Association of platelet to lymphocyte ratio with in-hospital major adverse cardiovascular events and the severity of coronary artery disease assessed by the Gensini score in patients with acute myocardial infarction

BACKGROUND: The platelet to lymphocyte ratio (PLR) has recently emerged as a potential inflammatory biomarker and has been shown to be significantly associated with atherosclerotic coronary artery disease (CAD). Therefore, we aimed to explore the association of PLR with in-hospital major adverse cardiovascular events (MACEs) and the severity of CAD assessed by the Gensini score (GS) in patients with acute myocardial infarction (AMI) undergoing coronary angiography. METHODS: A total of 502 patients with AMI consecutively treated at the Affiliated Hospital of Qingdao University (Qingdao, China) and underwent coronary angiography from August 2017 to December 2018 were recruited in this study. The demographic, clinical, angiographic characteristics, and laboratory parameters were collected. According to the presence of in-hospital MACEs, the included patients were divided into the MACE group (n = 81) and the non-MACE group (n = 421). Further, according to tertiles of the GS, the patients were classified into three groups: the low GS group (GS ≤ 32 points, n = 173), medium GS group (32 points < GS ≤ 60 points, n = 169), and high GS group (60 points < GS ≤ 180 points, n = 160). The main statistical methods included Chi-squared test, non-parametric Mann-Whitney U test, Kruskal-Wallis H test, logistic regression, and receiver operating characteristic curves. RESULTS: The PLR in the MACE group was significantly higher than that in the non-MACE group (179.43 [132.84, 239.74] vs. 116.11 [87.98, 145.45], Z = –8.109, P < 0.001). Further, there were significant differences in PLR among the tertiles of GS (110.05 [84.57, 139.06] vs. 119.78 [98.44, 157.98] vs. 140.00 [102.27, 191.83], H = 19.524, P < 0.001). PLR was demonstrated to be an independent risk factor of in-hospital MACEs (odds ratio [OR]: 1.012, 95% confidential interval [CI]: 1.006–1.018, P < 0.001) and severe CAD assessed by the GS (OR: 1.004, 95% CI: 1.002–1.009, P = 0.042). The cutoff value of PLR for predicting the development of in-hospital MACEs was 151.28 with a sensitivity of 66.7% and a specificity of 78.1% (area under the curve [AUC]: 0.786, 95% CI: 0.730–0.842, P < 0.001), and a PLR of 139.31 was also identified to be an effective cutoff point for detecting a high GS (>60 points) with a sensitivity of 49.4% and a specificity of 69.6% (AUC: 0.611, 95% CI: 0.556–0.666, P < 0.001). CONCLUSIONS: PLR as a novel inflammatory marker is significantly and independently associated with the occurrence of in-hospital MACEs and the severity of CAD assessed by the GS in patients with AMI. As an easily available and inexpensive inflammatory indicator, PLR could be widely used as an efficient inflammatory biomarker for identifying high-risk patients and for individualizing targeted therapy to improve the prognosis of AMI.