Platelet‐to‐lymphocyte ratio a potential prognosticator in acute myocardial infarction: A prospective longitudinal study

Abstract Background The ratio of platelets to lymphocytes (PLR) can serve as a potential biomarker for predicting the prognosis of individuals with acute myocardial infarction (AMI). Aim The purpose of the research was to evaluate the in‐hospital outcomes of AMI patients and the predictive significance of PLR on major adverse cardiac events (MACE). Methods A total of 799 AMI patients who had successful primary PCI within 12 h of the onset of chest pain were separated into low PLR (n = 511) and high PLR (n = 288) groups using a PLR cutoff value of 178. At admission, total white blood cell, neutrophil, lymphocyte, and platelet counts were assessed. Results In patients with a high PLR group with PLR > 178, the incidence of MACE: heart rupture, acute heart failure, total adverse events, and mortality due to all events was considerably greater. In an analysis of the receiver operating characteristic curve, a high PLR > 178 accurately predicted adverse outcomes (73% specificity and 65% sensitivity). Age, hypertension, and PLR were found as independent predictors of adverse outcomes by multiple logistic regression. Conclusions AMI patients with high PLR had poor hospital outcomes. These findings recommend PLR as an independent risk factor for hospital‐acquired complications, suggesting that inflammation and prothrombotic state may contribute to the poor prognosis of high PLR patients.

improve the treatment of AMI and patients' prognoses by identifying prognostic and diagnostic biomarkers for early risk assessment and in-time therapeutic techniques. The relevance and importance of inflammatory processes in atherosclerosis have been shown by several research in both animals and humans. 4,5 Numerous studies have revealed a strong correlation between platelets to lymphocytes (PLR), a possible indicator of inflammation, and coronary artery disease (CAD), and concluded that PLR might serve as a valid predictor of mortality or major adverse cardiac events (MACEs) in addition to CAD. Similar to the potential marker NLR, neutrophil lymphocyte ratio, which reflects inflammation and the body's stress response via a decrease in the quantity of lymphocytes, 6-10 PLR, platelet lymphocyte ratio, also indicates inflammation and the activity of thrombotic processes via platelet or lymphocyte counts. 8,9,[11][12][13] Previous studies have demonstrated that NLR could serve as an emerging biomarker of the incidence and severity of acute coronary syndrome (ACS). 14,15 It has been reported that high NLR may lead to the incidence of cardiac events or even cardiac death in AMI patients. [15][16][17] However, whether PLR accurately predicts the prognostic outcome of patients with CAD is still controversial, and it still lacks knowledge about the connection between PLR and AMI.
Many researchers have indicated that elevated NLR is connected with higher clinical adverse events, whereas the PLR did not show this association or there is little knowledge of the association of PLR with clinical features of AMI. 18,19 This study is going to investigate the connection between the PLR and 30-day MACE with AMI patients following ST elevation myocardial infarction (STEMI) after they got successful PCI treatment.

| Setting
If the rise in troponin I is more than 1 ng/mL and J point is less than 2, the elevation of the new ST-segment is measured. In accordance with standards published by the American Heart Association and European Heart Association, discomfort within the first 12 h was classified as AMI. Individuals with any blood issue, including anemia, any systemic illness, regardless of whether it is caused by inflammation or autoimmunity, any renal or hepatic disease, cancer, or use of NSAIDs or steroids in the last 6 months will not be included.

| Participants
The research included AMI patients who had successful primary PCI within 12 h of the onset of chest symptoms. As the PLR cutoff value was 178, the patients (n = 799; male: 643, female: 156; mean age: 59.5−10.6 [SD] years) were divided into two groups. Participants signed the patient permission form after a thorough description of the projects' aims, advantages, and even potential risks.

