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
Acute myocardial infarction (AMI) is a critical manifestation of coronary artery disease (CAD), primarily caused by the rupture of atherosclerotic plaques or thrombosis, leading to acute occlusion of coronary arteries and subsequent myocardial cell necrosis. Despite advancements in reperfusion strategies, the prognosis for AMI patients remains suboptimal. Early risk stratification and timely interventions are crucial for improving outcomes. Inflammation plays a pivotal role in the pathogenesis of atherosclerosis, and inflammatory biomarkers have emerged as potential predictors of adverse cardiovascular events. Among these biomarkers, the platelet to lymphocyte ratio (PLR) has gained attention for its association with CAD and its potential to predict major adverse cardiovascular events (MACEs).
This study aimed to investigate the association of PLR with in-hospital MACEs and the severity of CAD, as assessed by the Gensini score (GS), in patients with AMI undergoing coronary angiography. The study included 502 consecutive AMI patients admitted to the Affiliated Hospital of Qingdao University from August 2017 to December 2018. Patients were divided into two groups based on the occurrence of in-hospital MACEs: the MACE group (n = 81) and the non-MACE group (n = 421). Additionally, patients were classified into three groups according to tertiles of the GS: low GS group (GS ≤ 32 points, n = 173), medium GS group (32 < GS ≤ 60 points, n = 169), and high GS group (60 < GS ≤ 180 points, n = 160).
The study collected demographic, clinical, angiographic, and laboratory data. The primary statistical methods included the Chi-squared test, Mann-Whitney U test, Kruskal-Wallis H test, logistic regression, and receiver operating characteristic (ROC) curve analysis. The results demonstrated that PLR was significantly higher in the MACE group compared to the non-MACE group (179.43 vs. 116.11, P < 0.001). Moreover, PLR varied significantly across the GS tertiles, with the highest PLR observed in the high GS group (140.00 vs. 119.78 vs. 110.05, P < 0.001). Multivariate logistic regression analysis identified PLR as an independent risk factor for in-hospital MACEs (odds ratio [OR]: 1.012, 95% confidence interval [CI]: 1.006–1.018, P < 0.001) and severe CAD (OR: 1.004, 95% CI: 1.002–1.009, P = 0.042).
The ROC curve analysis determined that a PLR cutoff value of 151.28 predicted in-hospital MACEs with a sensitivity of 66.7% and specificity of 78.1% (area under the curve [AUC]: 0.786, 95% CI: 0.730–0.842, P 60 points) with a sensitivity of 49.4% and specificity of 69.6% (AUC: 0.611, 95% CI: 0.556–0.666, P < 0.001). These findings suggest that PLR, as an easily accessible and inexpensive inflammatory marker, can serve as a valuable tool for risk stratification and personalized treatment in AMI patients.
Introduction
AMI is a leading cause of morbidity and mortality worldwide, primarily driven by the rupture of atherosclerotic plaques or thrombosis, which results in acute coronary occlusion and myocardial necrosis. Despite significant advancements in reperfusion therapies, the outcomes for AMI patients remain unsatisfactory. Early identification of high-risk patients and timely interventions are essential for improving prognosis. Inflammation is a critical factor in the development and progression of atherosclerosis, and inflammatory biomarkers have been increasingly recognized for their predictive value in cardiovascular diseases.
Among these biomarkers, PLR has emerged as a promising indicator of inflammation and cardiovascular risk. PLR combines two critical components of the inflammatory response: platelets, which play a role in thrombosis and plaque destabilization, and lymphocytes, which regulate immune responses. Elevated PLR has been associated with adverse outcomes in various cardiovascular conditions, including CAD, heart failure, and acute coronary syndromes. This study aimed to explore the relationship between PLR and in-hospital MACEs, as well as the severity of CAD assessed by the GS, in AMI patients undergoing coronary angiography.
