigated IRA patency in patients with STEMI, have found a
significant relationship between the co-peptit level and the
IRA22, while Jing L. et al., however, found a
significant relationship between the homocysteine level and
IRA23. CAR, an inflammatory marker, reflects the
stability of albumin and CRP levels within the body. Few studies have
reported the relationship between ACS and CAR. In studies performed,
high CAR elevation was associated with poor prognosis in patients with
STEMI and stable angina pectoris24,25. In a study
investigating the relationship between short-term majorĀ adverseĀ cardiac
events (MACE) and CAR, which included 652 ACS patients, it was seen that
increased CAR increased the likelihood of developing
MACE26. Another study has revealed that CAR could
predict no-reflow in patients with ST-elevation myocardial
infarction27. In our study, the value of CAR was found
to be statistically higher in patients without IRA patency in patient
with STEMI (Table 1).
In patients with STEMI, the IRA patency, which is well known for its
effects on major cardiac side effects and mortality, results in a
decreased duration of ischemia and necrotic area, and associated
inflammation in the ischemic area28,29. However, this
effect in the IRA patency is limited with the thrombus load. Because the
increased thrombus load in the IRA patency will disrupt coronary
perfusion after p-PCI with microvascular obstruction. Insufficient
perfusion will lead to increased ischemic area and associated
inflammation. Considering that using the parameters reflecting the
inflammatory process in patients with ACS in determining thrombus load
in the IRA patency will be useful for determining the prognosis of the
patients, the relationship between IRA patency and CAR was investigated
in patients with STEMI, and the rate of CAR was found to be
significantly higher in patients with TIMI 0-1 flow in IRA
(p<0.001).