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Acute myocardial infarction (MI) is the leading cause of death worldwide. It has been widely accepted that it is due to the insufficient blood supply to the cardiac tissue.
Early revascularization with primary percutaneous coronary intervention (pPCI) after acute ST elevation myocardial infarction (STEMI) is associated with high success rates for Thrombolysis in Myocardial Infarction (TIMI) flow attainment and improved prognosis.
However, successful reopening of epicardial coronary artery does not always mean optimal myocardial reperfusion in a sizeable portion of patients, mostly because of no-reflow phenomenon.
No-reflow is defined as inadequate myocardial perfusion after temporary occlusion of an epicardial coronary artery without evidence of persistent mechanical obstruction, thus implying ongoing myocardial ischaemia.
Angiographic no-reflow is defined as less than TIMI 3 flow or TIMI 3 flow with MBG 0 or 1 without angiographic evidence of mechanical vessel obstruction. No-reflow occurs in >30% of patients after thrombolysis or mechanical intervention for acute myocardial infarction and in 0.6% to 2% of elective PCI.
The cornerstones of the ‘no reflow’ phenomenon are myocyte swelling, endothelial cell swelling with luminal protrusions, and intravascular red blood cell aggregates. Later findings included presence of capillary leukocyte plugging and to a lesser extent, platelet and fibrin accumulation. Myocardial damage always precedes the microvascular abnormalities in the presence of total coronary occlusion not caused by a coronary thrombus and not vice versa.
No reflow is a multifactorial phenomenon and five mechanisms have been recognized: (A) pre-existing microvascular dysfunction, (B) distal micro-thrombo-embolization, (C) ischemic injury, (D) reperfusion injury and (E) individual susceptibility. All these factors are inter-related in a complex manner.
Recently, clinical research has focused on the predictive effects of blood cell-related biomarkers on admission and their usefulness in modifying the clinical approach of no-reflow phenomenon in patients with acute myocardial infarction (AMI). Recent investigations have suggested that monocytes, CRP, albumin & HDL may be involved in the pathogenesis of coronary artery disease. Here, we aimed to investigate the relationship between on admission monocyte count, HDL, CRP and albumin and post-intervention no-reflow in patients receiving primary PCI because it would be valuable to be able to predict which factors are associated with no-reflow in AMI patients.
The aim of our study was to depict the relationship between admission eGFR, Monocyte/HDL index, CRP/Albumin index in patients presenting with acute STEMI and angiographic no-reflow after primary PCI.
Results for age, gender, hypertension and diabetes mellitus didn’t show any statistical significance of value between the no-reflow and reflow group.
However, CRP [median (IQR) of 75.08 ± 19.59 in the no-reflow group vs 75.56 ± 15.57 in the reflow group with a value P < 0.001], albumin [median ± SD was 3.58 ± 0.38 g/dL vs 4.00 ± 0.35 g/dL, P < 0.001], monocytes [2.44 ± 0.71 10^3/uL vs 0.38 ± 0.16 10^3/uL, P < 0.001], CAR [median (IQR) of 7.17 (5.58 - 16.18) for the no-reflow and 1.62 (1.46 - 2) in the reflow group, P < 0.001] and MHI [median ± SD of 0.07 ± 0.03 vs 0.01 ± 0.01, P < 0.001] all showed positive correlations with the occurrence of no-reflow.
According to our multivariate analysis, CAR had the best predictive value for no-reflow, Odds ratio: 0.182, P < 0.001. It was also suggested the best cut-off value over which risk of no-reflow was high is >3.26 for CAR with AUC = 0.974, making it the most useful laboratory parameter for the prediction of no-reflow in STEMI patients undergoing primary PCI.
In summary, our study concluded that the CAR withdrawn before primary percutaneous coronary intervention had the best clinical value for risk stratification for the occurrence of no-reflow in STEMI patients.