| Variables
Patients included in the research were questioned on the presence of hyperlipidemia, hypertension, diabetes, and smoking. Patients' age, sex, weight, and height were recorded simultaneously. Hyperlipidemia was diagnosed when total cholesterol was higher than 200 mg/ dL, LDL was greater than 130 mg/dL, or triglycerides were greater than 150 mg/dL. Arterial hypertension was diagnosed when systolic or diastolic blood pressure exceeded 140 or 90 mmHg, respectively, more than twice, or when a history of antihypertensive drug use was present. Plasma glucose in the fasting state more than 126 mg/dL in any measurement, glycosylated hemoglobin fraction larger than 6.5%, or a history of using antidiabetic medication constituted hypertension. Current heavy cigarette consumers were smokers. On admission, we collect a blood sample from the patient and analyze it to determine the number of various cell types.

| Coronary angiography
The Gensini score is examined by two interventional cardiologists who protect the confidentiality of clinical information throughout the coronary angiography evaluation. If the stenosis of the infarct artery is less than 30% and the thrombolytic therapy of the myocardial infarction is effective, we consider the operation a success. Before conducting the coronary intervention, the patient is given aspirin and loading dosages of clopidogrel or troglitazone (300 and 300/180 mg, respectively). The patient mandated to continue taking clopidogrel (75 mg/day) or troglitazone (90 mg/day) for more than 1 year and aspirin (100 mg/day) for life after the operation. Other drugs, including low molecular weight heparin, ACEI/ARBs, IIb/IIIa receptor antagonists, beta-blockers, and nitrates, must be administered as prescribed.

| Statistical analysis
The graphical data were compared using the 22 χ 2 test, while the measurement data were analyzed using the two-sample t-test. Using ROC curves, the sensitivity and specificity of PLR and NLR for predicting 30-day MACE were determined. Multivariate logistic models examining independent correlations between NLR or PLR and 30-day MACE were adjusted for the following variables: age, sex, history of hyperlipidemia, hypertension, and diabetes, smoking, and BMI. Last but not least, Kaplan−Meier (KM) curves were created to quantify the cumulative risk of MACE 30 days after admission, and log-rank tests were then performed to examine the predictive ability of NLR and PLR. SPSS 16.0 was used to conduct statistical analysis.

| Clinical outcomes
The PLR ratio is calculated by dividing the absolute platelet count by the absolute lymphocyte count. It is a novel inflammatory marker that has the potential to be employed in the prediction of inflammation and mortality in a variety of disorders.  Table 2

| ROC curve analysis
As illustrated in Figure 1, ROC analysis revealed that the PLR cutoff value was 178, with 65% sensitivity and 73% specificity for According to the correlation study, PLR shows a positive connection with NLR (r = .267, p = .001).

| Multivariate analysis
In the modified multivariate logistic model, NLR and PLR continue to correlate independently with 30-day MACE (Table 3). For the purpose of analyzing "time-to-event" data, the KM approach is utilized. The all-cause mortality rate is frequently included as the outcome in KM analyses; however, alternative outcomes, such as the occurrence of a cardiovascular event, could also be included. KM analysis, as seen in Figure 2, further corroborated this finding.
Specifically, those with a PLR larger than 178 had a higher accumulative risk of 30-day MACE (log rank, p .001). With the exception of the lymphocyte count, all the previously stated blood parameters, NLR and PLR, were more prevalent in the high-PLR T A B L E 1 Comparison of major adverse cardiac events between of the study groups.

| DISCUSSION
Platelets are essential components of thrombosis and have been linked to the development and progression of coronary thrombosis. 21 Platelets also play an essential part in the development of atherosclerosis. 22 In AMI patients, an increase in platelet count is related with an increase in infarct size and worsening. 23 More platelets at baseline are related with a worse outcome in AMI patients. 24,25 However, lymphocytes act as a controlled and static inflammatory pathway, which is suggestive of a repressed immune response. 26 PLR provides an insight of pathways associated with aggregation and inflammation. It may serve as an indicator of thrombotic and inflammatory processes that cause heart damage. 27  Formal analysis and writing-reviewing and editing.