• Kardiol Pol · Jan 2016

    Association of monocyte count on admission with angiographic no-reflow after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction.

    • Zuoyan Wang, Lihui Ren, Na Liu, Licheng Lei, Huiming Ye, and Jianjun Peng.
    • Department of Cardiology, Beijing Shijitan Hospital, Capital Medical University.. pjj0630@163.com.
    • Kardiol Pol. 2016 Jan 1; 74 (10): 1160-1166.

    BackgroundThe no-reflow phenomenon during primary percutaneous coronary intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI) can lead to poor outcomes. It has been shown that the monocytes may be involved in the pathogenesis of coronary artery disease and associated with high risk of myocardial infarction.AimTo assess the relation between admission monocyte count and angiographic no-reflow after pPCI.MethodsA total of 236 patients with acute STEMI, who underwent pPCI, were enrolled. The patients were divided into two groups (no-reflow and normal reflow) based on post-pPCI Thrombolysis in Myocardial Infarction (TIMI) flow grade. No reflow was defined as TIMI flow grades ≤ 2, and normal reflow was defined as TIMI 3 flow grade. The monocyte count and other laboratory parameters were measured on admission before pPCI.ResultsThere were 43 (18.2%) patients in the no-reflow group and 193 (81.8%) patients in the normal-reflow group. Patients with no-reflow had significantly higher admission monocyte count (0.76 ± 0.48 × 109/L vs. 0.55 ± 0.29 × 109/L, p = 0.004). Also, white blood cell and neutrophil counts were significantly higher while haemoglobin was significantly lower in the no-reflow group. In multivariate analysis, monocyte count remained an independent predictor of angiographic no-reflow phenomenon (odds ratio [OR] 2.665, 95% confidence interwal [CI] 1.102-6.445, p = 0.030) together with low haemoglobin concentration (OR 0.978, 95% CI 0.961-0.995, p = 0.013).ConclusionsMonocyte count on admission and low haemoglobin concentration were independent clinical predictors of no-reflow following pPCI in patients with STEMI. Our findings suggest that admission monocyte count may be available for early risk stratification of no-reflow after pPCI and might allow the improvement of strategies to prevent this phenomenon.

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