Methods
The study included 502 consecutive AMI patients admitted to the Affiliated Hospital of Qingdao University from August 2017 to December 2018. Patients were diagnosed with AMI based on the fourth universal definition of myocardial infarction. Exclusion criteria included prior AMI, coronary revascularization, significant cardiac diseases, hematological disorders, systemic inflammatory or autoimmune diseases, malignancy, severe renal or hepatic insufficiency, recent infections, and the use of anti-inflammatory medications.
Demographic, clinical, and laboratory data were collected, including age, sex, body mass index (BMI), smoking status, hypertension, diabetes mellitus (DM), and previous medications. Blood samples were collected for complete blood count analysis, and PLR was calculated as the ratio of platelet count to lymphocyte count. Coronary angiography was performed using the standard Judkin’s technique, and the severity of CAD was assessed using the GS. Patients were divided into two groups based on the occurrence of in-hospital MACEs and classified into three groups according to GS tertiles.
Results
The study population comprised 502 AMI patients, with 81 patients experiencing in-hospital MACEs. The MACE group had significantly higher PLR values compared to the non-MACE group (179.43 vs. 116.11, P < 0.001). Additionally, PLR varied significantly across the GS tertiles, with the highest PLR observed in the high GS group (140.00 vs. 119.78 vs. 110.05, P < 0.001). Multivariate logistic regression analysis identified PLR as an independent risk factor for in-hospital MACEs (OR: 1.012, 95% CI: 1.006–1.018, P < 0.001) and severe CAD (OR: 1.004, 95% CI: 1.002–1.009, P = 0.042).
ROC curve analysis determined that a PLR cutoff of 151.28 predicted in-hospital MACEs with a sensitivity of 66.7% and specificity of 78.1% (AUC: 0.786, 95% CI: 0.730–0.842, P 60 points) with a sensitivity of 49.4% and specificity of 69.6% (AUC: 0.611, 95% CI: 0.556–0.666, P < 0.001).
Discussion
The findings of this study highlight the significant association between PLR and in-hospital MACEs, as well as the severity of CAD assessed by the GS, in AMI patients. Elevated PLR was independently associated with adverse outcomes, suggesting its potential as a valuable biomarker for risk stratification and personalized treatment in AMI patients.
Platelets play a crucial role in the pathophysiology of atherosclerosis and thrombosis. Activated platelets contribute to plaque destabilization and thrombus formation, leading to acute coronary events. Lymphocytes, on the other hand, regulate immune responses and inflammation. A decrease in lymphocyte count has been associated with adverse outcomes in cardiovascular diseases, reflecting impaired immune regulation and increased inflammation.
The combination of elevated platelet count and decreased lymphocyte count, as reflected by PLR, provides a comprehensive measure of the inflammatory and thrombotic processes underlying AMI. The study demonstrated that PLR was significantly higher in patients experiencing in-hospital MACEs and those with severe CAD, as assessed by the GS. These findings are consistent with previous studies that have reported the predictive value of PLR in cardiovascular diseases.
The ROC curve analysis further validated the utility of PLR as a predictive marker for in-hospital MACEs and severe CAD. The identified cutoff values for PLR provide clinicians with practical thresholds for identifying high-risk patients and guiding therapeutic interventions. The study also highlighted the potential of PLR as an inexpensive and readily available biomarker that can be integrated into routine clinical practice for risk stratification in AMI patients.
Limitations
The study has several limitations. First, it was a single-center retrospective study with a relatively small sample size. Second, the study analyzed only the admission PLR, and the dynamic changes in PLR during the course of the disease were not evaluated. Third, the severity of CAD was assessed solely based on the GS, and other clinical characteristics, such as plaque vulnerability, were not considered. Future multi-center prospective studies are warranted to further validate the findings and explore the combined effects of PLR with other traditional risk factors.
Conclusion
In conclusion, this study demonstrated that PLR is significantly associated with in-hospital MACEs and the severity of CAD assessed by the GS in AMI patients. PLR, as an easily accessible and inexpensive inflammatory marker, can serve as a valuable tool for risk stratification and personalized treatment in AMI patients. The integration of PLR into routine clinical practice may enhance the identification of high-risk patients and improve the prognosis of AMI.
doi.org/10.1097/CM9.0000000000000650
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