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).