Neutrophil Percentage/Albumin Ratio as an Independent Predictor of the No-Reflow Phenomenon in Patients with ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

TL;DR

This study shows that a blood marker called NPAR can predict poor heart reperfusion in patients with heart attacks undergoing a specific treatment.

Contribution

The study identifies NPAR as a novel independent predictor of the no-reflow phenomenon in STEMI patients undergoing pPCI.

Findings

NPAR was significantly higher in patients with the no-reflow phenomenon compared to those without.

Multivariate analysis confirmed NPAR as an independent predictor of the no-reflow phenomenon.

A cutoff value of 18.45 for NPAR predicted the no-reflow phenomenon with high sensitivity and specificity.

Abstract

Objectives: Despite achieving a high rate of revascularization in epicardial coronary arteries with primary percutaneous coronary intervention (pPCI), suboptimal coronary reperfusion is encountered in more than half of patients. This condition, termed the ‘no-reflow phenomenon’ (NRP), has been associated with ventricular arrhythmias, left ventricular dysfunction, impaired ventricular remodeling, myocardial reinfarction, and increased mortality. The neutrophil percentage/albumin ratio (NPAR) has been associated with the severity and prognosis of cardiovascular patients. The aim of this study is to investigate the relationship between NRP and NPAR in patients undergoing pPCI with a diagnosis of ST-elevation myocardial infarction (STEMI). Methods: A total of 758 patients diagnosed with STEMI and undergoing pPCI were included in this study. A total of 105 patients were detected to have NFP during pPCI (13.8%). Slow flow, such as thrombolysis in myocardial infarction (TIMI) 0, 1, or 2, observed in the distal part of the coronary artery after pPCI, was operationally defined as NRP. Reflow was defined as TIMI 3. NPAR was obtained by dividing the neutrophil percentage by albumin. Results: Statistically, there was a significant difference between the groups in terms of mean age, body mass index (BMI), and left ventricular ejection fraction (LVEF), which were higher in the NRP group [54 (45–62) vs. 60 (53–67), 26.5 (23.6–30.8) vs. 28.4 (26–31), and 39.2 ± 6.9 vs. 31.8 ± 5.1; p < 0.001, for all]. When laboratory parameters were examined between the two groups, white blood cell (WBC) count, neutrophil count, neutrophil percentage, C-reactive protein (CRP), neutrophil/lymphocyte ratio (NLR), NPAR and CRP/albumin ratio (CAR) levels were found to be statistically significantly higher in the patient group with NRP (p < 0.05). Multivariate analysis identified NPAR as an independent predictor of NRP (5.482, 3.254–9.234, p < 0.001). ROC analysis demonstrated that the best cutoff value of 18.45 for NPAR was to predict NRP with 80% sensitivity and 75% specificity (area under ROC curve = 0.826 (95% CI: 0.770–0.881), p < 0.001). Conclusions: We found that NPAR levels at admission were independently associated with the development of NRP pPCI in patients with STEMI.

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